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{{BioPsy}} |
{{BioPsy}} |
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| + | {{For|an introduction to concepts and terminology used in this article|Chemical synapse}} |
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| − | [[Image:Aspartic Acid.png|thumb|Chemical structure of '''[[D-aspartic acid]]''', a common amino acid neurotransmitter.]] |
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| + | {{Synapse map}} |
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| − | '''Neurotransmitters''' are [[chemistry|chemicals]] that are used to relay, amplify and modulate signals between a [[neuron]] and another [[cell (biology)|cell]]. It does this through the process of [[receptor binding]] to a [[neuroreceptor]], which triggers aresponse in the neuron to alter its functioning. |
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| + | '''Neurotransmitters''' are [[endogenous]] [[chemistry|chemicals]] that transmit signals from a [[neuron]] to a target [[cell (biology)|cell]] across a [[synapse]].<ref>{{DorlandsDict|six/000072138|Neurotransmitter}}</ref> Neurotransmitters are packaged into [[synaptic vesicles]] clustered beneath the membrane in the axon terminal, on the presynaptic side of a synapse. They are released into and diffuse across the [[synaptic cleft]], where they bind to specific receptors in the membrane on the postsynaptic side of the synapse.<ref>Elias, L. J, & Saucier, D. M. (2005). Neuropsychology: Clinical and Experimental Foundations. Boston: Pearson</ref> Release of neurotransmitters usually follows arrival of an [[action potential]] at the synapse, but may also follow [[Membrane_potential#Graded_potentials|graded electrical potentials]]. Low level "baseline" release also occurs without electrical stimulation. Many neurotransmitters are synthesized from plentiful and simple precursors, such as [[amino acid]]s, which are readily available from the diet and which require only a small number of biosynthetic steps to convert.<ref name=twsNovK11>{{cite news |
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| + | |author= Robert Sapolsky |
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| + | |title= Biology and Human Behavior: The Neurological Origins of Individuality, 2nd edition |
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| + | |publisher= ''The Teaching Company'' |
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| + | |quote=see pages 13 & 14 of Guide Book |
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| + | |year=2005 |
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| + | }}</ref> |
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| + | ==Discovery== |
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| − | According to the prevailing beliefs of the 1960s, a chemical can be classified as a neurotransmitter if it meets the following conditions: |
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| + | Until the early 20th century, scientists assumed that the majority of synaptic communication in the brain was electrical. However, through the careful [[Histology|histological]] examinations of [[Ramón y Cajal]] (1852–1934), a 20 to 40 nm gap between neurons, known today as the [[synaptic cleft]], was discovered. The presence of such a gap suggested communication via chemical messengers traversing the synaptic cleft, and in 1921 German pharmacologist [[Otto Loewi]] (1873–1961) confirmed that neurons can communicate by releasing chemicals. Through a series of experiments involving the vagus nerves of frogs, Loewi was able to manually slow the heart rate of frogs by controlling the amount of saline solution present around the vagus nerve. Upon completion of this experiment, Loewi asserted that sympathetic regulation of cardiac function can be mediated through changes in chemical concentrations. Furthermore, Otto Loewi is accredited with discovering [[acetylcholine]] (ACh)—the first known neurotransmitter.<ref>Saladin, Kenneth S. ''Anatomy and Physiology: The Unity of Form and Function''. McGraw Hill. 2009 ISBN 0-07-727620-5</ref> Some neurons do, however, communicate via [[electrical synapse]]s through the use of [[gap junction]]s, which allow specific ions to pass directly from one cell to another.<ref name="gap">{{cite web |url=http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/J/Junctions.html |title=Junctions Between Cells |accessdate=2010-11-22}}</ref> |
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| − | == |
+ | ==Identifying neurotransmitters== |
| + | The chemical identity of neurotransmitters is often difficult to determine experimentally. For example, it is easy using an electron microscope to recognize vesicles on the presynaptic side of a synapse, but it may not be easy to determine directly what chemical is packed into them. The difficulties led to many historical controversies over whether a given chemical was or was not clearly established as a transmitter. In an effort to give some structure to the arguments, neurochemists worked out a set of experimentally tractable rules. According to the prevailing beliefs of the 1960s, a chemical can be classified as a neurotransmitter if it meets the following conditions: |
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| + | Modern advances in pharmacology, genetics, and chemical neuroanatomy have greatly reduced the importance of these rules. A series of experiments that may have taken several years in the 1960s can now be done, with much better precision, in a few months. Thus, it is unusual nowadays for the identification of a chemical as a neurotransmitter to remain controversial for very long periods of time. |
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| − | Some more precise divisions are as follows: |
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| ⚫ | |||
| − | * Around 10 '''small-molecule neurotransmitters''' or '''small signalling molecules''' are known: |
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| ⚫ | |||
| − | ** [[acetylcholine]] (Ach) |
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| − | ** [[monoamine]]s ([[epinephrine]] (E), [[norepinephrine]] (NE), [[dopamine]] (DA), [[serotonin]] (5-HT) and [[melatonin]]) |
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| − | ** An imbalance in norepinephrine and serotonin are one of the causes of anxiety disorders including separation anxiety |
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| − | * 3 or 4 '''excitory amino acids''', depending on exact definition used: (primarily [[glutamic acid]], [[gamma aminobutyric acid]] (GABA), [[aspartic acid]] & [[glycine]]) |
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| − | ** [[Purines]], (Adenosine, [[adenosine triphosphate|ATP]], [[Guanosine triphosphate|GTP]] and their derivatives) |
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| − | ** Fatty acids are also receiving attention as the potential [[Cannabinoids#Endogenous Cannabinoids|endogenous cannabinoid]].{{Fact|date=February 2007}} |
