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{{For|an introduction to concepts and terminology used in this article|Chemical synapse}}
{{Use dmy dates|date=October 2014}}
{{Synapse map}}
'''Neurotransmitters''' are [[endogenous]] [[chemistry|chemicals]] that transmit signals across a [[synapse]] from one [[neuron]] ([[brain]] [[cell (biology)|cell]]) to another 'target' neuron.<ref>{{DorlandsDict|six/000072138|Neurotransmitter}}</ref> Neurotransmitters are packaged into [[synaptic vesicles]] clustered beneath the [[Cell membrane|membrane]] in the [[axon terminal]], on the presynaptic side of a synapse. Neurotransmitters are released into and diffuse across the [[synaptic cleft]], where they bind to specific [[Receptor (biochemistry)|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> 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. Neurotransmitters play a major role in shaping everyday life and functions. Scientists do not yet know exactly how many neurotransmitters exist, but more than 100&nbsp;chemical messengers have been identified.<ref>{{cite web|last1=Cherry|first1=Kendra|title=What is a Nuerotransmitter?|url=http://psychology.about.com/od/nindex/g/neurotransmitter.htm|accessdate=6 October 2014}}</ref>
 
Most neurotransmitters are about the size of a single amino acid, but some neurotransmitters may be the size of larger proteins or [[peptides]]. A released neurotransmitter is typically available in the synaptic cleft for a short time before it is metabolized by enzymes, pulled back into the presynaptic neuron through [[reuptake]], or bound to a [[postsynaptic receptor]]. Nevertheless, short-term exposure of the receptor to neurotransmitter is typically sufficient for causing a postsynaptic response by way of [[Neurotransmission|synaptic transmission]].

In response to a threshold [[action potential]] or [[Membrane potential#Graded potentials|graded electrical potential]], a neurotransmitter is released at the presynaptic terminal. Low level "baseline" release also occurs without electrical stimulation. The released neurotransmitter may then move across the synapse to be detected by and bind with receptors in the postsynaptic neuron. Binding of neurotransmitters may influence the postsynaptic neuron in either an [[Inhibitory synapse|inhibitory]] or [[Excitatory synapse|excitatory]] way. This neuron may be connected to many more neurons, and if the total of excitatory influences is greater than that of inhibitory influences, it will also "fire". That is to say, it will create a new action potential at its [[axon hillock]] to release neurotransmitters and pass on the information to yet another neighboring neuron.<ref name=twsNovK11>{{cite news
 |author= Robert Sapolsky
 |title= Biology and Human Behavior: The Neurological Origins of Individuality, 2nd edition
 |publisher= ''The Teaching Company''
 |quote=see pages 13 & 14 of Guide Book
 |year=2005
}}</ref>

==Discovery==
Until the early 20th century, scientists assumed that the majority of synaptic communications within the brain were electrical. However, careful [[Histology|histological]] examinations by [[Ramón y Cajal]] (1852–1934), led to the discovery of what is presently known as the [[synaptic cleft]], a 20 to 40&nbsp;nm gap between neurons. The presence of synaptic clefts suggested communications via chemical messengers traversing the synaptic cleft. Furthermore, in 1921, German pharmacologist [[Otto Loewi]] (1873–1961) confirmed that neurons can communicate by releasing chemicals. Loewi led a series of experiments involving the vagus nerves of frogs and 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 regulations of cardiac function can be mediated through changes in chemical concentrations. Otto Loewi is now 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, nevertheless, 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=22 November 2010}}</ref>

Neurons form elaborate networks through which nerve impulses (action potentials) travel. Each neuron has 15,000 connections with neighboring neurons. Neurons do not make physical contact with one another (except in the case of an electrical synapse through a gap junction); instead, neurons interact at synapses- a junction within two nerve cells, consisting of a miniature gap which impulses pass by a neurotransmitter. A neuron transports information through nerve impulse. When a nerve impulse arrives at the synapse, it releases neurotransmitters which influence another cell, either in an inhibitory or excitatory way. The next neuron may be connected to many more neurons, and if the total of excitatory influences is greater than that of inhibitory influences, it will also "fire". That is to say, it will create a new action potential at its axon hillock, releasing neurotransmitters and passing on the information to yet another neighboring neuron.

==Identification==
There are four main criteria for identifying neurotransmitters:
# The chemical must be synthesized in the neuron or otherwise be present in it. 
# When the neuron is active, the chemical must be released and produce a response in some target. 
# The same response must be obtained when the chemical is experimentally placed on the target. 
# A mechanism must exist for removing the chemical from its site of activation after its work is done.

