query: neurons that release norepinephrine as a neurotransmitter are called

pos: Norepinephrine and Kjell Fuxe, who assigned them labels starting with the letter "A" (for "aminergic"). In their scheme, areas A1 through A7 contain the neurotransmitter norepinephrine (A8 through A14 contain dopamine). Noradrenergic cell group A1 is located in the caudal ventrolateral part of the medulla, and plays a role in the control of body fluid metabolism. Noradrenergic cell group A2 is located in a brainstem area called the solitary nucleus; these cells have been implicated in a variety of responses, including control of food intake and responses to stress. Cell groups A5 and A7 project mainly to the spinal cord. The

pos: Norepinephrine less costly in terms of energy expenditure. The sympathetic effects of norepinephrine include: The noradrenergic neurons in the brain form a neurotransmitter system, that, when activated, exerts effects on large areas of the brain. The effects are manifested in alertness, arousal, and readiness for action. Noradrenergic neurons (i.e., neurons whose primary neurotransmitter is norepinephrine) are comparatively few in number, and their cell bodies are confined to a few relatively small brain areas, but they send projections to many other brain areas and exert powerful effects on their targets. These noradrenergic cell groups were first mapped in 1964 by Annica Dahlström

pos: Motor neuron PNS, which synapses onto the muscle. All vertebrate motor neurons are cholinergic, that is, they release the neurotransmitter acetylcholine. Parasympathetic ganglionic neurons are also cholinergic, whereas most sympathetic ganglionic neurons are noradrenergic, that is, they release the neurotransmitter noradrenaline. (see Table) Motor neuron A motor neuron (or motoneuron) is a neuron whose cell body is located in the motor cortex, brainstem or the spinal cord, and whose axon (fiber) projects to the spinal cord or outside of the spinal cord to directly or indirectly control effector organs, mainly muscles and glands. There are two types of motor neuron – upper

pos: Henry Hallett Dale for Medicine. During the 1940s Dale was embroiled in the scientific debate over the nature of signaling at the synapse. Dale and others believed that signaling at the synapse was chemical, while John Carew Eccles and others believed that the synapse was electrical. It was later found that most synaptic signalling is chemical, but there are some synapses that are electrical. Dale also originated the scheme used to differentiate neurons according to the neurotransmitters they release. Thus, neurons releasing noradrenaline (known in the United States as norepinephrine) are called noradrenergic, neurons releasing GABA are GABAergic, and so on. This is

pos: Norepinephrine transporter cotransport with Na and Cl. The sequential binding of the ions results in the eventual reuptake of norepinephrine. The ion gradients of Na and Cl make this reuptake energetically favorable. The gradient is generated by the Na+/K+-ATPase which transports three sodium ions out and two potassium ions into the cell. NETs have conductances similar to those of ligand-gated ion channels. The expression of NET results in a leak-channel activity. NETs are restricted to noradrenergic neurons and are not present on neurons that release dopamine or epinephrine. The transporters can be found along the cell body, axons, and dendrites of the

pos: Arousal cortex. When stimulated, these systems produce cortical activity and alertness. The noradrenergic system is a bundle of axons that originate in the locus coeruleus and ascends up into the neocortex, limbic system, and basal forebrain. Most of the neurons are projected to the posterior cortex which is important with sensory information, and alertness. The activation of the locus coeruleus and release of norepinephrine causes wakefulness and increases vigilance. The neurons that project into the basal forebrain impact cholinergic neurons that results in a flood of acetylcholine into the cerebral cortex. The acetylcholinergic system has its neurons located in the pons

pos: Nitrous oxide also potentiate the antinociceptive effects of . Several experiments have shown that opioid receptor antagonists applied directly to the brain block the antinociceptive effects of , but these drugs have no effect when injected into the spinal cord. Conversely, α-adrenoceptor antagonists block the pain-reducing effects of when given directly to the spinal cord, but not when applied directly to the brain. Indeed, α-adrenoceptor knockout mice or animals depleted in norepinephrine are nearly completely resistant to the antinociceptive effects of . Apparently -induced release of endogenous opioids causes disinhibition of brain stem noradrenergic neurons, which release norepinephrine into the spinal cord

neg: Neurotransmitter neurons that use the transmitter, and the chemical properties of the receptors that the transmitter binds to. Here are a few examples of important neurotransmitter actions: Neurons expressing certain types of neurotransmitters sometimes form distinct systems, where activation of the system affects large volumes of the brain, called volume transmission. Major neurotransmitter systems include the noradrenaline (norepinephrine) system, the dopamine system, the serotonin system, and the cholinergic system, among others. Trace amines have a modulatory effect on neurotransmission in monoamine pathways (i.e., dopamine, norepinephrine, and serotonin pathways) throughout the brain via signaling through trace amine-associated receptor 1. A brief comparison

neg: Neurotransmitter release and prevent neurotransmitter reuptake. Amphetamine, for example, is an indirect agonist of postsynaptic dopamine, norepinephrine, and serotonin receptors in each their respective neurons; it produces both neurotransmitter release into the presynaptic neuron and subsequently the synaptic cleft and prevents their reuptake from the synaptic cleft by activating TAAR1, a presynaptic G protein-coupled receptor, and binding to a site on VMAT2, a type of monoamine transporter located on synaptic vesicles within monoamine neurons. An antagonist is a chemical that acts within the body to reduce the physiological activity of another chemical substance (as an opiate); especially one that opposes the

neg: Attentional blink processing. According to the LC-NE hypothesis, when a salient, or meaningful stimulus is presented, neurons in the locus coeruleus release norepinephrine, a neurotransmitter that benefits the detection of the stimulus. The effect of this release lasts for 100 ms after the salient stimulus is presented and benefits the second target when presented immediately after the first one, accounting for lag 1 sparing. Eventually the neurons in the locus coeruleus enter a refractory period, due to the auto-inhibitory effect of norepinephrine. According to the hypothesis, targets presented during this refractory period cannot trigger a release of norepinephrine, resulting in the attentional

neg: Autoreceptor of the cell membrane: in the dendrites, the cell body, the axon, or the axon terminals. Canonically, a presynaptic neuron releases a neurotransmitter across a synaptic cleft to be detected by the receptors on a postsynaptic neuron. Autoreceptors on the presynaptic neuron will also detect this neurotransmitter and often function to control internal cell processes, typically inhibiting further release or synthesis of the neurotransmitter. Thus, release of neurotransmitter is regulated by negative feedback. Autoreceptors are usually G protein-coupled receptors (rather than transmitter-gated ion channels) and act via a second messenger. As an example, norepinephrine released from sympathetic neurons may interact

neg: PGO waves is what keeps PGO wave amplitudes at very low levels during periods of a mammal being awake. The three specific aminergic neurotransmitters are serotonin, dopamine and norepinephrine. Cholinergic neurons are neurons that use acetylcholine as a neurotransmitter. Through different studies, these types of neurons have been proven to promote PGO wave generation, thus being an excitatory neuromodulator for triggering neurons. Nitroxergic neurons use nitric oxide (NO) as a neurotransmitter. In theory, the increase of nitric oxide is seen as an excitatory neuromodulator in PGO wave generation. This stems from animal testing that has shown increases in PGO waves as nitric

neg: Guanadrel Guanadrel Guanadrel is an antihypertensive agent. It is used in the form of its sulfate. Guanadrel is a postganglionic adrenergic blocking agent. Uptake of guanadrel and storage in sympathetic neurons occurs via the norepinephrine pump; guanadrel slowly displaces norepinephrine from its storage in nerve endings and thereby blocks the release of norepinephrine normally produced by nerve stimulation. The reduction in neurotransmitter release in response to sympathetic nerve stimulation, as a result of catecholamine depletion, leads to reduced arteriolar vasoconstriction, especially the reflex increase in sympathetic tone that occurs with a change in position. Guanadrel is rapidly and well absorbed from