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| − | * Over 50 [[neuroactive peptides]] ([[vasopressin]], [[somatostatin]], [[neurotensin]], etc.) have been found, among them hormones such as [[Luteinizing hormone]] (LH) or [[insulin]] that have specific local actions in addition to their long-range signalling properties. This group also includes [[hypothalmic releasing hormones]], the neurohypophyseal hormones, [[pituitary peptides]] and the [[gastrointestinal peptides]]. |
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| − | * Histamine |
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| − | * Single ions, such as synaptically-released [[zinc]], are also considered neurotransmitters by some.{{Fact|date=March 2007}} |
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| − | * Gaseous including :[[Nitrogen monoxide]] (NO) also called [[Nitric Oxide] and [[Carbon monoxide]] (CO))] |
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| − | + | Major neurotransmitters: |
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| + | *[[Amino acid]]s: [[glutamate]],<ref name=twsNovK11/> [[aspartate]], [[D-serine]], [[γ-aminobutyric acid]] (GABA), [[glycine]] |
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| − | ==Effects== |
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| + | *[[Monoamine]]s and other [[biogenic amines]]: [[dopamine]] (DA), [[norepinephrine]] (noradrenaline; NE, NA), [[epinephrine]] (adrenaline), [[histamine]], [[serotonin]] (SE, 5-HT) |
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| + | *[[Peptide]]s: [[somatostatin]], [[substance P]], [[opioid peptide]]s<ref>http://www.ncbi.nlm.nih.gov/pubmed/38738</ref> |
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| + | *Others: [[acetylcholine]] (ACh), [[adenosine]], [[anandamide]], [[nitric oxide]], etc. |
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| + | In addition, over 50 neuroactive [[peptide]]s have been found, and new ones are discovered regularly. Many of these are "co-released" along with a small-molecule transmitter, but in some cases a peptide is the primary transmitter at a synapse. [[β-endorphin]] is a relatively well known example of a peptide neurotransmitter; it engages in highly specific interactions with [[opioid receptors]] in the [[central nervous system]]. |
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| − | * [[Acetylcholine]] - voluntary movement of the muscles |
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| − | * [[Norepinephrine]] - wakefulness or arousal |
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| − | * [[Dopamine]] - voluntary movement and motivation, "wanting", pleasure, associated with addiction and love |
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| − | * [[Serotonin]] - memory, emotions, wakefulness, sleep and temperature regulation |
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| − | * [[gamma aminobutyric acid|GABA]] - inhibition of motor neurons |
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| − | * [[Glycine]] - spinal reflexes and motor behaviour |
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| − | * [[Neuromodulator]]s - sensory transmission - especially pain |
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| + | Single [[ion]]s, such as synaptically released [[zinc]], are also considered neurotransmitters by some,<ref>Kodirov,Sodikdjon A., Shuichi Takizawa, Jamie Joseph, Eric R. Kandel, Gleb P. Shumyatsky, and Vadim Y. Bolshakov. Synaptically released zinc gates long-term potentiation in fear conditioning pathways. ''PNAS'', October 10, 2006. 103(41): 15218-23. {{doi|10.1073/pnas.0607131103}}</ref> as are some gaseous molecules such as [[nitric oxide]] (NO), [[hydrogen sulfide]] (H<sub>2</sub>S), and [[carbon monoxide]] (CO).<ref>[http://www.marsdd.com/events/details/international-symposium-on-nitric-oxide-and-other-gaseous-neurotransmitters/ Nitric oxide and other gaseous neurotransmitters]</ref> Because they are not packaged into vesicles they are not classical neurotransmitters by the strictest definition, however they have all been shown experimentally to be released by presynaptic terminals in an activity-dependent way. |
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| − | {{Main|Neurotransmitter systems}} |
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| + | By far the most prevalent transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain.<ref name=twsNovK11/> The next most prevalent is GABA, which is inhibitory at more than 90% of the synapses that do not use glutamate. Even though other transmitters are used in far fewer synapses, they may be very important functionally—the great majority of psychoactive drugs exert their effects by altering the actions of some neurotransmitter systems, often acting through transmitters other than glutamate or GABA. Addictive drugs such as cocaine and amphetamine exert their effects primarily on the dopamine system. The addictive [[opiate]] drugs exert their effects primarily as functional analogs of [[opioid peptides]], which, in turn, regulate dopamine levels. |
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| − | The major neurotransmitter systems are the [[noradrenaline]] (norepinephrine) system, the [[dopamine]] system, the [[serotonin]] system and the [[cholinergic]] system. |
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| + | ===Excitatory and inhibitory=== |
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| − | Drugs targeting the neurotransmitter of such systems affects the whole system, and explains the mode of action of many drugs; |
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| + | Some neurotransmitters are commonly described as "excitatory" or "inhibitory". The only direct effect of a neurotransmitter is to activate one or more types of receptors. The effect on the postsynaptic cell depends, therefore, entirely on the properties of those receptors. It happens that for some neurotransmitters (for example, glutamate), the most important receptors all have excitatory effects: that is, they increase the probability that the target cell will fire an [[action potential]]. For other neurotransmitters, such as GABA, the most important receptors all have inhibitory effects (although there is [[Gamma-Aminobutyric_acid#Brain_development|evidence that GABA is excitatory]] during early brain development). There are, however, other neurotransmitters, such as acetylcholine, for which both excitatory and inhibitory receptors exist; and there are some types of receptors that activate complex metabolic pathways in the postsynaptic cell to produce effects that cannot appropriately be called either excitatory or inhibitory. Thus, it is an oversimplification to call a neurotransmitter excitatory or inhibitory—nevertheless it is convenient to call glutamate excitatory and GABA inhibitory so this usage is seen frequently. |
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| − | * [[Cocaine]], for example, blocks the reuptake of [[dopamine]], leaving these neurotransmitters in the [[synapse|synaptic gap]] longer. |
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| − | * [[Prozac]] is a [[serotonin reuptake inhibitor|selective serotonin reuptake inhibitor]] (SSRI), hence potentiating the effect of naturally released serotonin. |