However, given advances in pharmacology, genetics, and chemical neuroanatomy, the term "neurotransmitter" can be applied to chemicals that:
* carry messages between neurons via influence on the postsynaptic membrane.
* have little or no effect on membrane voltage, but have a common carrying function such as changing the structure of the [[synapse]]. 
* also communicate by sending reverse-direction messages that have an impact on the release or reuptake of transmitters.

Various techniques and experiments such as staining, stimulating, and collecting can be used to identify neurotransmitters throughout the [[central nervous system]].<ref name="Kolb Intro to Brain & Behavior">{{cite book|last1=Whishaw|first1=Bryan Kolb, Ian Q.|title=An introduction to brain and behavior|date=2014|publisher=Worth Publishers|location=New York, NY|isbn=978-1429242288|pages=150–151|edition=4th}}</ref>

==Types==
There are numerous ways to classify neurotransmitters. However, for classification purposes, the main neurotransmitters are: [[amino acids]], [[amine]]s ([[monoamine]]s and other [[biogenic amines]]),  [[peptides]], and certain soluble gases. 

Major neurotransmitters:

*'''[[Amino acid]]s:''' [[glutamate]],<ref name=twsNovK11/> [[aspartate]], [[D-serine]], [[γ-aminobutyric acid]] (GABA), [[glycine]]
*'''[[Amine]]s:''' [[dopamine]] (DA), [[norepinephrine]] (noradrenaline; NE, NA), [[epinephrine]] (adrenaline), [[histamine]], [[serotonin]] (SER, 5-HT)
**'''Trace amines''': [[phenethylamine]], [[N-methylphenethylamine|''N''-methylphenethylamine]], [[tyramine]], [[3-iodothyronamine]], [[octopamine]], [[tryptamine]], etc.
*'''[[Peptide]]s:''' [[somatostatin]], [[substance P]], [[cocaine and amphetamine regulated transcript]], [[opioid peptide]]s<ref name="pmid38738">{{cite journal | author = Snyder SH, Innis RB | title = Peptide neurotransmitters | journal = Annu. Rev. Biochem. | volume = 48 | issue = | pages = 755–82 | year = 1979 | pmid = 38738 | doi = 10.1146/annurev.bi.48.070179.003543 | url = }}</ref>
*'''Soluble gasess:''' [[nitric oxide]] (NO), [[carbon monoxide]] (CO)
*Others: [[acetylcholine]] (ACh), [[adenosine]], [[anandamide]], etc.

In addition, over fifty neuroactive [[peptide]]s have been discovered and more recent peptides are found regularly. Many of these are "co-released" along with a small-molecule transmitter. Nevertheless, in some cases a peptide is the primary transmitter at a synapse. [[β-endorphin]] is a relatively well known example of a peptide neurotransmitter because it engages in highly specific interactions with [[opioid receptors]] in the [[central nervous system]].

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'', 10 October 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/mars-library/international-symposium-on-nitric-oxide-dr-john-andrews/ Nitric oxide and other gaseous neurotransmitters]</ref> Because they are not packaged into vesicles, they are not classical neurotransmitters by the strictest definition; they have all been presented experimentally to be released by presynaptic terminals in an activity-dependent way.

The most prevalent transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain.<ref name=twsNovK11/> Next is Gamma-Aminobutyric Acid, or GABA, which is inhibitory at more than 90% of the synapses that do not use glutamate. Although other transmitters are used in 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===
A neurotransmitter can influence the function of a neuron through a remarkable number of mechanisms. In its direct actions in influencing a neuron’s electrical excitability, however, a neurotransmitter acts in only one of two ways. It influences transmembrane ion flow either to increase or to decrease the probability that the cell with which it comes in contact will produce an action potential. Thus, despite the wide variety of synapses, they all convey messages of only these two types, excitatory or inhibitory, and they are labeled as such. Type I synapses are [[excitatory]] in their actions, whereas type II synapses are [[inhibitory]]. Each type has a different appearance and is located on different parts of the neurons under its influence.Each neuron receives thousands of excitatory and inhibitory signals every second.

Type I (excitatory) synapses are typically located on the shafts or the spines of dendrites, whereas type II (inhibitory) synapses are typically located on a cell body. In addition, Type I synapses have round synaptic vesicles, whereas the vesicles of type II synapses are flattened. The material on the presynaptic and postsynaptic membranes is denser in a Type I synapse than it is in a type II, and the type I synaptic cleft is wider. Finally, the active zone on a Type I synapse is larger than that on a Type II synapse.

The different locations of type I and type II synapses divide a neuron into two zones: an excitatory dendritic tree and an inhibitory cell body. You can think of excitatory and inhibitory messages as interacting from these two different perspectives.