neg: Clonidine (PFC), among other areas. The alpha-2A adrenergic receptors are found on the presynaptic cleft of a given neuron, and, when activated by an agonist, the effect on downstream neurons is inhibitory. The inhibition is accomplished by preventing the secretion of the neurotransmitter norepinephrine. Thus, clonidine's agonism on alpha-2A adrenergic receptors in the PFC inhibits the action of downstream neurons by preventing the secretion of norepinephrine. This mechanism is similar to the brain's physiological inhibition of PFC neurons by the locus ceruleus (LC), which secretes norepinephrine into the PFC. Although norepinephrine can also bind to target adrenergic receptors on the downstream

neg: Dale's principle this form it is certainly false. Many neurons release more than one neurotransmitter, in what is called "cotransmission". Although there were earlier hints, the first formal proposal of this discovery did not come until 1976. Most neurons release several different chemical messengers. In modern neuroscience, neurons are often classified by their neurotransmitter and most important cotransmitter, for example striatal GABA neurons utilize either opioid peptides or substance P as the primary cotransmitter. In a 1976 publication, however, Eccles interpreted the principle in a subtly different way: "I proposed that Dale’s Principle be defined as stating that at all the axonal

neg: Catecholamine such as norepinephrine have a hydroxyl group on the ethyl chain. Catecholamines are produced mainly by the chromaffin cells of the adrenal medulla and the postganglionic fibers of the sympathetic nervous system. Dopamine, which acts as a neurotransmitter in the central nervous system, is largely produced in neuronal cell bodies in two areas of the brainstem: the ventral tegmental area and the substantia nigra, the latter of which contains neuromelanin-pigmented neurons. The similarly neuromelanin-pigmented cell bodies of the locus ceruleus produce norepinephrine. Epinephrine is produced in small groups of neurons in the human brain which express its synthesizing enzyme, phenylethanolamine

neg: PC12 cell line moles of neurotransmitter released. The vesicles hold catecholamines, mostly dopamine but also limited amount of norepinephrine, and release of these neurotransmitters give rise to spikes due to changes in current similar to chromaffin cells. PC12 cell line use has given much information to the function of proteins underlying vesicle fusion. This cell line has been used to understand the role of synaptotagmin in vesicle-cell membrane fusion. Their embryological origin with neuroblastic cells means they can easily differentiate into neuron-like cells even though they are not considered adult neurons. Neuron-like means they share properties similar to neurons, in this case it

neg: Vesicular monoamine transporter 2 Vesicular monoamine transporter 2 The vesicular monoamine transporter 2 (VMAT2) also known as solute carrier family 18 member 2 (SLC18A2) is a protein that in humans is encoded by the "SLC18A2" gene. VMAT2 is an integral membrane protein that transports monoamines—particularly neurotransmitters such as dopamine, norepinephrine, serotonin, and histamine—from cellular cytosol into synaptic vesicles. In nigrostriatal pathway and mesolimbic pathway dopamine-releasing neurons, VMAT2 function is also necessary for the vesicular release of the neurotransmitter GABA. VMAT2 is believed to possess at least two distinct binding sites, which are characterized by tetrabenazine (TBZ) and reserpine binding to the transporter. Amphetamine (TBZ

neg: Locus coeruleus ceruleus The norepinephrine from locus ceruleus cells in addition to its neurotransmitter role locally diffuses from "varicosities". As such it provides an endogenous anti-inflammatory agent in the microenvironment around the neurons, glial cells, and blood vessels in the neocortex and hippocampus. It has been shown that norepinephrine stimulates mouse microglia to suppress Aβ-induced production of cytokines and promotes phagocytosis of Aβ. This suggests that degeneration of the locus ceruleus might be responsible for increased Aβ deposition in AD brains. Degeneration of pigmented neurons in this region in Alzheimer's and Parkinson's disease can be visualized in vivo with Neuromelanin MRI. It

neg: Norepinephrine In 1945 Ulf von Euler published the first of a series of papers that established the role of norepinephrine as a neurotransmitter. He demonstrated the presence of norepinephrine in sympathetically innervated tissues and brain, and adduced evidence that it is the "sympathin" of Cannon and Rosenblueth. Norepinephrine Noradrenaline (NA), also called norepinephrine (NE) or noradrenalin, is an organic chemical in the catecholamine family that functions in the brain and body as a hormone and neurotransmitter. The name "noradrenaline", derived from Latin roots meaning "at/alongside the kidneys", is more commonly used in the United Kingdom; in the United States, "norepinephrine," derived

neg: Dopaminergic pathways SNc. The excitatory orexinergic inputs to the VTA originate in the lateral hypothalamus and may regulate the baseline firing of VTA dopaminergic neurons. Dopaminergic pathways Dopaminergic pathways, sometimes called dopaminergic projections, are the sets of projection neurons in the brain that synthesize and release the neurotransmitter dopamine. Individual neurons in these pathways are referred to as dopamine neurons. Dopamine neurons have axons that run the entire length of the pathway. The neurons' somata produce the enzymes that synthesize dopamine, and they are then transmitted via the projecting axons to their synaptic destinations, where most of the dopamine is produced. Dopaminergic

neg: TAAR1 efflux. Consequently, the efficacy of a particular TAAR1 ligand in producing these effects in different monoamine neurons is a function of both its binding affinity at TAAR1 and its capacity to move across the presynaptic membrane at each type of neuron. The variability between a TAAR1 ligand's substrate affinity at the various monoamine transporters accounts for much of the difference in its capacity to produce neurotransmitter release and reuptake inhibition in different types of monoamine neurons. E.g., a TAAR1 ligand which can easily pass through the norepinephrine transporter, but not the serotonin transporter, will produce – all else equal –

neg: Dopaminergic pathways Dopaminergic pathways Dopaminergic pathways, sometimes called dopaminergic projections, are the sets of projection neurons in the brain that synthesize and release the neurotransmitter dopamine. Individual neurons in these pathways are referred to as dopamine neurons. Dopamine neurons have axons that run the entire length of the pathway. The neurons' somata produce the enzymes that synthesize dopamine, and they are then transmitted via the projecting axons to their synaptic destinations, where most of the dopamine is produced. Dopaminergic nerve cell bodies in such areas as the substantia nigra pars compacta tend to be pigmented due to the presence of the black

neg: Monoamine neurotransmitter It has also been found that monoamine neurotransmitters play an important role in the secretion and production of neurotrophin-3 by astrocytes, a chemical which maintains neuron integrity and provides neurons with trophic support. Drugs used to increase (or reduce) the effect of monoamine neurotransmitters are used to treat patients with psychiatric and neurological disorders, including depression, anxiety, schizophrenia and Parkinson's disease. Specific transporter proteins called monoamine transporters that transport monoamines in or out of a cell exist. These are the dopamine transporter (DAT), serotonin transporter (SERT), and the norepinephrine transporter (NET) in the outer cell membrane and the vesicular monoamine

neg: Quantal neurotransmitter release release and instead use gap junctions between neurons to send current flows between neurons. The goal of any synapse is to produce either an excitatory postsynaptic potential (EPSP) or an inhibitory postsynaptic potential (IPSP), which generate or repress the expression, respectively, of an action potential in the postsynaptic neuron. It is estimated that an action potential will trigger the release of approximately 20% of an axon terminal's neurotransmitter load. Neurotransmitters are synthesized in the axon terminal where they are stored in vesicles. These neurotransmitter-filled vesicles are the quanta that will be released into the synapse. Quantal vesicles release their contents