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| − | * [[AMPT]] prevents the conversion of tyrosine to [[L-DOPA]], the precursor to dopamine; [[reserpine]] prevents dopamine storage within [[vesicles]]; and [[deprenyl]] inhibits [[monoamine oxidase]] (MAO)-B and thus increases dopamine levels. |
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| + | ==Actions== |
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| ⚫ | Diseases may affect specific neurotransmitter systems. For example, [[Parkinson's disease]] is at least in part related to failure of dopaminergic cells in |
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| + | {{Main|Neuromodulation}} |
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| + | As explained above, the only direct action of a neurotransmitter is to activate a receptor. Therefore, the effects of a neurotransmitter system depend on the connections of the neurons that use the transmitter, and the chemical properties of the receptors that the transmitter binds to. |
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| + | |||
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| + | *[[Glutamate]] is used at the great majority of fast excitatory synapses in the brain and spinal cord. It is also used at most synapses that are "modifiable", i.e. capable of increasing or decreasing in strength. Excess glutamate can overstimulate the brain and causes seizures.{{citation needed|date=December 2012}} [[Synaptic plasticity|Modifiable synapses]] are thought to be the main memory-storage elements in the brain. Excessive glutamate release can lead to [[excitotoxicity]] causing cell death. |
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| + | *[[GABA]] is used at the great majority of fast inhibitory synapses in virtually every part of the brain. Many sedative/tranquilizing drugs act by enhancing the effects of GABA. Correspondingly [[glycine]] is the inhibitory transmitter in the spinal cord. |
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| + | *[[Acetylcholine]] is distinguished as the transmitter at the [[neuromuscular junction]] connecting motor nerves to muscles. The paralytic arrow-poison [[curare]] acts by blocking transmission at these synapses. Acetylcholine also operates in many regions of the brain, but using [[Acetylcholine receptor#Receptor types|different types of receptors]], including [[Nicotinic acetylcholine receptor|nicotinic]] and [[Muscarinic acetylcholine receptor|muscarinic]] receptors.<ref>http://www.ebi.ac.uk/interpro/potm/2005_11/Page2.htm</ref> |
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| + | *[[Dopamine]] has a number of important functions in the brain; this includes regulation of motor behavior, pleasures related to motivation and also emotional arousal. It plays a critical role in the [[reward system]]; people with [[Parkinson's disease]] have been linked to low levels of dopamine and people with [[schizophrenia]] have been linked to high levels of dopamine.<ref>Schacter, Gilbert and Weger. Psychology.United States of America.2009.Print.</ref> |
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| + | *[[Serotonin]] is a [[monoamine neurotransmitter]]. Most is produced by and found in the intestine (approximately 90%), and the remainder in [[central nervous system]] neurons. It functions to regulate appetite, sleep, memory and learning, temperature, mood, behaviour, muscle contraction, and function of the [[cardiovascular system]] and [[endocrine system]]. It is speculated to have a role in depression, as some depressed patients are seen to have lower concentrations of metabolites of serotonin in their [[cerebrospinal fluid]] and brain tissue.<ref name=serotonin>{{cite web|url = http://www.chm.bris.ac.uk/motm/serotonin/depression.htm|author = University of Bristol|title=Introduction to Serotonin|accessdate=2009-10-15}}</ref> |
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| + | *[[Substance P]] is an undecapeptide responsible for transmission of pain from certain sensory neurons to the central nervous system. It also aids in controlling relaxation of the vasculature and lowering blood pressure through the release of nitric oxide.<ref>http://www.wellnessresources.com/health_topics/sleep/substance_p.php</ref> |
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| + | *[[Opioid peptides]] are neurotransmitters that act within pain pathways and the emotional centers of the brain; some of them are [[analgesic]]s and elicit pleasure or euphoria.<ref>Schacter, Gilbert and Weger. Psychology. 2009.Print.</ref> |
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| ⚫ | 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. |
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| + | |||
| + | Drugs targeting the neurotransmitter of such systems affect the whole system; this fact explains the complexity of action of some drugs. [[Cocaine]], for example, blocks the reuptake of [[dopamine]] back into the [[presynaptic]] neuron, leaving the neurotransmitter molecules in the [[synapse|synaptic gap]] longer. Since the dopamine remains in the synapse longer, the neurotransmitter continues to bind to the receptors on the [[postsynaptic]] neuron, eliciting a pleasurable emotional response. Physical addiction to cocaine may result from prolonged exposure to excess dopamine in the synapses, which leads to the [[downregulation]] of some postsynaptic receptors. After the effects of the drug wear off, one might feel depressed because of the decreased probability of the neurotransmitter binding to a receptor. [[Prozac]] is a [[serotonin reuptake inhibitor|selective serotonin reuptake inhibitor]] (SSRI), which blocks re-uptake of serotonin by the presynaptic cell. This increases the amount of serotonin present at the synapse and allows it to remain there longer, hence potentiating the effect of naturally released serotonin.<ref name="InhibitingSerotoninSynthesis">{{cite journal|author = Yadav, V. et al|title = Lrp5 Controls Bone Formation by Inhibiting Serotonin Synthesis in the Duodenum|journal = Cell|volume = 135|issue = 5|pages = 825–837|year = 2008|doi = 10.1016/j.cell.2008.09.059|pmid = 19041748|pmc = 2614332|last2 = Ryu|first2 = Je-Hwang|last3 = Suda|first3 = Nina|last4 = Tanaka|first4 = Kenji F.|last5 = Gingrich|first5 = Jay A.|last6 = Schütz|first6 = Günther|last7 = Glorieux|first7 = Francis H.|last8 = Chiang|first8 = Cherie Y.|last9 = Zajac|first9 = Jeffrey D.}}</ref> [[AMPT]] prevents the conversion of tyrosine to [[L-DOPA]], the precursor to dopamine; [[reserpine]] prevents dopamine storage within [[Synaptic vesicle|vesicles]]; and [[deprenyl]] inhibits [[monoamine oxidase]] (MAO)-B and thus increases dopamine levels. |
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| + | |||
| ⚫ | Diseases may affect specific neurotransmitter systems. For example, [[Parkinson's disease]] is at least in part related to failure of dopaminergic cells in deep-[[brain nuclei]], for example the [[substantia nigra]]. [[L-DOPA|Levodopa]] is a precursor of dopamine, and is the most widely used drug to treat Parkinson's disease. |
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A brief comparison of the major neurotransmitter systems follows: |