From an inhibitory perspective, you can picture excitation coming in over the dendrites and spreading to the [[axon hillock]] to trigger an [[action potential]]. If the message is to be stopped, it is best stopped by applying inhibition on the cell body, close to the axon hillock where the action potential originates. Another way to conceptualize excitatory–inhibitory interaction is to picture excitation overcoming inhibition. If the cell body is normally in an inhibited state, the only way to generate an action potential at the axon hillock is to reduce the cell body’s inhibition. In this “open the gates” strategy, the excitatory message is like a racehorse ready to run down the track, but first the inhibitory starting gate must be removed.<ref>Kolb, B., & Whishaw, I. Q. (2014). An introduction to brain and behavior. Worth Publishers.</ref>

==Actions==
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. [[Synaptic plasticity|Modifiable synapses]] are thought to be the main memory-storage elements in the brain. Excessive glutamate release can overstimulate the brain and lead to [[excitotoxicity]] causing cell death resulting in seizures or strokes.<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1609133/#!po=50.0000 Glutamate: Seizures and strokes]- PLoS Biol. 2006 November; 4(11): e371. Published online 2006 October 17. doi: 10.1371/journal.pbio.0040371 by author Liza Gross- Courtesy Public Library of Science (2006); PubMed (PMC) of NCBI, Retrieved 2013-16-13</ref> Excitotoxicity has been implicated in certain chronic diseases including [[ischemic stroke]], [[epilepsy]], [[Amyotrophic lateral sclerosis]], [[Alzheimer's disease]], [[Huntington disease]], and [[Parkinson's disease]].<ref name="pmid21729715">{{cite journal | author = Yang JL, Sykora P, Wilson DM, Mattson MP, Bohr VA | title = The excitatory neurotransmitter glutamate stimulates DNA repair to increase neuronal resiliency | journal = Mech. Ageing Dev. | volume = 132 | issue = 8–9 | pages = 405–11 | year = 2011 | date = August 2011 | pmid = 21729715 | pmc = 3367503 | doi = 10.1016/j.mad.2011.06.005 | url = }}</ref>
*[[GABA]] is used at the great majority of fast inhibitory synapses in virtually every part of the brain. Many [[sedative|sedative/tranquilizing drugs]] act by enhancing the effects of GABA.<ref>[http://www.sleepfoundation.org/article/orexin-receptor-antagonists-new-class-sleeping-pill Orexin receptor antagonists a new class of sleeping pill], National Sleep Foundation.</ref> 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 [[Acetylcholine receptor#Receptor types|different types of receptors]], including [[Nicotinic acetylcholine receptor|nicotinic]] and [[Muscarinic acetylcholine receptor|muscarinic]] receptors.<ref>{{cite web|url=http://www.ebi.ac.uk/interpro/potm/2005_11/Page2.htm |title=Acetylcholine Receptors |publisher=Ebi.ac.uk |accessdate=25 August 2014}}</ref>
*[[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>
*[[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=15 October 2009}}</ref>
*[[Norepinephrine]] which focuses on the central nervous system, based on patients sleep patterns, focus and alertness. It is synthesized from [[tyrosine]].
*[[Epinephrine]] which is also synthesized from tyrosine takes part in controlling the adrenal glands. It plays a role in sleep, with ones ability to stay become alert, and the [[fight-or-flight response]].
*[[Histamine]] works with the central nervous system (CNS), specifically the hypothalamus ([[tuberomamillary nucleus]]) and CNS [[mast cell]]s.
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.

