Editing Neurotransmitter (section)

== Actions ==
Neurons communicate with each other through [[synapse]]s, specialized contact points where neurotransmitters transmit signals. When an [[action potential]] reaches the [[presynaptic terminal]], the action potential can trigger the release of neurotransmitters into the synaptic cleft. These neurotransmitters then bind to receptors on the postsynaptic membrane, influencing the receiving neuron in either an [[Inhibitory postsynaptic potential|inhibitory]] or [[Excitatory postsynaptic potential|excitatory]] manner. If the overall excitatory influences outweigh the inhibitory influences, the receiving neuron may generate its own action potential, continuing the transmission of information to the next neuron in the network. This process allows for the flow of information and the formation of complex neural networks.<ref>{{Citation |last1=Purves |first1=Dale |title=Excitatory and Inhibitory Postsynaptic Potentials |date=2001 |url=https://www.ncbi.nlm.nih.gov/books/NBK11117/ |work=Neuroscience. 2nd edition |access-date=2023-07-14 |publisher=Sinauer Associates |language=en |last2=Augustine |first2=George J. |last3=Fitzpatrick |first3=David |last4=Katz |first4=Lawrence C. |last5=LaMantia |first5=Anthony-Samuel |last6=McNamara |first6=James O. |last7=Williams |first7=S. Mark}}</ref>

===Modulation===
A neurotransmitter may have an excitatory, inhibitory or modulatory effect on the target cell. The effect is determined by the receptors the neurotransmitter interacts with at the post-synaptic membrane. Neurotransmitter influences trans-membrane ion flow either to increase (excitatory) or to decrease (inhibitory) the probability that the cell with which it comes in contact will produce an action potential. Synapses containing receptors with excitatory effects are called Type I synapses, while Type II synapses contain receptors with inhibitory effects.<ref>{{cite journal | vauthors = Peters A, Palay SL | title = The morphology of synapses | journal = Journal of Neurocytology | volume = 25 | issue = 12 | pages = 687–700 | date = December 1996 | pmid = 9023718 | doi = 10.1007/BF02284835 | s2cid = 29365393 }}</ref> Thus, despite the wide variety of synapses, they all convey messages of only these two types. The two types are different appearance and are primarily located on different parts of the neurons under its influence.<ref>{{Cite book|url=https://www.worldcat.org/oclc/881146319|title=Hole's human anatomy & physiology|vauthors=Shier D, Butler J, Lewis R|date=5 January 2015|isbn=978-0-07-802429-0|edition=Fourteenth|location=New York, NY|oclc=881146319}}</ref> Receptors with modulatory effects are spread throughout all synaptic membranes and binding of neurotransmitters sets in motion signaling cascades that help the cell regulate its function.<ref name=":1">{{cite journal | vauthors = Di Chiara G, Morelli M, Consolo S | title = Modulatory functions of neurotransmitters in the striatum: ACh/dopamine/NMDA interactions | journal = Trends in Neurosciences | volume = 17 | issue = 6 | pages = 228–233 | date = June 1994 | pmid = 7521083 | doi = 10.1016/0166-2236(94)90005-1 | s2cid = 32085555 }}</ref> Binding of neurotransmitters to receptors with modulatory effects can have many results. For example, it may result in an increase or decrease in sensitivity to future stimulus by recruiting more or less receptors to the synaptic membrane.{{cn|date=January 2025}}

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 post-synaptic 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.{{cn|date=January 2025}}

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. From an inhibitory perspective, excitation comes in over the dendrites and spreads 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 name="Kolb Intro to Brain and Behavior">{{cite book|title=An introduction to brain and behavior|vauthors=Whishaw B, Kolb IQ|date=2014|publisher=Worth Publishers|isbn=978-1429242288|edition=4th|location=New York, NY}}</ref>