A brief comparison of the major neurotransmitter systems follows: |
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|+Neurotransmitter systems |
|+Neurotransmitter systems |
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|- |
|- |
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| − | ! System !! Origin <ref name=Rang> |
+ | ! System !! Origin <ref name=Rang>{{cite book |author=Rang, H. P. |title=Pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2003 |pages= 474 for noradrenaline system, page 476 for dopamine system, page 480 for serotonin system and page 483 for cholinergic system. |isbn=0-443-07145-4 |oclc= |doi=}}</ref> !! Effects<ref name=Rang/> |
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|- |
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!rowspan=2| Noradrenaline system |
!rowspan=2| Noradrenaline system |
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| − | | [[locus coeruleus]] |
+ | | ''[[locus coeruleus]]'' |
| − | |rowspan=2| |
+ | |rowspan=2| |
*arousal |
*arousal |
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*reward |
*reward |
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|- |
|- |
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| − | | [[Lateral tegmental field]] |
+ | | [[Lateral tegmental field]] |
|- |
|- |
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! Dopamine system |
! Dopamine system |
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|| [[dopamine]] [[neural pathway|pathways]]: |
|| [[dopamine]] [[neural pathway|pathways]]: |
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| − | * |
+ | *[[mesocortical pathway]] |
| − | * |
+ | *[[mesolimbic pathway]] |
| − | * |
+ | *[[nigrostriatal pathway]] |
| − | * |
+ | *[[tuberoinfundibular pathway]] |
|| [[motor system]], reward, [[cognition]], [[endocrine]], [[nausea]] |
|| [[motor system]], reward, [[cognition]], [[endocrine]], [[nausea]] |
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|- |
|- |
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!rowspan=2| Serotonin system |
!rowspan=2| Serotonin system |
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| − | | caudal [[dorsal raphe nucleus]] |
+ | | caudal [[dorsal raphe nucleus]] |
| − | |rowspan=2| Increase ([[extraversion and introversion| |
+ | |rowspan=2| Increase ([[extraversion and introversion|introversion]]), [[Mood (psychology)|mood]], [[satiety]], [[body temperature]] and [[sleep]], while decreasing [[nociception]]. |
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|- |
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| − | | rostral [[dorsal raphe nucleus]] |
+ | | rostral [[dorsal raphe nucleus]] |
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|- |
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!rowspan=3| Cholinergic system |
!rowspan=3| Cholinergic system |
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| − | | ''pontomesencephalotegmental complex'' |
+ | | ''pontomesencephalotegmental complex'' |
| − | |rowspan=3| |
+ | |rowspan=3| |
*[[learning]] |
*[[learning]] |
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*[[Memory#Short-term|short-term memory]] |
*[[Memory#Short-term|short-term memory]] |
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*reward |
*reward |
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| − | | [[basal optic nucleus of Meynert]] |
+ | | [[basal optic nucleus of Meynert]] |
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|- |
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| medial [[septal nucleus]] |
| medial [[septal nucleus]] |
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|} |
|} |
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| − | == |
+ | ==Common neurotransmitters== |
| − | {| class="wikitable" class="sortable wikitable" |
+ | {| class="wikitable" class="sortable wikitable" |
| '''Category''' || '''Name''' || '''Abbreviation''' || '''[[Metabotropic]]''' || '''[[Ionotropic]]''' |
| '''Category''' || '''Name''' || '''Abbreviation''' || '''[[Metabotropic]]''' || '''[[Ionotropic]]''' |
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| − | |- |
+ | |- |
| − | + | |Small: Amino acids || [[Aspartate]] || || - || - |
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| ⚫ | |||
| − | | [[Neuropeptide]]s || [[N-Acetylaspartylglutamate]] || [[NAAG]] || [[Metabotropic glutamate receptor]]s; selective agonist of [[mGluR3]] || - |
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|- |
|- |
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| − | + | |[[Neuropeptide]]s || [[N-Acetylaspartylglutamate]] || NAAG || [[Metabotropic glutamate receptor]]s; selective agonist of [[mGluR3]] || - |
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| − | |- |
+ | |- |
| − | + | |Small: Amino acids || [[Glutamate]] (glutamic acid) || Glu || [[Metabotropic glutamate receptor]] || [[NMDA receptor]], [[Kainate receptor]], [[AMPA receptor]] |
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| − | |- |
+ | |- |
| − | + | |Small: Amino acids || [[Gamma-aminobutyric acid]] || GABA || [[GABAB receptor|GABA<sub>B</sub> receptor]] || [[GABAA receptor|GABA<sub>A</sub>]], [[GABAA-rho receptor|GABA<sub>A</sub>-ρ receptor]] |
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| − | |- |
+ | |- |
| − | + | |Small: Amino acids || [[Glycine]] || Gly || - || [[Glycine receptor]] |
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| − | |- |
+ | |- |
| − | + | |Small: Acetylcholine || [[Acetylcholine]] || Ach || [[Muscarinic acetylcholine receptor]] || [[Nicotinic acetylcholine receptor]] |
|
| − | |- |
+ | |- |
| − | + | |Small: Monoamine ([[Phenylalanine|Phe]]/[[Tyrosine|Tyr]]) || [[Dopamine]] || DA || [[Dopamine receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |Small: Monoamine ([[Phenylalanine|Phe]]/[[Tyrosine|Tyr]]) || [[Norepinephrine]] (noradrenaline) || NE || [[Adrenergic receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |Small: Monoamine ([[Phenylalanine|Phe]]/[[Tyrosine|Tyr]]) || [[Epinephrine]] (adrenaline) || Epi || [[Adrenergic receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |Small: Monoamine ([[Phenylalanine|Phe]]/[[Tyrosine|Tyr]]) || [[Octopamine]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |Small: Monoamine ([[Phenylalanine|Phe]]/[[Tyrosine|Tyr]]) || [[Tyramine]] || || - |
|
| − | |- |
+ | |- |
| − | + | |Small: Monoamine ([[Tryptophan|Trp]]) || [[Serotonin]] (5-hydroxytryptamine) || 5-HT || [[Serotonin receptor]], all but 5-HT<sub>3</sub> || [[5-HT3|5-HT<sub>3</sub>]] |
|
| − | |- |
+ | |- |
| − | + | |Small: Monoamine ([[Tryptophan|Trp]]) || [[Melatonin]] || Mel || [[Melatonin receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |Small: Diamine ([[Histamine|His]]) || [[Histamine]] || H || [[Histamine receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Gastrins || [[Gastrin]] || || - || - |
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| − | |- |
+ | |- |
| − | + | |PP: Gastrins || [[Cholecystokinin]] || CCK || [[Cholecystokinin receptor]] || - |
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| − | |- |
+ | |- |