A brief comparison of the major neurotransmitter systems follows:
<!--"Neurotransmitter system" and other articles redirect to the anchor in the wikitable title-->
{| class="wikitable"
|+Neurotransmitter systems{{anchor|table}}
|-
! 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> !! Regulated effects and processes<ref name=Rang/>
|-
!Noradrenaline system<br /><ref name="VTA inputs">{{cite book | author = Malenka RC, Nestler EJ, Hyman SE | editor = Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | page = 155 | edition = 2nd | chapter = Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin | quote= Different subregions of the VTA receive glutamatergic inputs from the prefrontal cortex, orexinergic inputs from the lateral hypothalamus, cholinergic and also glutamatergic and GABAergic inputs from the laterodorsal tegmental nucleus and pedunculopontine nucleus, noradrenergic inputs from the locus ceruleus, serotonergic inputs from the raphe nuclei, and GABAergic inputs from the nucleus accumbens and ventral pallidum.}}</ref><ref name="Noradrenergic pathways">{{cite book | author = Malenka RC, Nestler EJ, Hyman SE | editor = Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | pages = 156–157 | edition = 2nd | chapter = Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin | quote=The locus ceruleus (LC), which is located on the floor of the fourth ventricle in the rostral pons, contains more than 50% of all noradrenergic neurons in the brain; it innervates both the forebrain (eg, it provides virtually all the NE to the cerebral cortex) and regions of the brainstem and spinal cord.&nbsp;... The other noradrenergic neurons in the brain occur in loose collections of cells in the brainstem, including the lateral tegmental regions.  These neurons project largely within the brainstem and spinal cord. {{abbr|NE|norepinephrine}}, along with {{abbr|5HT|serotonin}}, {{abbr|ACh|acetylcholine}}, histamine, and orexin, is a critical regulator of the sleep-wake cycle and of levels of arousal.&nbsp;... {{abbr|LC|locus ceruleus}} firing may also increase anxiety&nbsp;...Stimulation of β-adrenergic receptors in the amygdala results in enhanced memory for stimuli encoded under strong negative emotion&nbsp;... Epinephrine occurs in only a small number of central neurons, all located in the medulla. Epinephrine is involved in visceral functions, such as control of respiration.<!--Note: the noradrenergic pathways are based upon a projection diagram that can't be quoted.-->}}</ref>
| '''Noradernergic pathways''':
* [[Locus coeruleus]] (LC) projections
:* LC → [[Amygdala]] & [[Hippocampus]]
:* LC → [[Brain stem]] & [[Spinal cord]]
:* LC → [[Cerebellum]]
:* LC → [[Cerebral cortex]]
:* LC → [[Hypothalamus]]
:* LC → [[Tectum]]
:* LC → [[Thalamus]]
:* LC → [[Ventral tegmental area]]
* [[Lateral tegmental field]] (LTF) projections
:* LTF → [[Brain stem]] & [[Spinal cord]]
:* LTF → [[Olfactory bulb]]
|
* Anxiety
* arousal
* [[cognitive control]] & [[working memory]] (co-regulated by dopamine)
* hunger
* negative emotional memory
* respiration
* reward (minor role)
* [[sleep-wake cycle]]
|-
! Dopamine system<br /><ref name="Malenka pathways">{{cite book | author = Malenka RC, Nestler EJ, Hyman SE | editor = Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | pages = 147–148, 154–157 | edition = 2nd | chapter = Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin | quote=Neurons from the {{abbr|SNc|Substantia nigra pars compacta}} densely innervate the dorsal striatum where they play a critical role in the learning and execution of motor programs.  Neurons from the {{abbr|VTA|Ventral tegmental area}} innervate the ventral striatum (nucleus accumbens), olfactory bulb, amygdala, hippocampus, orbital and medial prefrontal cortex, and cingulate cortex. VTA {{abbr|DA|Dopamine}} neurons play a critical role in motivation, reward-related behavior, attention, and multiple forms of memory.&nbsp;... Thus, acting in diverse terminal fields, dopamine confers motivational salience ("wanting") on the reward itself or associated cues (nucleus accumbens shell region), updates the value placed on different goals in light of this new experience (orbital prefrontal cortex), helps consolidate multiple forms of memory (amygdala and hippocampus), and encodes new motor programs that will facilitate obtaining this reward in the future (nucleus accumbens core region and dorsal striatum).&nbsp;... {{Abbr|DA|Dopamine}} has multiple actions in the prefrontal cortex.  It promotes the "cognitive control" of behavior: the selection and successful monitoring of behavior to facilitate attainment of chosen goals.  Aspects of cognitive control in which DA plays a role include working memory, the ability to hold information "on line" in order to guide actions, suppression of prepotent behaviors that compete with goal-directed actions, and control of attention and thus the ability to overcome distractions.&nbsp;... Noradrenergic projections from the {{abbr|LC|locus coeruleus}} thus interact with dopaminergic projections from the VTA to regulate cognitive control.&nbsp;...}}</ref>
| '''[[Dopaminergic pathways]]''':
* [[Ventral tegmental area]] (VTA) projections
:* VTA → [[Amygdala]]
:* VTA → [[Cingulate gyrus]]
:* VTA → [[Hippocampus]]
:* VTA → [[Nucleus accumbens]]
:* VTA → [[Olfactory bulb]]
:* VTA → [[Prefrontal cortex]]
*[[Nigrostriatal pathway]]
:* [[Substantia nigra]] → [[Dorsal striatum]]
*[[Tuberoinfundibular pathway]]
:* [[Arcuate nucleus]] → [[Hypothalamus]]
|
* [[Cognitive control]] & [[working memory]] (co-regulated by norepinephrine)
* [[endocrine]] function
* [[mood (psychology)|mood]]
* motivation
* [[motor system]] function
* reward (primary mediator)
|-
!Histamine system<br /><ref name="Histamine pathways">{{cite book | author = Malenka RC, Nestler EJ, Hyman SE | editor = Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | pages = 175–176 | edition = 2nd | chapter = Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin | quote = Within the brain, histamine is synthesized exclusively by neurons with their cell bodies in the tuberomammillary nucleus (TMN) that lies within the posterior hypothalamus. There are approximately 64000 histaminergic neurons per side in humans. These cells project throughout the brain and spinal cord. Areas that receive especially dense projections include the cerebral cortex, hippocampus, neostriatum, nucleus accumbens, amygdala, and hypothalamus. &nbsp;... While the best characterized function of the histamine system in the brain is regulation of sleep and arousal, histamine is also involved in learning and memory&nbsp;...It also appears that histamine is involved in the regulation of feeding and energy balance.}}</ref>
|'''Histaminergic pathways''':
*[[Tuberomamillary nucleus]] (TMN) projections
:* TMN → [[Cerebral cortex]]
:* TMN → [[Hippocampus]]
:* TMN → [[Neostriatum]]
:* TMN → [[Nucleus accumbens]]
:* TMN → [[Amygdala]]
:* TMN → [[Hypothalamus]]
|
* Arousal
* feeding and energy balance 
* learning
* memory
* sleep
|-
! Serotonin system<br /><ref name="VTA inputs" /><ref name="Serotonergic pathways">{{cite book | author = Malenka RC, Nestler EJ, Hyman SE | editor = Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | pages = 158–160 | edition = 2nd | chapter = Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin | quote= [The] dorsal raphe preferentially innervates the cerebral cortex, thalamus, striatal regions (caudate-putamen and nucleus accumbens), and dopaminergic nuclei of the midbrain (eg, the substantia nigra and ventral tegmental area), while the median raphe innervates the hippocampus, septum, and other structures of the limbic forebrain.&nbsp;... it is clear that 5HT influences sleep, arousal, attention, processing of sensory information in the cerebral cortex, and important aspects of emotion (likely including aggression) and mood regulation.&nbsp;...The rostral nuclei, which include the nucleus linearis, dorsal raphe, medial raphe, and raphe pontis, innervate most of the brain, including the cerebellum.  The caudal nuclei, which comprise the raphe magnus, raphe pallidus, and raphe obscuris, have more limited projections that terminate in the cerebellum, brainstem, and spinal cord.}}</ref><ref>{{cite web|last1=Nestler|first1=Eric J.|title=BRAIN REWARD PATHWAYS|url=http://neuroscience.mssm.edu/nestler/brainRewardpathways.html|website=Icahn School of Medicine at Mount Sinai|publisher=Nestler Lab|accessdate=16 August 2014|quote=The dorsal raphe is the primary site of serotonergic neurons in the brain, which, like noradrenergic neurons, pervasively modulate brain function to regulate the state of activation and mood of the organism.}}</ref>
|'''Serotonergic pathways''':
[[Caudal nuclei]] (CN):<br />
[[Raphe magnus]], [[raphe pallidus]], [[raphe obscuris]]
* Caudal projections
:* CN → [[Cerebral cortex]]
:* CN → [[Thalamus]]
:* CN → [[Caudate putamen]] & [[nucleus accumbens]]
:* CN → [[Substantia nigra]] & [[ventral tegmental area]]
[[Rostral nuclei]] (RN):<br />
[[Nucleus linearis]], [[dorsal raphe]], [[medial raphe]], [[raphe pontis]]
* Rostral projections
:* RN → [[Amygdala]]
:* RN → [[Cingulate gyrus]]
:* RN → [[Hippocampus]]
:* RN → [[Hypothalamus]]
:* RN → [[Neocortex]]
:* RN → [[Septum]]
:* RN → [[Thalamus]]
:* RN → [[Ventral tegmental area]]
|
* Arousal
* attention
* [[body temperature]]
* emotion and [[Mood (psychology)|mood]]
* reward (minor role)
* [[satiety]]
* sensory perception
* sleep
|-
! GABA system<br /><ref name="tVTA projections">{{cite journal | author = Barrot M, Sesack SR, Georges F, Pistis M, Hong S, Jhou TC | title = Braking dopamine systems: a new GABA master structure for mesolimbic and nigrostriatal functions | journal = J. Neurosci. | volume = 32 | issue = 41 | pages = 14094–101 |date=October 2012  | pmid = 23055478 | pmc = 3513755 | doi = 10.1523/JNEUROSCI.3370-12.2012 | url = | last2 = Sesack | last3 = Georges | last4 = Pistis | last5 = Hong | last6 = Jhou }}</ref>
|'''[[GABA]]ergic pathways''':
*[[Globus pallidus]] (GP) projections
:*&nbsp;