neg: Tamas Bartfai release first norepinephrine at 0.5–3 Hz and then neuropeptide Y at 3–20 Hz stimulation. Both neurotransmitters cause vasoconstriction, but the effects of norepinephrine are now widely prolonged by neuropeptide Y. Their work showed that the chemical palette of neurons were expanded qualitatively and frequency dependently. Cytokines, such as interleukin-1 can be synthesized and released by neurons. Bartfai's group showed interleukin-1, then called the endogenous pyrogen, is released from the adrenal medulla and brain and demonstrated that the endogenous pyrogen can control body temperature by acting at receptors and hyperpolarizing hypothalamic gabaergic interneurons that control thermogenesis in brown adipose tissue, and

neg: Monoamine releasing agent releaser of dopamine (~6- and 10-fold lower for dopamine than norepinephrine or serotonin, respectively). Even more selective include agents like fenfluramine, a selective SRA, and ephedrine, a selective NRA. The differences in selectivity of these agents is the result of different affinities as substrates for the monoamine transporters, and thus differing ability to gain access into monoaminergic neurons and induce monoamine neurotransmitter release via the TAAR1 and VMAT2 proteins. As of present, no selective DRAs are known. This is because it has proven extremely difficult to separate DAT affinity from NET affinity and retain releasing efficacy at the same time.

neg: Norepinephrine Norepinephrine Noradrenaline (NA), also called norepinephrine (NE) or noradrenalin, is an organic chemical in the catecholamine family that functions in the brain and body as a hormone and neurotransmitter. The name "noradrenaline", derived from Latin roots meaning "at/alongside the kidneys", is more commonly used in the United Kingdom; in the United States, "norepinephrine," derived from Greek roots having that same meaning, is usually preferred. "Norepinephrine" is also the international nonproprietary name given to the drug. Regardless of which name is used for the substance itself, parts of the body that produce or are affected by it are referred to as

neg: Cell signaling Norepinephrine can also be produced by neurons to function as a neurotransmitter within the brain. Estrogen can be released by the ovary and function as a hormone or act locally via paracrine or autocrine signaling. Active species of oxygen and nitric oxide can also act as cellular messengers. This process is dubbed redox signaling. In a multicellular organism, signaling between cells occurs either through release into the extracellular space, divided in paracrine signaling (over short distances) and endocrine signaling (over long distances), or by direct contact, known as juxtacrine signaling. Autocrine signaling is a special case of paracrine signaling where

neg: Norepinephrine beta receptors into subtypes β, β, and β. All of these function as G protein-coupled receptors, meaning that they exert their effects via a complex second messenger system. Alpha-2 receptors usually have inhibitory effects, but many are located pre-synaptically (i.e., on the surface of the cells that release norepinephrine), so the net effect of alpha-2 activation is often a decrease in the amount of norepinephrine released. Alpha-1 receptors and all three types of beta receptors usually have excitatory effects. Inside the brain norepinephrine functions as a neurotransmitter, and is controlled by a set of mechanisms common to all monoamine neurotransmitters.

neg: Autonomic nervous system and digest" response, promotes calming of the nerves return to regular function, and enhancing digestion. Functions of nerves within the parasympathetic nervous system include: The enteric nervous system is the intrinsic nervous system of the gastrointestinal system. It has been described as "the Second Brain of the Human Body". Its functions include: At the effector organs, sympathetic ganglionic neurons release noradrenaline (norepinephrine), along with other cotransmitters such as ATP, to act on adrenergic receptors, with the exception of the sweat glands and the adrenal medulla: A full table is found at Table of neurotransmitter actions in the ANS. Caffeine is

neg: Olfactory memory responsiveness to an odor as a result of prolonged exposure (restricted to a certain repeated stimulus), which involves adaptation of cells in the olfactory system. Receptor neurons and mitral cells located in the olfactory system adapt in response to odors. This includes the involvement of piriform cortical neurons which adapt rapidly, more completely and selectively to novel odors and are also thought to play a very important role in the habituation of odors. Norepinephrine is considered to have an effect on the functioning of the mitral cells by increasing their responsiveness. Acetylcholine is also regarded as an important neurotransmitter involved

neg: Glutamate-glutamine cycle Glutamate-glutamine cycle In biochemistry, the glutamate-glutamine cycle is a sequence of events by which an adequate supply of the neurotransmitter glutamate is maintained in the central nervous system. Neurons are unable to synthesize either the neurotransmitter glutamate or γ-aminobutyric acid (GABA) from glucose. Discoveries of glutamine and glutamate pools within intercellular compartments led to suggestions of the glutamate-glutamine cycle working between neurons and astrocytes. The glutamate/GABA-glutamine cycle is a metabolic pathway that describes the release of glutamate or GABA from neurons which are then taken up into astrocytes (star-shaped glial cells). In return, astrocytes release glutamine to be taken up

neg: Hypofrontality and mediodorsal thalamus) can be, in part, explained. Dopaminergic activity is the release (or lack thereof) of the neurotransmitter dopamine and the resulting cellular responses. The limbic striatum and mediodorsal thalamus (parts of the brain) have connections with a part of the prefrontal cortex called the corticolimbothalamic circuit. The corticolimbothalamic circuit has a high concentration of GABAergic interneurons, which are neurons that predominantly work with the inhibitory neurotransmitter GABA. As a result of the impaired synaptic connections, the GABAergic interneurons of the corticolimbothalamic circuit would adapt to release increasingly high amounts of GABA to send a signal of the correct

neg: Neurotransmitter receptor associated G-protein by exchanging its bound GDP for a GTP. The G-protein's α subunit, together with the bound GTP, can then dissociate from the β and γ subunits to further affect intracellular signaling proteins or target functional proteins directly depending on the α subunit type (G, G, G, G). Neurotransmitter receptors are subject to ligand-induced desensitization: That is, they can become unresponsive upon prolonged exposure to their neurotransmitter. Neurotransmitter receptors are present on both postsynaptic neurons "and" presynaptic neurons with the former being used to receive neurotransmitters and the latter for the purpose of preventing further release of a given

neg: Wade Regehr dye alters the fluorenscence properties when attached to calcium, and changes in intracellular calcium are associated with neuronal activity (firing of action potentials). Using fluorescence-microscopy techniques, calcium levels are detected, and therefore the influx of calcium in the presynaptic neuron. Calcium processes affect the release of neurotransmitter from the axon terminal. (Occasionally this happens in reverse). Chemical synapses are characterized by the presynaptic release of neurotransmitters that diffuse across a synaptic cleft to bind with postsynaptic receptors. A neurotransmitter is a chemical messenger that is synthesized within neurons themselves and released by these same neurons to communicate with their postsynaptic

neg: Grey column structure, are islet, central, vertical, and radial cells. The interneurons can also be divided by their function: excitatory or inhibitory. The excitatory interneurons release glutamate as their main neurotransmitter and the inhibitory interneurons use GABA and/or glycine as their main neurotransmitter. The neurons of this layer are only C fibers and contain almost no myelin. These laminae are also known as the nucleus proprius and contain a much smaller density of neurons than lamina II. There are projection neurons scattered throughout these layers. Mechanosensitive A beta fibers terminate in these layers. The layers receive input from lamina II and also

neg: Neurotransmitter in some cases, a neurotransmitter utilizes retrograde neurotransmission, a type of feedback signaling in neurons where the neurotransmitter is released postsynaptically and binds to target receptors located on the presynaptic neuron. Nicotine, a compound found in tobacco, is a direct agonist of most nicotinic acetylcholine receptors, mainly located in cholinergic neurons. Opiates, such as morphine, heroin, hydrocodone, oxycodone, codeine, and methadone, are μ-opioid receptor agonists; this action mediates their euphoriant and pain relieving properties. Indirect agonists increase the binding of neurotransmitters at their target receptors by stimulating the release or preventing the reuptake of neurotransmitters. Some indirect agonists trigger neurotransmitter