| − | + | |PP: Neurohypophyseals || [[Vasopressin]] || AVP || [[Vasopressin receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Neurohypophyseals || [[Oxytocin]] || OT || [[Oxytocin receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Neurohypophyseals || [[Neurophysin I]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Neurohypophyseals || [[Neurophysin II]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Neuropeptide Y || [[Neuropeptide Y]] || NY || [[Neuropeptide Y receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Neuropeptide Y || [[Pancreatic polypeptide]] || PP || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Neuropeptide Y || [[Peptide YY]] || PYY || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: [[Opioid]]s || [[Corticotropin]] (adrenocorticotropic hormone) || ACTH || [[Corticotropin receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Opioids || [[Dynorphin]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Opioids || [[Endorphin]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Opioids || [[Enkephaline]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Secretins || [[Secretin]] || || [[Secretin receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Secretins || [[Motilin]] || || [[Motilin receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Secretins || [[Glucagon]] || || [[Glucagon receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Secretins || [[Vasoactive intestinal peptide]] || VIP || [[Vasoactive intestinal peptide receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Secretins || [[Growth hormone-releasing factor]] || GRF || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Somatostatins || [[Somatostatin]] || || [[Somatostatin receptor]] || - |
|
| − | |- |
+ | |- |
| − | + | |SS: Tachykinins || [[Neurokinin A]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |SS: Tachykinins || [[Neurokinin B]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |SS: Tachykinins || [[Substance P]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Other || [[Bombesin]] || || - || - |
|
| − | |- |
+ | |- |
| − | + | |PP: Other || [[Gastrin releasing peptide]] || GRP || - || - |
|
| − | |- |
+ | |- |
| − | + | |Gas || [[Nitric oxide]] || NO || Soluble [[guanylyl cyclase]] || - |
|
| − | |- |
+ | |- |
| − | + | |Gas || [[Carbon monoxide]] || CO || - || [[Heme]] bound to [[potassium channel]]s |
|
| − | |- |
+ | |- |
| − | + | |Other || [[Anandamide]] || AEA || [[Cannabinoid receptor]] || - |
|
| ⚫ | |||
| − | |||
| + | |Other || [[Adenosine triphosphate]] || ATP || [[P2Y12]] || [[P2X receptor]] |
||
|} |
|} |
||
| + | ==Precursors of neurotransmitters== |
||
| − | ==Production and destruction cycles== |
||
| + | While intake of neurotransmitter [[Precursor (chemistry)|precursors]] does increase neurotransmitter synthesis, evidence is mixed as to whether [[neurotransmitter release]] (firing) is increased. Even with increased neurotransmitter release, it is unclear whether this will result in a long-term increase in neurotransmitter signal strength, since the nervous system can adapt to changes such as increased neurotransmitter synthesis and may therefore maintain constant firing.<ref name="NeurotransmitterPrecursorsDepression">{{cite journal|author = Meyers, Stephen|title = Use of Neurotransmitter Precursors for Treatment of Depression|journal = Alternative Medicine Review|volume = 5|pages = 64–71|year = 2000|pmid =10696120|doi =|url = http://www.thorne.com/altmedrev/.fulltext/5/1/64.pdf|issue = 1}}</ref> Some neurotransmitters may have a role in depression, and there is some evidence to suggest that intake of precursors of these neurotransmitters may be useful in the treatment of mild and moderate depression.<ref name="NeurotransmitterPrecursorsDepression"/><ref name="ManagementDepressionSerotoninPrecursors">{{cite journal|author =|title = Management of depression with serotonin precursors|journal = Biol Psychiatry|volume = 16|pages = 291–310|year = 1981|pmid = 6164407|issue = 3|last1 =Van Praag|first1 =HM}}</ref> |
||
| − | When neurotransmitters are released into the [[synapse]] only some binds with receptors, the rest may be broken down by enzymes in the synaptic fluid or is reabsorbed quickly into the presynaptic neuron via a [[reuptake transporter pump]]. This allows for the neurotransmitter to be repackaged in the vesicles and to be recycled. |
||
| − | |||
| ⚫ | |||
| − | Many of these neurochemicals have been studied with a view to identifying the genetic mechanisms underlying their production and control |
||
| − | |||
| − | {{Main|Genetic factors influencing neurotransmitter production and action}} |
||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | ---- |
||
| + | ===Dopamine precursors=== |
||
| − | == See also == |
||
| + | [[L-DOPA|<small>L</small>-DOPA]], a precursor of [[dopamine]] that crosses the [[blood–brain barrier]], is used in the treatment of [[Parkinson's disease]]. |
||
| − | * [[Catecholamines]] |
||
| − | * [[Cholecystokinin]] |
||
| − | * [[Endorphins]] |
||
| − | * [[Factors affecting neurotransmitter action]] |
||
| ⚫ | |||
| ⚫ | |||
| ⚫ | |||
| − | * [[Neurokinins]] |
||
| − | * [[Neurotensin]] |
||
| + | ===Norepinephrine precursors=== |
||
| − | ==References & Bibliography== |
||
| + | 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.<ref name="NeurotransmitterPrecursorsDepression"/> |
||
| − | ==Key texts== |
||
| − | ===Books=== |
||
| − | * Kopn,L.J. (ed.) Neurotransmitters, Baltmore: Williams & Wilkins. |
||
| + | ===Serotonin precursors=== |
||
| + | Administration of [[L-tryptophan]], a precursor for [[serotonin]], is seen to double the production of serotonin in the brain. It is significantly more effective than a placebo in the treatment of mild and moderate depression.<ref name="NeurotransmitterPrecursorsDepression"/> This conversion requires [[vitamin C]].<ref name=serotonin /> [[5-hydroxytryptophan]] (5-HTP), also a precursor for [[serotonin]], is also more effective than a placebo.<ref name="NeurotransmitterPrecursorsDepression"/> |
||
| + | ==Degradation and elimination== |
||
| − | ===Papers=== |
||
| + | A neurotransmitter must be broken down once it reaches the post-synaptic cell to prevent further excitatory or inhibitory signal transduction. For example, [[acetylcholine| acetylcholine (ACh)]], an excitatory neurotransmitter, is broken down by [[acetylcholinesterase]] (AChE). [[Choline]] is taken up and recycled by the pre-synaptic neuron to synthesize more ACh. |
||
| − | |||
| + | Other neurotransmitters such as [[dopamine]] are able to [[diffusion|diffuse]] away from their targeted synaptic junctions and are eliminated from the body via the kidneys, or destroyed in the liver. Each neurotransmitter has very specific degradation pathways at regulatory points, which may be the target of the body's own regulatory system or [[recreational drug]]s. |
||
| − | ==Additional material== |
||
| − | ===Books=== |
||
| − | == |
+ | ==See also== |
| + | *[[Amino acid neurotransmitters]] |
||
| ⚫ | |||
| + | *[[Kiss-and-run fusion]] |
||
| ⚫ | |||
| + | *[[Neuromuscular transmission]] |
||
| + | *[[Neuropeptide]] |
||
| ⚫ | |||
==References== |
==References== |
||
| − | {{Reflist}} |
+ | {{Reflist|2}} |
==External links== |
==External links== |
||
| − | {{ |