*[[Tail of the ventral tegmental area]] (tVTA) projections
:*tVTA → [[ventral tegmental area|VTA]]
:*tVTA → [[Raphe nuclei]]
:*tVTA → [[Preoptic area]]
:*tVTA → [[Lateral hypothalamus]]
:*tVTA → [[Substantia nigra]]
:*tVTA → [[Periaqueductal gray]]
:*tVTA → [[Pontine tegmentum]]
|
*(coming soon)
|-
! Acetylcholine system<br /><ref name="VTA inputs" /><ref name="Cholinergic pathways">{{cite book | author = Malenka RC, Nestler EJ, Hyman SE | editor = Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | pages = 167–175 | edition = 2nd | chapter = Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin | quote= The basal forebrain cholinergic nuclei are {{sic|hide=y|comprised| of}} the medial septal nucleus (Ch1), the vertical nucleus of the diagonal band (Ch2), the horizontal limb of the diagonal band (Ch3), and the nucleus basalis of Meynert (Ch4).  Brainstem cholinergic nuclei include the pedunculopontine nucleus (Ch5), the laterodorsal tegmental nucleus (Ch6), the medial habenula (Ch7), and the parabigeminal nucleus (Ch8).}}</ref>
|'''Cholinergic pathways''':
* [[Nucleus basalis of Meynert]] (NBM) projections
:*NBM → [[Hippocampus]]
:*NBM → [[Cerebral cortex]]
:*NBM → [[Limbic cortex]] & [[sensory cortex]]