neg: Quantal neurotransmitter release receptors that neurons are able to send a plethora of potential signals to each other. Estimations of quantal release time courses can be roughly estimated from the original quantal release events following presynaptic simulation. Such estimations cannot be reliably used in all synapses, but can be useful tools in developing the understanding of neurotransmitter release time courses in general. As described above, the synaptic vesicle will remain fused to the presynaptic membrane after its neurotransmitter contents have been released into the synapse. The repeated additions to the axon terminal membrane would eventually result in the uncontrolled growth of the axon

neg: Gonadotropin-releasing hormone so they receive shared synaptic input, a process that allows them to synchronize their GnRH release. The GnRH neurons are regulated by many different afferent neurons, using several different transmitters (including norepinephrine, GABA, glutamate). For instance, dopamine appears to stimulate LH release (through GnRH) in estrogen-progesterone-primed females; dopamine may inhibit LH release in ovariectomized females. Kisspeptin appears to be an important regulator of GnRH release. GnRH release can also be regulated by estrogen. It has been reported that there are kisspeptin-producing neurons that also express estrogen receptor alpha. GnRH is found in organs outside of the hypothalamus and pituitary, and

neg: Neuron of the neurons in the brain release either glutamate or GABA, these labels encompass the great majority of neurons. There are also other types of neurons that have consistent effects on their targets, for example, "excitatory" motor neurons in the spinal cord that release acetylcholine, and "inhibitory" spinal neurons that release glycine. The distinction between excitatory and inhibitory neurotransmitters is not absolute, however. Rather, it depends on the class of chemical receptors present on the postsynaptic neuron. In principle, a single neuron, releasing a single neurotransmitter, can have excitatory effects on some targets, inhibitory effects on others, and modulatory effects

neg: Norepinephrine can either be broken down by monoamine oxidase or repackaged into vesicles by VMAT, making it available for future release. Norepinephrine is the main neurotransmitter used by the sympathetic nervous system, which consists of about two dozen sympathetic chain ganglia located next to the spinal cord, plus a set of prevertebral ganglia located in the chest and abdomen. These sympathetic ganglia are connected to numerous organs, including the eyes, salivary glands, heart, lungs, liver, gallbladder, stomach, intestines, kidneys, urinary bladder, reproductive organs, muscles, skin, and adrenal glands. Sympathetic activation of the adrenal glands causes the part called the adrenal medulla

neg: Reverse transport the cytosol of a neuron or glial cell. When these transporters operate in reverse, they produce neurotransmitter efflux (i.e., the movement of neurotransmitters from the cytosol to the extracellular space via transporter-mediated release, as opposed to exocytotic release). In neurons, transporter reversal facilitates the release of neurotransmitters into the synaptic cleft, resulting in a higher concentration of synaptic neurotransmitters and increased signaling through the corresponding neurotransmitter receptors. For example, many monoamine releasing agents cause monoamine neurotransmitter efflux (i.e., the release of monoamine neurotransmitters from neurons into the synaptic cleft via monoamine transporter-mediated release) by triggering reverse transport at vesicular monoamine

neg: Serotonin–norepinephrine–dopamine reuptake inhibitor limbic structures of the brain. Its existence was proved by demonstration of the "pleasure centers," that were discovered as the location from which electrical self-stimulation is readily evoked. The main neurotransmitter involved in the reward is dopamine, but other monoamines and acetylcholine may also participate. The anatomical core of the reward system are dopaminergic neurons of the ventral tegmentum that project to the nucleus accumbens, amygdala, prefrontal cortex and other forebrain structures. There are several groups of substances that activate the reward system and they may produce addiction, which in humans is a chronic, recurrent disease, characterized by absolute dominance

neg: Neurotransmitter the dopamine system. The addictive opiate drugs exert their effects primarily as functional analogs of opioid peptides, which, in turn, regulate dopamine levels. Neurons form elaborate networks through which nerve impulses—action potentials—travel. Each neuron has as many as 15,000 connections with neighboring neurons. Neurons do not touch each other (except in the case of an electrical synapse through a gap junction); instead, neurons interact at contact points called synapses: a junction within two nerve cells, consisting of a miniature gap within which impulses are carried by a neurotransmitter. A neuron transports its information by way of a nerve impulse called

neg: Serotonin–norepinephrine reuptake inhibitor by autoreceptors through the rate-limiting enzyme tyrosine hydroxylase, an effect mediated by decreased cyclic AMP-mediated phosphorylation-activation of the enzyme. α receptors also cause decreased intracellular cyclic AMP expression which results in smooth muscle relaxation or decreased secretion. TCAs activate a negative feedback mechanism through their effects on presynaptic receptors. One probable explanation for the effects on decreased neurotransmitter release is that, as the receptors activate, inhibition of neurotransmitter release occurs (including suppression of voltage-gated Ca currents and activation of G protein-coupled receptor-operated K currents). Repeated exposure of agents with this type of mechanism leads to inhibition of neurotransmitter release, but

neg: Pars reticulata Pars reticulata The pars reticulata is a portion of the substantia nigra. Most of the neurons that project out of the pars reticulata are inhibitory GABAergic neurons (i.e., these neurons release GABA, which is an inhibitory neurotransmitter). Neurons in the pars reticulata are much less densely packed than those in the pars compacta (they were sometimes named pars diffusa). They are smaller and thinner than the dopaminergic neurons and conversely identical and morphologically similar to the pallidal neurons (see primate basal ganglia). Their dendrites as well as the pallidal are preferentially perpendicular to the striatal afferents. The massive striatal afferents

neg: Familial hemiplegic migraine by creating a R192Q knock-in mouse. They confirmed that the R192Q mutant activates at more negative potentials and that neurons producing these channels have much larger whole-cell current. This resulted in a much larger quantal content (the number of neurotransmitter packets released per action potential) and generally enhanced neurotransmitter release in R192Q expressing neurons versus wild-type. Consequently, these mutant mice were more susceptible to cortical-spreading-depression than their wild-type counterparts. The most recent experiments on this mutant, however, have contradicted some of these results. In Ca2.1 knockout neurons transfected with human channels, P/Q-type currents from mutant channels are actually smaller than

neg: Locus coeruleus the LC, in particular the pontine raphe nucleus and dorsal raphe nucleus. The locus coeruleus receives inputs from a number of other brain regions, primarily: The projections from the locus coeruleus consist of neurons that utilize norepinephrine as their primary neurotransmitter. These projections include the following connections: It is related to many functions via its widespread projections. The LC-NA system modulates cortical, subcortical, cerebellar, brainstem, and spinal cord circuits. Some of the most important functions influenced by this system are: The locus coeruleus is a part of the reticular activating system, and is almost completely inactivated in rapid eye movement

neg: Caffeine-induced anxiety disorder proteins which activate adenylate cyclase and some voltage gated Ca channels. A receptors are located in dopamine rich brain regions. A receptor mRNA was found in the same neurons as the dopamine receptor D within the dorsal striatum, nucleus accumbens and tuberculum olfactorium. A receptors are not found in neurons that express the dopamine receptor D receptors and Substance P. Within the striatum, part of the basal ganglia, activation of A receptors by adenosine increases GABA release, an inhibitory neurotransmitter. When caffeine binds to the receptor, less inhibitory neurotransmitter is released, supporting caffeine’s role as a central nervous system stimulant.