+ | {{Commons|Neurotransmitter|Neurotransmitter}} |
| − | * |
+ | *[http://micro.magnet.fsu.edu/micro/gallery/neurotrans/neurotrans.html Molecular Expressions Photo Gallery: The Neurotransmitter Collection] |
| − | * |
+ | *[http://www.benbest.com/science/anatmind/anatmd10.html Brain Neurotransmitters] |
| − | * |
+ | *[http://www.neurotransmitter.net/neurosignaling.html Endogenous Neuroactive Extracellular Signal Transducers] |
| − | * |
+ | *{{MeshName|Neurotransmitter}} |
| + | *[http://faculty.washington.edu/chudler/chnt1.html neuroscience for kids website] |
||
| + | *[http://www.brainexplorer.org/neurological_control/Neurological_Neurotransmitters.shtml brain explorer website] |
||
| + | *[http://en.wikibooks.org/wiki/Neuroscience/Cellular_Neurobiology/Neurotransmitters wikibooks cellular neurobiology] |
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| + | {{Neuroscience}} |
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| + | {{Neurotransmitters}} |
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{{Cell signaling}} |
{{Cell signaling}} |
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| ⚫ | |||
| − | [[Category:Neurotransmitters]] |
+ | [[Category:Neurotransmitters| ]] |
| ⚫ | |||
[[Category:Molecular neuroscience]] |
[[Category:Molecular neuroscience]] |
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| − | [[bn:নিউরোট্রান্সমিটার]] |
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| − | [[bg:Невротрансмитер]] |
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| − | [[ca:Neurotransmissor]] |
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| − | [[cs:Neurotransmitér]] |
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| − | [[ko:신경전달물질]] |
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| − | [[hr:Neurotransmiter]] |
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| − | [[it:Neurotrasmettitore]] |
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| − | [[he:מוליך עצבי]] |
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| − | [[lt:Mediatorius (biochemija)]] |
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| − | [[hu:Ingerületátvivő anyagok]] |
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| − | [[ja:神経伝達物質]] |
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| − | [[no:Nevrotransmitter]] |
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| − | [[pl:Neuroprzekaźnik]] |
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Latest revision as of 00:09, 5 October 2013
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Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
- For an introduction to concepts and terminology used in this article, see Chemical synapse.
| Structure of a typical chemical synapse |
|---|
Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a target cell across a synapse.[1] Neurotransmitters are packaged into synaptic vesicles clustered beneath the membrane in the axon terminal, on the presynaptic side of a synapse. They are released into and diffuse across the synaptic cleft, where they bind to specific receptors in the membrane on the postsynaptic side of the synapse.[2] Release of neurotransmitters usually follows arrival of an action potential at the synapse, but may also follow graded electrical potentials. Low level "baseline" release also occurs without electrical stimulation. Many neurotransmitters are synthesized from plentiful and simple precursors, such as amino acids, which are readily available from the diet and which require only a small number of biosynthetic steps to convert.[3]
Discovery
Until the early 20th century, scientists assumed that the majority of synaptic communication in the brain was electrical. However, through the careful histological examinations of Ramón y Cajal (1852–1934), a 20 to 40 nm gap between neurons, known today as the synaptic cleft, was discovered. The presence of such a gap suggested communication via chemical messengers traversing the synaptic cleft, and in 1921 German pharmacologist Otto Loewi (1873–1961) confirmed that neurons can communicate by releasing chemicals. Through a series of experiments involving the vagus nerves of frogs, Loewi was able to manually slow the heart rate of frogs by controlling the amount of saline solution present around the vagus nerve. Upon completion of this experiment, Loewi asserted that sympathetic regulation of cardiac function can be mediated through changes in chemical concentrations. Furthermore, Otto Loewi is accredited with discovering acetylcholine (ACh)—the first known neurotransmitter.[4] Some neurons do, however, communicate via electrical synapses through the use of gap junctions, which allow specific ions to pass directly from one cell to another.[5]
Identifying neurotransmitters
The chemical identity of neurotransmitters is often difficult to determine experimentally. For example, it is easy using an electron microscope to recognize vesicles on the presynaptic side of a synapse, but it may not be easy to determine directly what chemical is packed into them. The difficulties led to many historical controversies over whether a given chemical was or was not clearly established as a transmitter. In an effort to give some structure to the arguments, neurochemists worked out a set of experimentally tractable rules. According to the prevailing beliefs of the 1960s, a chemical can be classified as a neurotransmitter if it meets the following conditions:
- There are precursors and/or synthesis enzymes located in the presynaptic side of the synapse.
- The chemical is present in the presynaptic element.
- It is available in sufficient quantity in the presynaptic neuron to affect the postsynaptic neuron.
- There are postsynaptic receptors and the chemical is able to bind to them.
- A biochemical mechanism for inactivation is present.
Modern advances in pharmacology, genetics, and chemical neuroanatomy have greatly reduced the importance of these rules. A series of experiments that may have taken several years in the 1960s can now be done, with much better precision, in a few months. Thus, it is unusual nowadays for the identification of a chemical as a neurotransmitter to remain controversial for very long periods of time.
Types of neurotransmitters
There are many different ways to classify neurotransmitters. Dividing them into amino acids, peptides, and monoamines is sufficient for some classification purposes.
Major neurotransmitters:
- Amino acids: glutamate,[3] aspartate, D-serine, γ-aminobutyric acid (GABA), glycine
- Monoamines and other biogenic amines: dopamine (DA), norepinephrine (noradrenaline; NE, NA), epinephrine (adrenaline), histamine, serotonin (SE, 5-HT)
- Peptides: somatostatin, substance P, opioid peptides[6]
- Others: acetylcholine (ACh), adenosine, anandamide, nitric oxide, etc.
In addition, over 50 neuroactive peptides have been found, and new ones are discovered regularly. Many of these are "co-released" along with a small-molecule transmitter, but in some cases a peptide is the primary transmitter at a synapse. β-endorphin is a relatively well known example of a peptide neurotransmitter; it engages in highly specific interactions with opioid receptors in the central nervous system.