Brainstem cholinergic nuclei (BCN):<br />
[[Pedunculopontine nucleus]], [[laterodorsal tegmental nucleus]], [[medial habenula]], [[parabigeminal nucleus]]
* Brainstem nuclei projections
:*BCN → [[Ventral tegmental area]]
:*BCN → [[Thalamus]]

Forebrain cholinergic nuclei (FCN):<br />
[[Medial septal nucleus]] & [[nucleus of diagonal band|diagonal band]]
* Forebrain nuclei projections
:*FCN → [[Hippocampus]]
:*FCN → [[Cerebral cortex]]
:*FCN → [[Limbic cortex]] & [[sensory cortex]]
|
*Arousal
*emotional states
*[[learning]]
*[[motor system]] function
*[[Memory#Short-term|short-term memory]]
*reward (minor role)
|}

===Drug effects===
Drugs can influence behavior by altering neurotransmitter activity. For instance, drugs can decrease the rate of synthesis of neurotransmitters by affecting the synthetic enzyme(s) for that neurotransmitter. When neurotransmitter synthesis' are blocked, the amount of 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 antagonist]]s. 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 [[agonist]]s. An example of a receptor agonist is Valium, a benzodiazepine that mimics effects of the endogenous neurotransmitter gamma-aminobutyric acid (GABA) to decrease anxiety. Other drugs interfere with the deactivation of a neurotransmitter after it has been released, thereby prolonging the action of a neurotransmitter. This can be accomplished by blocking reuptake or inhibiting degradative enzymes. Lastly, drugs can also prevent an action potential from occurring, blocking neuronal activity throughout the central and peripheral [[nervous system]]. Drugs such as tetrodotoxin that block neural activity are typically lethal. [[File:ΔFosB.svg|thumb|Chronic high-dose use of dopaminergic stimulants.]]

Drugs targeting the neurotransmitter of major systems affect the whole system which can explain 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]] for an extended period of time. 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, an individual can become depressed due to decreased probability of the neurotransmitter binding to a receptor. [[Fluoxetine]] is a [[serotonin reuptake inhibitor|selective serotonin reuptake inhibitor]] (SSRI), which blocks re-uptake of serotonin by the presynaptic cell which increases the amount of serotonin present at the synapse and furthermore allows it to remain there longer, providing potential for the effect of naturally released serotonin.<ref name="InhibitingSerotoninSynthesis">{{cite journal | author = Yadav VK, Ryu JH, Suda N, Tanaka KF, Gingrich JA, Schütz G, Glorieux FH, Chiang CY, Zajac JD, Insogna KL, Mann JJ, Hen R, Ducy P, Karsenty G | title = Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum | journal = Cell | volume = 135 | issue = 5 | pages = 825–37 | year = 2008 | date = November 2008 | pmid = 19041748 | pmc = 2614332 | doi = 10.1016/j.cell.2008.09.059 | url = }}</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.