neg: Psychopharmacology amino acid neurotransmitter. The reinforcing qualities of alcohol leading to repeated use – and thus also the mechanisms of withdrawal from chronic alcohol use – are partially due to the substance’s action on the dopamine system. This is also due to alcohol’s effect on the opioid systems, or endorphins, that have opiate-like effects, such as modulating pain, mood, feeding, reinforcement, and response to stress. Antidepressants reduce symptoms of mood disorders primarily through the regulation of norepinephrine and serotonin (particularly the 5-HT receptors). After chronic use, neurons adapt to the change in biochemistry, resulting in a change in pre- and postsynaptic

neg: Psychopharmacology effects almost entirely by acting on neurotransmitters and by modifying one or more aspects of synaptic transmission. Neurotransmitters can be viewed as chemicals through which neurons primarily communicate; psychoactive drugs affect the mind by altering this communication. Drugs may act by 1) serving as a precursor for the neurotransmitter; 2) inhibiting neurotransmitter synthesis; 3) preventing storage of neurotransmitter in the presynaptic vesicle; 4) stimulating or inhibiting neurotransmitter release; 5) stimulating or blocking post-synaptic receptors; 6) stimulating autoreceptors, inhibiting neurotransmitter release; 7) blocking autoreceptors, increasing neurotransmitter release; 8) inhibiting neurotransmission breakdown; or 9) blocking neurotransmitter reuptake by the presynaptic neuron. The

neg: Occipital horn syndrome Such individuals also often endure inconvenient dysautonomic signs and symptoms related to a partial deficiency in dopamine-β-hydroxylase (DBH) activity. DBH, another copper-dependent enzyme, normally converts dopamine to norepinephrine, a crucial neurotransmitter in norepinephrinergic neurons. A natural mouse model of OHS, the so-called mottled blotchy model, recapitulates the connective tissue abnormalities, DBH deficiency and mild CNS damage seen in humans. The initial diagnosis of Menkes disease (MD) and its milder variants such as Occipital Horn Syndrome is based on the clinical symptoms. Low serum copper and ceruloplasmin levels support the clinical suspicion of OHS, but biochemical confirmation in tissue culture is

neg: Heart that lies over the heart called the cardiac plexus. The vagus nerve is a long, wandering nerve that emerges from the brainstem and provides parasympathetic stimulation to a large number of organs in the thorax and abdomen, including the heart. The nerves from the sympathetic trunk emerge through the T1-T4 thoracic ganglia and travel to both the sinoatrial and atrioventricular nodes, as well as to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (also known as noradrenaline) at the neuromuscular junction of the

neg: Active zone Active zone The active zone or synaptic active zone is a term first used by Couteaux and Pecot-Dechavassinein in 1970 to define the site of neurotransmitter release. Two neurons make near contact through structures called synapses allowing them to communicate with each other. As shown in the adjacent diagram, a synapse consists of the presynaptic bouton of one neuron which stores vesicles containing neurotransmitter (uppermost in the picture), and a second, postsynaptic neuron which bears receptors for the neurotransmitter (at the bottom), together with a gap between the two called the synaptic cleft (with synaptic adhesion molecules, SAMs, holding the

neg: Vertigo discharge of the central vestibular neurons and may modulate synaptic transmission in all three neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. Gamma-Aminobutyric acid (GABA) is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections between the cerebellar Purkinje cells, and the lateral vestibular nucleus, and the vertical VOR. Three other neurotransmitters work centrally. Dopamine may accelerate vestibular compensation. Norepinephrine modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. Histamine is present only centrally, but its role is unclear. Dopamine,

neg: Neuron on others still. For example, photoreceptor cells in the retina constantly release the neurotransmitter glutamate in the absence of light. So-called OFF bipolar cells are, like most neurons, excited by the released glutamate. However, neighboring target neurons called ON bipolar cells are instead "inhibited" by glutamate, because they lack the typical ionotropic glutamate receptors and instead express a class of inhibitory metabotropic glutamate receptors. When light is present, the photoreceptors cease releasing glutamate, which relieves the ON bipolar cells from inhibition, activating them; this simultaneously removes the excitation from the OFF bipolar cells, silencing them. It is possible to identify

neg: Somatic nervous system the efferent somatic nervous system involves a sequence that begins in the upper cell bodies of motor neurons (upper motor neurons) within the precentral gyrus (which approximates the primary motor cortex). Stimuli from the precentral gyrus are transmitted from upper motor neurons and down the corticospinal tract, via axons to control skeletal (voluntary) muscles. These stimuli are conveyed from upper motor neurons through the ventral horn of the spinal cord, and across synapses to be received by the sensory receptors of alpha motor neurons (large lower motor neurons) of the brainstem and spinal cord. Upper motor neurons release a neurotransmitter,

neg: N-type calcium channel channels are highly known for their function in the nervous system, but they are also involved with the function of the heart and kidneys. They are important in neurotransmitter release because they are localized at the synaptic terminals. In the peripheral nervous system, N-type channels are known to be involved in the release of many neurotransmitters like glutamate, GABA, acetylcholine, dopamine, and norepinephrine. When extracellular calcium flows into N-type calcium channels due to an action potential, it triggers the fusion of the secretory vesicles. Studies on the cardiovascular system reveal when ω-Conotoxin is introduced, it causes the inhibition of norepinephrine,

neg: David Sulzer accumulated like genuine neurotransmitters into neurons and synaptic vesicles. This is used to observe neurotransmitter release and reuptake from individual synapses in video. Sulzer, along with his mentor Stephen Rayport, showed that the neurotransmitter glutamate is released from dopamine neurons, an important exception to the Dale's principle that a neuron releases the same transmitter from each of its synapses. By introducing the "weak base hypothesis" of amphetamine action, for measuring amphetamine's effects on the quantal size of dopamine release, intracellular patch electrochemistry to measure dopamine levels in the cytosol, and providing real-time measurement of dopamine release by reverse transport, Sulzer's

neg: Psychopharmacology receptor density and second messenger function. Monoamine oxidase inhibitors (MAOIs) are the oldest class of antidepressants. They inhibit monoamine oxidase, the enzyme that metabolizes the monoamine neurotransmitters in the presynaptic terminals that are not contained in protective synaptic vesicles. The inhibition of the enzyme increases the amount of neurotransmitter available for release. It increases norepinephrine, dopamine, and 5-HT and thus increases the action of the transmitters at their receptors. MAOIs have been somewhat disfavored because of their reputation for more serious side effects. Tricyclic antidepressants (TCAs) work through binding to the presynaptic transporter proteins and blocking the reuptake of norepinephrine

neg: Benzofuranylpropylaminopentane when a neuron is stimulated by receiving an impulse from a neighbouring neuron. So while both amphetamine and BPAP increase the amount of neurotransmitters that get released, amphetamine causes neurons to dump neurotransmitter stores into the synapse regardless of external input, while with BPAP the pattern of neurotransmitter release is not changed, but when the neuron would normally release neurotransmitter, a larger amount than normal is released. Other drugs which produce this effect are the endogenous trace amines phenethylamine and tryptamine, and the neuroprotective MAO-B inhibitor selegiline. However, while selegiline is a potent monoamine oxidase inhibitor, BPAP is only a

neg: Brain in irregular patterns; other neurons are quiet most of the time, but occasionally emit a burst of action potentials. Axons transmit signals to other neurons by means of specialized junctions called synapses. A single axon may make as many as several thousand synaptic connections with other cells. When an action potential, traveling along an axon, arrives at a synapse, it causes a chemical called a neurotransmitter to be released. The neurotransmitter binds to receptor molecules in the membrane of the target cell. Synapses are the key functional elements of the brain. The essential function of the brain is cell-to-cell communication,