Single ions, such as synaptically released zinc, are also considered neurotransmitters by some,[7] as are some gaseous molecules such as nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO).[8] Because they are not packaged into vesicles they are not classical neurotransmitters by the strictest definition, however they have all been shown experimentally to be released by presynaptic terminals in an activity-dependent way.
By far the most prevalent transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain.[3] The next most prevalent is GABA, which is inhibitory at more than 90% of the synapses that do not use glutamate. Even though other transmitters are used in far fewer synapses, they may be very important functionally—the great majority of psychoactive drugs exert their effects by altering the actions of some neurotransmitter systems, often acting through transmitters other than glutamate or GABA. Addictive drugs such as cocaine and amphetamine exert their effects primarily on the dopamine system. The addictive opiate drugs exert their effects primarily as functional analogs of opioid peptides, which, in turn, regulate dopamine levels.
Excitatory and inhibitory
Some neurotransmitters are commonly described as "excitatory" or "inhibitory". The only direct effect of a neurotransmitter is to activate one or more types of receptors. The effect on the postsynaptic cell depends, therefore, entirely on the properties of those receptors. It happens that for some neurotransmitters (for example, glutamate), the most important receptors all have excitatory effects: that is, they increase the probability that the target cell will fire an action potential. For other neurotransmitters, such as GABA, the most important receptors all have inhibitory effects (although there is evidence that GABA is excitatory during early brain development). There are, however, other neurotransmitters, such as acetylcholine, for which both excitatory and inhibitory receptors exist; and there are some types of receptors that activate complex metabolic pathways in the postsynaptic cell to produce effects that cannot appropriately be called either excitatory or inhibitory. Thus, it is an oversimplification to call a neurotransmitter excitatory or inhibitory—nevertheless it is convenient to call glutamate excitatory and GABA inhibitory so this usage is seen frequently.
Actions
- Main article: Neuromodulation
As explained above, the only direct action of a neurotransmitter is to activate a receptor. Therefore, the effects of a neurotransmitter system depend on the connections of the 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:
- Glutamate is used at the great majority of fast excitatory synapses in the brain and spinal cord. It is also used at most synapses that are "modifiable", i.e. capable of increasing or decreasing in strength. Excess glutamate can overstimulate the brain and causes seizures.[citation needed] Modifiable synapses are thought to be the main memory-storage elements in the brain. Excessive glutamate release can lead to excitotoxicity causing cell death.
- GABA is used at the great majority of fast inhibitory synapses in virtually every part of the brain. Many sedative/tranquilizing drugs act by enhancing the effects of GABA. Correspondingly glycine is the inhibitory transmitter in the spinal cord.
- Acetylcholine is distinguished as the transmitter at the neuromuscular junction connecting motor nerves to muscles. The paralytic arrow-poison curare acts by blocking transmission at these synapses. Acetylcholine also operates in many regions of the brain, but using different types of receptors, including nicotinic and muscarinic receptors.[9]
- Dopamine has a number of important functions in the brain; this includes regulation of motor behavior, pleasures related to motivation and also emotional arousal. It plays a critical role in the reward system; people with Parkinson's disease have been linked to low levels of dopamine and people with schizophrenia have been linked to high levels of dopamine.[10]
- Serotonin is a monoamine neurotransmitter. Most is produced by and found in the intestine (approximately 90%), and the remainder in central nervous system neurons. It functions to regulate appetite, sleep, memory and learning, temperature, mood, behaviour, muscle contraction, and function of the cardiovascular system and endocrine system. It is speculated to have a role in depression, as some depressed patients are seen to have lower concentrations of metabolites of serotonin in their cerebrospinal fluid and brain tissue.[11]
- Substance P is an undecapeptide responsible for transmission of pain from certain sensory neurons to the central nervous system. It also aids in controlling relaxation of the vasculature and lowering blood pressure through the release of nitric oxide.[12]
- Opioid peptides are neurotransmitters that act within pain pathways and the emotional centers of the brain; some of them are analgesics and elicit pleasure or euphoria.[13]
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.
Drugs targeting the neurotransmitter of such systems affect the whole system; this fact explains the complexity of action of some drugs. Cocaine, for example, blocks the reuptake of dopamine back into the presynaptic neuron, leaving the neurotransmitter molecules in the synaptic gap longer. Since the dopamine remains in the synapse longer, the neurotransmitter continues to bind to the receptors on the postsynaptic neuron, eliciting a pleasurable emotional response. Physical addiction to cocaine may result from prolonged exposure to excess dopamine in the synapses, which leads to the downregulation of some postsynaptic receptors. After the effects of the drug wear off, one might feel depressed because of the decreased probability of the neurotransmitter binding to a receptor. Prozac is a selective serotonin reuptake inhibitor (SSRI), which blocks re-uptake of serotonin by the presynaptic cell. This increases the amount of serotonin present at the synapse and allows it to remain there longer, hence potentiating the effect of naturally released serotonin.[14] AMPT prevents the conversion of tyrosine to L-DOPA, the precursor to dopamine; reserpine prevents dopamine storage within vesicles; and deprenyl inhibits monoamine oxidase (MAO)-B and thus increases dopamine levels.
Diseases may affect specific neurotransmitter systems. For example, Parkinson's disease is at least in part related to failure of dopaminergic cells in deep-brain nuclei, for example the substantia nigra. Levodopa is a precursor of dopamine, and is the most widely used drug to treat Parkinson's disease.
A brief comparison of the major neurotransmitter systems follows:
| System | Origin [15] | Effects[15] |
|---|---|---|
| Noradrenaline system | locus coeruleus |
|
| Lateral tegmental field | ||
| Dopamine system | dopamine pathways: | motor system, reward, cognition, endocrine, nausea |
| Serotonin system | caudal dorsal raphe nucleus | Increase (introversion), mood, satiety, body temperature and sleep, while decreasing nociception. |
| rostral dorsal raphe nucleus | ||
| Cholinergic system | pontomesencephalotegmental complex |
|
| basal optic nucleus of Meynert | ||
| medial septal nucleus |
Common neurotransmitters
Precursors of neurotransmitters
While intake of neurotransmitter precursors does increase neurotransmitter synthesis, evidence is mixed as to whether neurotransmitter release (firing) is increased. Even with increased neurotransmitter release, it is unclear whether this will result in a long-term increase in neurotransmitter signal strength, since the nervous system can adapt to changes such as increased neurotransmitter synthesis and may therefore maintain constant firing.[16] Some neurotransmitters may have a role in depression, and there is some evidence to suggest that intake of precursors of these neurotransmitters may be useful in the treatment of mild and moderate depression.[16][17]
Dopamine precursors
L-DOPA, a precursor of dopamine that crosses the blood–brain barrier, is used in the treatment of Parkinson's disease.