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.


==List of neurotransmitters, peptides, and gasotransmitters==
{| class="wikitable" class="sortable wikitable"
|-
| '''Category''' || '''Name''' || '''Abbreviation''' || '''[[Metabotropic]]''' || '''[[Ionotropic]]'''
|-
|Small: Amino acids ([[Arginine|Arg]]) || [[Agmatine]] ||   || [[Alpha-2 adrenergic receptor|α<sub>2</sub> adrenergic receptor]] [[Imidazoline receptor]] || [[NMDA receptor]]
 |-
|Small: Amino acids || [[Aspartate]] || Asp ||  – || [[NMDA receptor]]
 |-
|Small: Amino acids || [[Glutamate]] (glutamic acid) || Glu  || [[Metabotropic glutamate receptor]] || [[NMDA receptor]] (co-agonist), [[Kainate receptor]], [[AMPA receptor]]
 |-
|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]]
 |-
|Small: Amino acids || [[Glycine]] || Gly  ||  –  || [[Glycine receptor]], [[NMDA receptor]] (co-agonist)
 |-
|Small: Amino acids || [[D-serine|<small>D</small>-serine]] || Ser  ||  –  || [[NMDA receptor]] (co-agonist)
 |-
|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 ([[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: Monoamine ([[Histamine|His]]) ||  [[Histamine]]  || H  ||  [[Histamine receptor]]  || –
 |-
|Small: Trace amine ([[Phenylalanine|Phe]]) || [[Phenethylamine]] || PEA || [[Trace amine-associated receptor]]s: {{abbrlink|hTAAR1|human trace amine associated receptor 1}}, {{abbrlink|hTAAR2|human trace amine associated receptor 2}} || –
 |-
|Small: Trace amine ([[Phenylalanine|Phe]]) || [[N-methylphenethylamine|''N''-methylphenethylamine]] || NMPEA || {{abbrlink|hTAAR1|human trace amine associated receptor 1}} || –
 |-
|Small: Trace amine ([[Phenylalanine|Phe]]/[[Tyrosine|Tyr]]) || [[Tyramine]]  || TYR || {{abbrlink|hTAAR1|human trace amine associated receptor 1}}, {{abbrlink|hTAAR2|human trace amine associated receptor 2}} || –
 |-
|Small: Trace amine ([[Phenylalanine|Phe]]/[[Tyrosine|Tyr]]) ||  [[Octopamine]]  || Oct || {{abbrlink|hTAAR1|human trace amine associated receptor 1}} || –
 |-
|Small: Trace amine ([[Phenylalanine|Phe]]/[[Tyrosine|Tyr]]) ||  [[Synephrine]]  || Syn || {{abbrlink|hTAAR1|human trace amine associated receptor 1}} || –
 |-
|Small: Trace amine ([[Phenylalanine|Phe]]/[[Tyrosine|Tyr]]) ||  [[3-methoxytyramine]]  || 3-MT || {{abbrlink|hTAAR1|human trace amine associated receptor 1}} || –
 |-
||Small: Trace amine ([[Tryptophan|Trp]]) || [[Tryptamine]] ||  || {{abbrlink|hTAAR1|human trace amine associated receptor 1}}, various [[5-HT receptor]]s ||
 |-
||Small: Trace amine ([[Tryptophan|Trp]]) || [[Dimethyltryptamine]] || DMT || {{abbrlink|hTAAR1|human trace amine associated receptor 1}}, various [[5-HT receptor]]s,  ||
 |-
|[[Neuropeptide]]s || [[N-Acetylaspartylglutamate|''N''-Acetylaspartylglutamate]] || NAAG || [[Metabotropic glutamate receptor]]s; selective agonist of [[mGluR3]] || –
 |-
|PP: Gastrins ||  [[Gastrin]]  ||   ||  – || –
 |-
|PP: Gastrins ||  [[Cholecystokinin]]   || CCK  ||  [[Cholecystokinin receptor]]  || –
 |-
|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 ||  [[Enkephaline]]  ||   ||  [[Delta opioid receptor|δ-opioid receptor]]  || –
 |-
|PP: Opioids ||  [[Dynorphin]]  ||   ||  [[Kappa opioid receptor|κ-opioid receptor]] || –
 |-
|PP: Opioids ||  [[Endorphin]]  ||   ||  [[Mu opioid receptor|μ-opioid receptor]]  || –
 |-
|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 || [[Cocaine and amphetamine regulated transcript]] || CART || Unknown [[Gi alpha subunit|G<sub>i</sub>/G<sub>o</sub>]]-coupled receptor<ref name="pmid21855138">{{cite journal | author = Lin Y, Hall RA, Kuhar MJ | title = CART peptide stimulation of G protein-mediated signaling in differentiated PC12 cells: identification of PACAP 6-38 as a CART receptor antagonist | journal = Neuropeptides | volume = 45 | issue = 5 | pages = 351–358 |date=October 2011 | pmid = 21855138 | pmc = 3170513 | doi = 10.1016/j.npep.2011.07.006 | last2 = Hall | last3 = Kuhar }}</ref> || 
 |-
|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 ||  [[2-Arachidonoylglycerol]]  || 2-AG  ||  [[Cannabinoid receptor]] || –
 |-
|Other ||  [[2-Arachidonyl glyceryl ether]]  || 2-AGE  ||  [[Cannabinoid receptor]] || –
 |-
|Other ||  [[N-Arachidonoyl dopamine|''N''-Arachidonoyl dopamine]]  || NADA  ||  [[Cannabinoid receptor]] || [[TRPV1]]
 |-
|Other ||  [[Virodhamine]]  ||   ||  [[Cannabinoid receptor]] || –
 |-
|Other ||  [[Adenosine triphosphate]]   || ATP  ||  [[P2Y12]] || [[P2X receptor]]
 |-
|Other ||  [[Adenosine]]   || Ado  ||  [[Adenosine receptor]] || –
|}