neg: Octopamine (neurotransmitter) replaces norepinephrine in sympathetic neurons with chronic use of monoamine oxidase inhibitors. It may be responsible for the common side effect of orthostatic hypotension with these agents, though there is also evidence that it is actually mediated by increased levels of "N"-acetylserotonin. One study noted that octopamine might be an important amine that influences the therapeutic effects of inhibitors such as monoamine oxidase inhibitors, especially because a large increase in octopamine levels was observed when animals were treated with this inhibitor. Octopamine was positively identified in the urine samples of mammals such as humans, rats, and rabbits treated with monoamine

neg: Synaptic fatigue (not true) When synaptic vesicles release neurotransmitters into the synapse that bind with post-synaptic membrane proteins to pass a signal, neurotransmitter re-uptake occurs to recycle neurotransmitters in the presynaptic cell in order to be released again. Neurotransmitter vesicles are recycled through the process of endocytosis. Because each presynaptic cell can link up to thousands of connections with other neurons, synaptic fatigue and its recovery can cause interactions with other neuronal circuits and can affect the kinetics with other processes of neurons. It is important that the recycling of neurotransmitters take place at an effective and efficient rate in order to

neg: Dopaminergic cell groups Dopaminergic cell groups Dopaminergic cell groups are collections of neurons in the central nervous system that synthesize the neurotransmitter dopamine. In the 1960s, dopamine neurons were first identified and named by Annica Dahlström and , who used histochemical fluorescence. The subsequent discovery of genes encoding enzymes that synthesize dopamine, and transporters that incorporate dopamine into synaptic vesicles or reclaim it after synaptic release, enabled scientists to identify dopaminergic neurons by labeling gene or protein expression that is specific to these neurons. In the mammalian brain, dopaminergic neurons form a semi-continuous population extending from the midbrain through the forebrain, with eleven

neg: Neuromuscular junction synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. In vertebrates, motor neurons release acetylcholine (ACh), a small molecule neurotransmitter, which diffuses across the synaptic cleft and binds to nicotinic acetylcholine receptors (nAChRs) on the cell membrane of the muscle fiber, also known as the sarcolemma. nAChRs are ionotropic receptors, meaning they serve as ligand-gated ion channels. The binding of ACh to the receptor can depolarize the muscle fiber, causing a cascade that eventually results in muscle contraction. Neuromuscular junction diseases can be of genetic and autoimmune origin.

neg: Cerebral cortex in shape and use glutamate as a neurotransmitter, however these migrating cells contribute neurons that are stellate-shaped and use GABA as their main neurotransmitter. These GABAergic neurons are generated by progenitor cells in the medial ganglionic eminence (MGE) that migrate tangentially to the cortex via the subventricular zone. This migration of GABAergic neurons is particularly important since GABA receptors are excitatory during development. This excitation is primarily driven by the flux of chloride ions through the GABA receptor, however in adults chloride concentrations shift causing an inward flux of chloride that hyperpolarizes postsynaptic neurons. Of all the different brain regions,

neg: Antidepressant hypnotics. They act by antagonizing serotonin receptors such as 5-HT and inhibiting the reuptake of serotonin, norepinephrine, and/or dopamine. Additionally, most also act as α-adrenergic receptor antagonists. The majority of the currently marketed SARIs belong to the phenylpiperazine class of compounds. They include trazodone and nefazodone. Norepinephrine reuptake inhibitors (NRIs or NERIs) are a type of drug that acts as a reuptake inhibitor for the neurotransmitter norepinephrine (noradrenaline) by blocking the action of the norepinephrine transporter (NET). This in turn leads to increased extracellular concentrations of norepinephrine. NRIs are commonly used in the treatment of conditions like ADHD and narcolepsy

neg: Photoreceptor cell they are not being stimulated, they depolarize and release glutamate continuously. In the dark, cells have a relatively high concentration of cyclic guanosine 3'-5' monophosphate (cGMP), which opens ion channels (largely sodium channels, though calcium can enter through these channels as well). The positive charges of the ions that enter the cell down its electrochemical gradient change the cell's membrane potential, cause depolarization, and lead to the release of the neurotransmitter glutamate. Glutamate can depolarize some neurons and hyperpolarize others. When light hits a photoreceptive pigment within the photoreceptor cell, the pigment changes shape. The pigment, called iodopsin or rhodopsin,

neg: Neurochemistry published in 1954 was titled "Biochemistry of the Developing Nervous System". These meetings led to the formation of the International Society for Neurochemistry and the American Society for Neurochemistry. These early gatherings discussed the tentative nature of possible neurotransmitter substances such as acetylcholine, histamine, substance P, and serotonin. By 1972, ideas were more concrete. Neurochemicals such as norepinephrine, dopamine, and serotonin were classified as "putative neurotransmitters in certain neuronal tracts in the brain." Neurochemistry Neurochemistry is the study of neurochemicals, including neurotransmitters and other molecules such as psychopharmaceuticals and neuropeptides, that influence the function of neurons. This field within neuroscience

neg: Neurotransmitter -DOPA, a precursor of dopamine that crosses the blood–brain barrier, is used in the treatment of Parkinson's disease. For depressed patients where low activity of the neurotransmitter norepinephrine is implicated, there is only little evidence for benefit of neurotransmitter precursor administration. L-phenylalanine and L-tyrosine are both precursors for dopamine, norepinephrine, and epinephrine. These conversions require vitamin B6, vitamin C, and S-adenosylmethionine. A few studies suggest potential antidepressant effects of L-phenylalanine and L-tyrosine, but there is much room for further research in this area. Administration of L-tryptophan, a precursor for serotonin, is seen to double the production of serotonin in the

neg: Dopamine make up the dopamine system which is neuromodulatory. Dopaminergic neurons (dopamine-producing nerve cells) are comparatively few in number—a total of around 400,000 in the human brain—and their cell bodies are confined in groups to a few relatively small brain areas. However their axons project to many other brain areas, and they exert powerful effects on their targets. These dopaminergic cell groups were first mapped in 1964 by Annica Dahlström and Kjell Fuxe, who assigned them labels starting with the letter "A" (for "aminergic"). In their scheme, areas A1 through A7 contain the neurotransmitter norepinephrine, whereas A8 through A14 contain dopamine.

neg: Traumatic memories emotional arousal and the activation of stress hormones. These memories become consolidated, stable, and enduring long-term memories (LTMs) through the synthesis of proteins only a few hours after the initial experience. The release of the neurotransmitter Norepinephrine (Noradrenaline) plays a large role in consolidation of traumatic memory. Stimulation of beta-adrenergic receptors during arousal and stress strengthens memory consolidation. Increased release of Norepinephrine inhibits the prefrontal cortex, which plays a role in emotion control as well as extinction or suppression of memory. Additionally, the release also serves to stimulate the amygdala which plays a key role in generating fear behaviors. Memory

neg: Cardiac physiology The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (also known as noradrenaline) at the neuromuscular junction of the cardiac nerves. This shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increased heartrate. It opens chemical or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions. Norepinephrine binds to the beta–1 receptor. High blood pressure medications are used to block these receptors and so reduce the heart rate. The cardiovascular centres receive input from a series of

neg: Summation (neurophysiology) depolarization of the postsynaptic cell, whereas the hyperpolarization produced by an inhibitory neurotransmitter will mitigate the effects of an excitatory neurotransmitter. This depolarization is called an EPSP, or an excitatory postsynaptic potential, and the hyperpolarization is called an IPSP, or an inhibitory postsynaptic potential. The only influences that neurons can have on one another are excitation, inhibition, and—through modulatory transmitters—biasing one another's excitability. From such a small set of basic interactions, a chain of neurons can produce only a limited response. A pathway can be facilitated by excitatory input; removal of such input constitutes "disfacillitation". A pathway may also be