Norepinephrine precursors
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.[16]
Serotonin precursors
Administration of L-tryptophan, a precursor for serotonin, is seen to double the production of serotonin in the brain. It is significantly more effective than a placebo in the treatment of mild and moderate depression.[16] This conversion requires vitamin C.[11] 5-hydroxytryptophan (5-HTP), also a precursor for serotonin, is also more effective than a placebo.[16]
Degradation and elimination
A neurotransmitter must be broken down once it reaches the post-synaptic cell to prevent further excitatory or inhibitory signal transduction. For example, acetylcholine (ACh), an excitatory neurotransmitter, is broken down by acetylcholinesterase (AChE). Choline is taken up and recycled by the pre-synaptic neuron to synthesize more ACh. Other neurotransmitters such as dopamine are able to diffuse away from their targeted synaptic junctions and are eliminated from the body via the kidneys, or destroyed in the liver. Each neurotransmitter has very specific degradation pathways at regulatory points, which may be the target of the body's own regulatory system or recreational drugs.
See also
- Amino acid neurotransmitters
- Gasotransmitters
- Kiss-and-run fusion
- Nervous system
- Neuromuscular transmission
- Neuropeptide
- Neuropsychopharmacology
References
- ↑ Template:DorlandsDict
- ↑ Elias, L. J, & Saucier, D. M. (2005). Neuropsychology: Clinical and Experimental Foundations. Boston: Pearson
- ↑ 3.0 3.1 3.2 includeonly>Robert Sapolsky. "Biology and Human Behavior: The Neurological Origins of Individuality, 2nd edition", 'The Teaching Company'. “see pages 13 & 14 of Guide Book”
- ↑ Saladin, Kenneth S. Anatomy and Physiology: The Unity of Form and Function. McGraw Hill. 2009 ISBN 0-07-727620-5
- ↑ Junctions Between Cells. URL accessed on 2010-11-22.
- ↑ http://www.ncbi.nlm.nih.gov/pubmed/38738
- ↑ Kodirov,Sodikdjon A., Shuichi Takizawa, Jamie Joseph, Eric R. Kandel, Gleb P. Shumyatsky, and Vadim Y. Bolshakov. Synaptically released zinc gates long-term potentiation in fear conditioning pathways. PNAS, October 10, 2006. 103(41): 15218-23. DOI:10.1073/pnas.0607131103
- ↑ Nitric oxide and other gaseous neurotransmitters
- ↑ http://www.ebi.ac.uk/interpro/potm/2005_11/Page2.htm
- ↑ Schacter, Gilbert and Weger. Psychology.United States of America.2009.Print.
- ↑ 11.0 11.1 University of Bristol. Introduction to Serotonin. URL accessed on 2009-10-15.
- ↑ http://www.wellnessresources.com/health_topics/sleep/substance_p.php
- ↑ Schacter, Gilbert and Weger. Psychology. 2009.Print.
- ↑ Yadav, V. et al (2008). Lrp5 Controls Bone Formation by Inhibiting Serotonin Synthesis in the Duodenum. Cell 135 (5): 825–837.
- ↑ 15.0 15.1 Rang, H. P. (2003). Pharmacology, 474 for noradrenaline system, page 476 for dopamine system, page 480 for serotonin system and page 483 for cholinergic system., Edinburgh: Churchill Livingstone.
- ↑ 16.0 16.1 16.2 16.3 16.4 Meyers, Stephen (2000). Use of Neurotransmitter Precursors for Treatment of Depression. Alternative Medicine Review 5 (1): 64–71.
- ↑ (1981) Management of depression with serotonin precursors. Biol Psychiatry 16 (3): 291–310.
External links
- Molecular Expressions Photo Gallery: The Neurotransmitter Collection
- Brain Neurotransmitters
- Endogenous Neuroactive Extracellular Signal Transducers
- MeSH Neurotransmitter
- neuroscience for kids website
- brain explorer website
- wikibooks cellular neurobiology
Neurotransmitters | ||||
|---|---|---|---|---|
| Amino acids |
Alanine · Aspartate · Cycloserine · DMG · GABA · Glutamate · Glycine · Hypotaurine · Kynurenic acid (Transtorine) · NAAG (Spaglumic acid) · NMG (Sarcosine) · Serine · Taurine · TMG (Betaine) | |||
| Endocannabinoids |
2-AG · 2-AGE (Noladin ether) · AEA (Anandamide) · NADA · OAE (Virodhamine) · Oleamide ·PEA (Palmitoylethanolamide) ·RVD-Hpα ·Hp (Hemopressin) | |||
| Gasotransmitters |
Carbon monoxide · Hydrogen sulfide · Nitric oxide · Nitrous oxide | |||
| Monoamines |
Dopamine · Epinephrine (Adrenaline) · Melatonin · NAS (Normelatonin) · Norepinephrine (Noradrenaline) · Serotonin (5-HT) | |||
| Purines |
| |||
| Trace amines |
3-ITA · 5-MeO-DMT · Bufotenin · DMT · NMT · Octopamine · Phenethylamine · Synephrine · Thyronamine · Tryptamine · Tyramine | |||
| Others |
1,4-BD · Acetylcholine · GBL · GHB · Histamine | |||
|
See also Template:Neuropeptides | ||||
| {| class="navbox collapsible uncollapsed nowraplinks" style="margin:auto; " | ||||
| ||||
|}
Cell physiology: cell signaling | |
|---|---|
| Key concepts |
Ligand - Cell signaling networks - Signal transduction - Apoptosis - Second messenger system (Ca2+ signaling, Lipid signaling) |
| Processes |
Paracrine - Autocrine - Juxtacrine - Neurotransmitters - Endocrine (Neuroendocrine) |
| Types of proteins |
Receptor (Transmembrane, Intracellular) - Transcription factor (General, Preinitiation complex, TFIID, TFIIH) - Adaptor protein |
Neurotransmitter systems | |||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| Acetylcholine | |||||||||||
| BA/M |
| ||||||||||
| AA |
| ||||||||||
| This page uses Creative Commons Licensed content from Wikipedia (view authors). |