==Precursors==
{{Phenylalanine biosynthesis|caption=In humans, catecholamines and phenethylaminergic trace amines are derived from the amino acid phenylalanine.|align=right}}
While intake of neurotransmitter [[Precursor (chemistry)|precursors]] does increase neurotransmitter synthesis, evidence is mixed as to whether [[neurotransmitter release]] and postsynaptic receptor 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|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>

===Catecholamine and trace amine precursors===
[[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]]. 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"/>

===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"/>

==Elimination Of neurotransmitters==
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. Neurotransmitters are terminated in three different ways:
# Diffusion – the neurotransmitter detaches from receptor, drifting out of the synaptic cleft, here it becomes absorbed by [[glial cells]].
# Enzyme degradation – special chemicals called [[enzymes]] break it down.
# Reuptake – re-absorption of a neurotransmitter into the neuron. Transporters, or [[membrane transport protein]]s, pump neurotransmitters from the synaptic cleft back into [[axon terminal]]s (the presynaptic neuron) where they are stored.<ref>"General, Organic ans Biological Chemistry Structures of Life" by Karen C. Timberlake p.661</ref>

For example [[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 targeted by the body's regulatory system or by [[recreational drug]]s.

==Agonists==
{{Main|Agonist}}
An agonist is a chemical capable of binding to a receptor, such as a neurotransmitter receptor, and initiating the same reaction typically produced by the binding of the endogenous substance.<ref>{{cite web|url=http://www.merriam-webster.com/dictionary/agonist |title=Agonist - Definition and More from the Free Merriam-Webster Dictionary |publisher=Merriam-webster.com |accessdate=25 August 2014}}</ref> An agonist of a neurotransmitter will thus initiate the same receptor response as the transmitter.<ref>{{cite web|title=Drug Receptor Interactions|url=http://www.elmhurst.edu/~chm/vchembook/660drugreceptor.html|publisher=Virtual Chembook, Elmhurst College}}</ref>

[[Nicotine]], found in [[tobacco]], is an agonist for acetylcholine at nicotinic receptors.<ref name=Fallows>{{cite web|url=http://ocw.mit.edu/ans7870/SP/SP.236/S09/lecturenotes/drugchart.htm |title=Neurotransmitters and Drugs Chart |publisher=Ocw.mit.edu |accessdate=25 August 2014}}</ref> [[Opiate]] agonists include [[morphine]], [[heroin]], [[hydrocodone]], [[oxycodone]], [[codeine]], and [[methadone]]. These drugs activate [[mu opioid receptor]]s that typically respond to endogenous transmitters such as [[enkephalin]]s. When these receptors are activated, individuals experience euphoria, [[analgesia|pain relief]], and drowsiness.<ref name=Fallows/>

==See also==
{{Portal|Neuroscience}}
*[[Gasotransmitters]]
*[[Kiss-and-run fusion]]
*[[Neuromuscular transmission]]
*[[Neuropsychopharmacology]]

==References==
{{Reflist|30em}}

==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]

{{Neuroscience}}
{{Neurotransmitters}}
{{Cell signaling}}
{{Neurotransmitter systems}}

[[:Category:Neurotransmitters| ]]
[[:Category:Molecular neuroscience]]
[[:Category:Neuroscience]]