neg: Dale's principle branches of a neurone, there was liberation of the same transmitter substance or substances." The addition of "or substances" is critical. With this change, the principle allows for the possibility of neurons releasing more than one transmitter, and only asserts that the same set are released at all synapses. In this form, it continues to be an important rule of thumb, with only a few known exceptions, including David Sulzer and Stephen Rayport's finding that dopamine neurons also release glutamate as a neurotransmitter, but at separate release sites. Dale's principle In neuroscience, Dale's principle (or Dale's law) is a rule

neg: Plasma membrane monoamine transporter Plasma membrane monoamine transporter The plasma membrane monoamine transporter (PMAT) is a low-affinity monoamine transporter protein which in humans is encoded by the "SLC29A4" gene. It is known alternatively as the human equilibrative nucleoside transporter-4 (hENT4). Unlike other members of the ENT family, it is impermeable to most nucleosides, with the exception of the inhibitory neurotransmitter and ribonucleoside adenosine, which it is permeable to in a highly pH-dependent manner. This protein is an integral membrane protein that transports the monoamine neurotransmitters (serotonin, dopamine, norepinephrine) as well as adenosine, from synaptic spaces into presynaptic neurons or neighboring glial cells. It is

neg: Anterior grey column and West Nile virus. The anterior grey column is the target for some spasmolytic medications. Norepinephrine release here, (as induced by cyclobenzaprine) reduces spasms by innervation (reducing nerve activity) of alpha motor neurons via interaction with gamma fibers. Anterior grey column The anterior grey column (also called the anterior cornu, anterior horn of spinal cord or ventral horn) is the front column of grey matter in the spinal cord. It is one of the three grey columns. The anterior grey column contains motor neurons that affect the skeletal muscles while the posterior grey column receives information regarding touch and sensation.

neg: Clonidine neuron (otherwise inducing a stimulatory effect), norepinephrine also binds to alpha-2A adreneric receptors (akin to clonidine's mechanism of action), inhibiting the release of norepinephrine by that neuron and inducing an inhibitory effect. Because the PFC is required for working memory and attention, it is thought that clonidine's inhibition of PFC neurons helps to eliminate irrelevant attention (and subsequent behaviors), improving the person's focus and correcting deficits in attention. Clonidine stimulates release of growth hormone releasing hormone from the hypothalamus, which in turn stimulates pituitary release of growth hormone. This effect has been used as part of a "growth hormone test,"

neg: Nicotinic agonist hyperactivity disorder: those experiments showed positive outcomes. One of the first nAChR active compounds, besides nicotine, that was marketed as a drug was galantamine, a plant alkaloid that works as a weak cholinesterase inhibitor (IC50=5µM) as well as an allosteric sensitizer for nAChRs (EC50=50 nM). In the human nervous system nicotinic cholinergic signals are extended throughout the system, where the neurotransmitter acetylcholine (ACh) plays a key role in activating ligand-gated ion channels. The cholinergic system is a vital nervous pathway, where cholinergic neurons synthesize, store and release the neurotransmitter ACh. The main receptors that convert the ACh messages are the

neg: Axon terminal Axon terminal Axon terminals (also called synaptic boutons or terminal boutons) are distal terminations of the telodendria (branches) of an axon. An axon, also called a nerve fiber, is a long, slender projection of a nerve cell, or neuron, that conducts electrical impulses called action potentials away from the neuron's cell body, or soma, in order to transmit those impulses to other neurons, muscle cells or glands. Neurons are interconnected in complex arrangements, and use electrochemical signals and neurotransmitter chemicals to transmit impulses from one neuron to the next; axon terminals are separated from neighboring neurons by a small gap

neg: Psychoactive drug to a psychoactive substance can cause changes in the structure and functioning of neurons, as the nervous system tries to re-establish the homeostasis disrupted by the presence of the drug (see also, neuroplasticity). Exposure to antagonists for a particular neurotransmitter can increase the number of receptors for that neurotransmitter or the receptors themselves may become more responsive to neurotransmitters; this is called sensitization. Conversely, overstimulation of receptors for a particular neurotransmitter may cause a decrease in both number and sensitivity of these receptors, a process called desensitization or tolerance. Sensitization and desensitization are more likely to occur with long-term exposure,

neg: Dopamine Reward was seen to be mediated instead by octopamine, a neurotransmitter closely related to norepinephrine. More recent studies however have shown that dopamine does play a part in reward learning in fruit flies. Also it has been found that the rewarding effect of octopamine is due to its activating a set of dopaminergic neurons not previously accessed in the research. Many plants, including a variety of food plants, synthesize dopamine to varying degrees. The highest concentrations have been observed in bananas—the fruit pulp of red and yellow bananas contains dopamine at levels of 40 to 50 parts per million by

neg: Neurotransmitter role in neurotransmitter activities. Apart from recreational use, medications that directly and indirectly interact one or more transmitter or its receptor are commonly prescribed for psychiatric and psychological issues. Notably, drugs interacting with serotonin and norepinephrine are prescribed to patients with problems such as depression and anxiety—though the notion that there is much solid medical evidence to support such interventions has been widely criticized. A neurotransmitter must be broken down once it reaches the post-synaptic cell to prevent further excitatory or inhibitory signal transduction. This allows new signals to be produced from the adjacent nerve cells. When the neurotransmitter has

neg: Neuromuscular junction death. Snake venoms act as toxins at the neuromuscular junction and can induce weakness and paralysis. Venoms can act as both presynaptic and postsynaptic neurotoxins. Presynaptic neurotoxins, commonly known as β-neurotoxins, affect the presynaptic regions of the neuromuscular junction. The majority of these neurotoxins act by inhibiting the release of neurotransmitters, such as acetylcholine, into the synapse between neurons. However, some of these toxins have also been known to enhance neurotransmitter release. Those that inhibit neurotransmitter release create a neuromuscular blockade that prevents signaling molecules from reaching their postsynaptic target receptors. In doing so, the victim of these snake bite

neg: Neurotransmitter neurotransmitters available for release becomes substantially lower, resulting in a decrease in neurotransmitter activity. Some drugs block or stimulate the release of specific neurotransmitters. Alternatively, drugs can prevent neurotransmitter storage in synaptic vesicles by causing the synaptic vesicle membranes to leak. Drugs that prevent a neurotransmitter from binding to its receptor are called receptor antagonists. For example, drugs used to treat patients with schizophrenia such as haloperidol, chlorpromazine, and clozapine are antagonists at receptors in the brain for dopamine. Other drugs act by binding to a receptor and mimicking the normal neurotransmitter. Such drugs are called receptor agonists. An example

neg: Neuroblastoma detect neuroblastoma is the meta-iodobenzylguanidine scan, which is taken up by 90 to 95% of all neuroblastomas, often termed "mIBG-avid". The mechanism is that mIBG is taken up by sympathetic neurons, and is a functioning analog of the neurotransmitter norepinephrine. When it is radio-iodinated with I-131 or I-123 (radioactive iodine isotopes), it is a very good radiopharmaceutical for diagnosis and monitoring of response to treatment for this disease. With a half-life of 13 hours, I-123 is the preferred isotope for imaging sensitivity and quality. I-131 has a half-life of 8 days and at higher doses is an effective therapy as

neg: Phentermine phentermine may be impaired when driving or operating machinery. Consumption of alcohol with phentermine may produce adverse effects. There is no evidence that phentermine is safe for women who are pregnant. Other adverse effects include: Phentermine has some similarity in its pharmacodynamics with its parent compound, amphetamine, as they both are TAAR1 agonists, where the activation of TAAR1 in monoamine neurons facilitates the efflux or, release into the synapse, of these neurochemicals; at clinically relevant doses, phentermine primarily acts as a releasing agent of norepinephrine in neurons, although, to a lesser extent, it releases dopamine and serotonin into synapses as