===Neurotransmitter 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.
* [[Glutamate (neurotransmitter)|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>{{cite journal|vauthors=Gross L|date=November 2006|title="Supporting" players take the lead in protecting the overstimulated brain|journal=PLOS Biology|volume=4|issue=11|pages=e371|doi=10.1371/journal.pbio.0040371|pmc=1609133|pmid=20076484 |doi-access=free }}</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|vauthors=Yang JL, Sykora P, Wilson DM, Mattson MP, Bohr VA|date=August 2011|title=The excitatory neurotransmitter glutamate stimulates DNA repair to increase neuronal resiliency|journal=Mechanisms of Ageing and Development|volume=132|issue=8–9|pages=405–11|doi=10.1016/j.mad.2011.06.005|pmc=3367503|pmid=21729715}}</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>
* [[Glycine]] is the primary inhibitory neurotransmitter in the [[spinal cord]].<ref>{{Cite journal |last1=Rajendra |first1=Sundran |last2=Lynch |first2=Joseph W. |last3=Schofield |first3=Peter R. |date=January 1997 |title=The glycine receptor |url=https://linkinghub.elsevier.com/retrieve/pii/S0163725896001635 |journal=Pharmacology & Therapeutics |language=en |volume=73 |issue=2 |pages=121–146 |doi=10.1016/S0163-7258(96)00163-5|pmid=9131721 |url-access=subscription }}</ref>
* [[Acetylcholine]] was the first neurotransmitter discovered in the peripheral and central nervous systems. It activates skeletal muscles in the somatic nervous system and may either excite or inhibit internal organs in the autonomic system.<ref name="Kolb Intro to Brain & Behavior" /> It is main neurotransmitter 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 as a [[Neuromodulation|neuromodulatory]], but using [[Acetylcholine receptor#Receptor types|different types of receptors]], including [[Nicotinic acetylcholine receptor|nicotinic]] and [[Muscarinic acetylcholine receptor|muscarinic]] receptors.<ref>{{cite web|title=Acetylcholine Receptors|url=http://www.ebi.ac.uk/interpro/potm/2005_11/Page2.htm|access-date=25 August 2014|publisher=Ebi.ac.uk}}</ref>
* [[Dopamine]] has a number of important functions in the brain. This includes critical role in the [[reward system]], motivation and emotional arousal. It also plays an important role in fine motor control and [[Parkinson's disease]] has been linked to low levels of dopamine due to the loss of [[dopaminergic neurons]] in [[substantia nigra]] [[pars compacta]].<ref>{{Citation |last1=Fahn |first1=Stanley |title=Chapter 3 - Functional neuroanatomy of the basal ganglia |date=2011-01-01 |work=Principles and Practice of Movement Disorders (Second Edition) |pages=55–65 |editor-last=Fahn |editor-first=Stanley |url=https://linkinghub.elsevier.com/retrieve/pii/B9781437723694000032 |access-date=2024-11-25 |place=Edinburgh |publisher=W.B. Saunders |doi=10.1016/b978-1-4377-2369-4.00003-2 |isbn=978-1-4377-2369-4 |last2=Jankovic |first2=Joseph |last3=Hallett |first3=Mark |editor2-last=Jankovic |editor2-first=Joseph |editor3-last=Hallett |editor3-first=Mark|url-access=subscription }}</ref> [[Schizophrenia]], a highly heterogeneous and complicated disorder has 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 of it is produced by the intestine (approximately 90%),<ref>{{Citation |last1=Terry |first1=Natalie |title=Serotonergic Mechanisms Regulating the GI Tract: Experimental Evidence and Therapeutic Relevance |date=2017 |work=Gastrointestinal Pharmacology |pages=319–342 |editor-last=Greenwood-Van Meerveld |editor-first=Beverley |place=Cham |publisher=Springer International Publishing |language=en |doi=10.1007/164_2016_103 |isbn=978-3-319-56360-2 |pmc=5526216 |pmid=28035530 |last2=Margolis |first2=Kara Gross|volume=239 }}</ref> and the remainder by [[central nervous system]] neurons at the [[raphe nuclei]]. It functions to regulate appetite, sleep, memory and learning, temperature, mood, behaviour, muscle contraction, and the functions of the [[cardiovascular system]] and [[endocrine system]]. It is speculated to have a role in [[Depression (mood)|depression]], as some depressed patients have been reported to exhibit lower concentrations of metabolites of serotonin in their [[cerebrospinal fluid]] and brain tissue.<ref name="serotonin">{{cite web|author=University of Bristol|title=Introduction to Serotonin|url=http://www.chm.bris.ac.uk/motm/serotonin/depression.htm|access-date=15 October 2009}}</ref>
* [[Norepinephrine]] is a member of the [[catecholamine]] family of neurotransmitters. It is synthesized from the [[amino acid]] [[tyrosine]]. In the [[peripheral nervous system]], one of the primary roles of norepinephrine is to stimulate the release of the stress hormone [[epinephrine]] (i.e. [[adrenaline]]) from the [[adrenal gland]]s.<ref name=":0">{{Citation |last1=Sheffler |first1=Zachary M. |title=Physiology, Neurotransmitters |date=2023 |url=http://www.ncbi.nlm.nih.gov/books/NBK539894/ |work=StatPearls |access-date=2023-07-16 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30969716 |last2=Reddy |first2=Vamsi |last3=Pillarisetty |first3=Leela Sharath}}</ref> Norepinephrine is involved in the [[fight-or-flight response]]<ref>{{Cite journal |last=Fitzgerald |first=P. J. |date=April 2015 |title=Noradrenaline transmission reducing drugs may protect against a broad range of diseases. |url=https://onlinelibrary.wiley.com/doi/10.1111/aap.12019 |journal=Autonomic and Autacoid Pharmacology |language=en |volume=34 |issue=3–4 |pages=15–26 |doi=10.1111/aap.12019 |pmid=25271382 |issn=1474-8665|url-access=subscription }}</ref> and is also affected in [[anxiety disorder]]s<ref>{{Cite journal |last1=Bouras |first1=Nadia N. |last2=Mack |first2=Nancy R. |last3=Gao |first3=Wen-Jun |date=2023-04-17 |title=Prefrontal modulation of anxiety through a lens of noradrenergic signaling |journal=Frontiers in Systems Neuroscience |language=English |volume=17 |doi=10.3389/fnsys.2023.1173326 |doi-access=free |issn=1662-5137 |pmc=10149815 |pmid=37139472}}</ref>  and depression.<ref>{{Cite journal |last1=Moret |first1=Chantal |last2=Briley |first2=Mike |date=2011-05-31 |title=The importance of norepinephrine in depression |journal=Neuropsychiatric Disease and Treatment |language=English |volume=7 |issue=Supplement 1 |pages=9–13 |doi=10.2147/NDT.S19619 |doi-access=free |pmc=3131098 |pmid=21750623}}</ref>
* [[Epinephrine]], a neurotransmitter and [[hormone]] is synthesized from [[tyrosine]]. It is released from the [[adrenal gland]]s and also plays a role in the fight-or-flight response. Epinephrine has [[Vasoconstriction|vasoconstrictive]] effects, which promote increased heart rate, blood pressure, energy mobilization. Vasoconstriction influences [[metabolism]] by promoting the breakdown of [[glucose]] released into the bloodstream. Epinephrine also has [[Bronchodilator|bronchodilation]] effects, which is the relaxing of airways.<ref name=":0" />