neg: Reticular formation composed primarily of neurons that release monoamine neurotransmitters, namely dopamine, norepinephrine, serotonin, and histamine. The glutamate-releasing neurons in the ARAS were identified much more recently relative to the monoaminergic and cholinergic nuclei; the glutamatergic component of the ARAS includes one glutamatergic nucleus in the hypothalamus and various glutamatergic brainstem nuclei. The orexin neurons of the lateral hypothalamus innervate every component of the ascending reticular activating system and coordinate activity within the entire system. The key components of the ARAS are listed in the table below. The ARAS consists of evolutionarily ancient areas of the brain, which are crucial to survival

neg: End-plate potential membrane of the neuromuscular junction. End plate potentials are produced almost entirely by the neurotransmitter acetylcholine in skeletal muscle. Acetylcholine is the second most important excitatory neurotransmitter in the body following glutamate. It controls the somatosensory system which includes the senses of touch, vision, and hearing. It was the first neurotransmitter to be identified in 1914 by Henry Dale. Acetylcholine is synthesized in the cytoplasm of the neuron from choline and acetyl-CoA. Choline acyltransferase is the enzyme that synthesizes acetylcholine and is often used as a marker in research relating to acetylcholine production. Neurons that utilize acetylcholine are called cholinergic

neg: Neuromodulation from the target cells with the resulting activation of extrasynaptic receptors, and with a longer time course than for transmission at a single synapse. Such prolonged transmitter action is called tonic transmission, in contrast to the phasic transmission that occurs rapidly at single synapses. The major neurotransmitter systems are the noradrenaline (norepinephrine) system, the dopamine system, the serotonin system and the cholinergic system. Drugs targeting the neurotransmitter of such systems affects the whole system, and explains the mode of action of many drugs. Most other neurotransmitters, on the other hand, e.g. glutamate, GABA and glycine, are used very generally throughout

neg: Octopamine (neurotransmitter) Octopamine (neurotransmitter) Octopamine is an organic chemical closely related to norepinephrine, and synthesized biologically by a homologous pathway. Its name derives from the fact that it was first identified in the salivary glands of the octopus. In many types of invertebrates octopamine is an important neurotransmitter and hormone. In protostomes—arthropods, molluscs, and several types of worms—it substitutes for norephinephrine and performs functions apparently similar to those of norepinephrine in mammals, functions that have been described as mobilizing the body and nervous system for action. Octopamine exerts its effects by binding to and activating receptors located on the surface of cells.

neg: Fenfluramine the medication. Of the users tested, 20% of women, and 12% of men were affected. For all ex-users, there was a 7-fold increase of chances of needing surgery for faulty heart valves caused by the drug. In overdose, fenfluramine can cause serotonin syndrome and rapidly result in death. Fenfluramine acts primarily as a serotonin releasing agent. It increases the level of serotonin, a neurotransmitter that regulates mood, appetite and other functions. Fenfluramine causes the release of serotonin by disrupting vesicular storage of the neurotransmitter, and reversing serotonin transporter function. The drug also acts as a norepinephrine releasing agent to a

neg: Nervous system several widely occurring receptor types, but all of them are inhibitory. Because of this consistency, glutamatergic cells are frequently referred to as "excitatory neurons", and GABAergic cells as "inhibitory neurons". Strictly speaking, this is an abuse of terminology—it is the receptors that are excitatory and inhibitory, not the neurons—but it is commonly seen even in scholarly publications. One very important subset of synapses are capable of forming memory traces by means of long-lasting activity-dependent changes in synaptic strength. The best-known form of neural memory is a process called long-term potentiation (abbreviated LTP), which operates at synapses that use the neurotransmitter

neg: Acetylcholine the projections from the central nervous system to the autonomic ganglia, use acetylcholine as a neurotransmitter to innervate (or excite) cholinergic neurons (neurons expressing nicotinic acetylcholine receptors). In the parasympathetic nervous system the output connections, the projections from ganglion neurons to tissues that don't belong to the nervous system, also release acetylcholine but act on muscarinic receptors. In the sympathetic nervous system the output connections mainly release noradrenaline, although acetylcholine is released at a few points, such as the sudomotor innervation of the sweat glands. Acetylcholine in the serum exerts a direct effect on vascular tone by binding to muscarinic

neg: Sympathetic nervous system reach their destinations. A notable exception to the routes mentioned above is the sympathetic innervation of the suprarenal (adrenal) medulla. In this case, presynaptic neurons pass through paravertebral ganglia, on through prevertebral ganglia and then synapse directly with suprarenal tissue. This tissue consists of cells that have pseudo-neuron like qualities in that when activated by the presynaptic neuron, they will release their neurotransmitter (epinephrine) directly into the bloodstream. In the sympathetic nervous system and other components of the peripheral nervous system, these synapses are made at sites called ganglia. The cell that sends its fiber is called a preganglionic cell,

neg: Dopamine is modulated by two mechanisms: phasic and tonic transmission. Phasic dopamine release, like most neurotransmitter release in the nervous system, is driven directly by action potentials in the dopamine-containing cells. Tonic dopamine transmission occurs when small amounts of dopamine are released without being preceded by presynaptic action potentials. Tonic transmission is regulated by a variety of factors, including the activity of other neurons and neurotransmitter reuptake. Inside the brain, dopamine plays important roles in executive functions, motor control, motivation, arousal, reinforcement, and reward, as well as lower-level functions including lactation, sexual gratification, and nausea. The dopaminergic cell groups and pathways

neg: Dopamine beta hydroxylase deficiency homeostasis" overall. This shows that treatment modalities other than Droxidopa should be pursued as possible adjuncts for the hyperinsulinemia seen in DβH deficiency. Dopamine beta hydroxylase deficiency Dopamine beta (β)-hydroxylase deficiency (DβH deficiency) is a condition involving inadequate dopamine beta-hydroxylase. It is characterized by increased amounts of serum dopamine and the absence of norepinephrine (NE) and epinephrine. Dopamine is released, as a false neurotransmitter, in place of norepinephrine. Other names for norepinephrine include noradrenaline (NA) and noradrenalin. This condition is also sometimes referred to as "norepinephrine deficiency". Researchers of disorders such as schizophrenia are interested in studying this disorder, as

neg: Sympathetic nervous system parasympathetic nervous system which stimulates the body to "feed and breed" and to (then) "rest-and-digest". There are two kinds of neurons involved in the transmission of any signal through the sympathetic system: pre-ganglionic and post-ganglionic. The shorter preganglionic neurons originate from the thoracolumbar region of the spinal cord specifically at T1 to L2~L3, and travel to a ganglion, often one of the paravertebral ganglia, where they synapse with a postganglionic neuron. From there, the long postganglionic neurons extend across most of the body. At the synapses within the ganglia, preganglionic neurons release acetylcholine, a neurotransmitter that activates nicotinic acetylcholine receptors

neg: Muscle contraction are myogenic, the rate and strength of their contractions can be modulated by the autonomic nervous system. Postganglionic nerve fibers of parasympathetic nervous system release the neurotransmitter acetylcholine, which binds to muscarinic acetylcholine receptors (mAChRs) on smooth muscle cells. These receptors are metabotropic, or G-protein coupled receptors that initiate a second messenger cascade. Conversely, postganglionic nerve fibers of the sympathetic nervous system release the neurotransmitters epinephrine and norepinephrine, which bind to adrenergic receptors that are also metabotropic. The exact effects on the smooth muscle depend on the specific characteristics of the receptor activated—both parasympathetic input and sympathetic input can be