Editing Neurotransmitter (section)

===Elimination===
[[File:Synapse acetylcholine.png|thumb|Acetylcholine is cleaved in the synaptic cleft into acetic acid and choline.]]

In order to avoid continuous activation of receptors on the post-synaptic or target cell, neurotransmitters must be removed from the synaptic cleft.<ref>{{cite journal | vauthors = Chergui K, Suaud-Chagny MF, Gonon F | title = Nonlinear relationship between impulse flow, dopamine release and dopamine elimination in the rat brain in vivo | journal = Neuroscience | volume = 62 | issue = 3 | pages = 641–645 | date = October 1994 | pmid = 7870295 | doi = 10.1016/0306-4522(94)90465-0 | s2cid = 20465561 }}</ref>  Neurotransmitters are removed through one of three mechanisms:

# Diffusion – neurotransmitters drift out of the synaptic cleft, where they are absorbed by [[glial cells]]. These glial cells, usually [[astrocyte]]s, absorb the excess neurotransmitters.
#* Astrocytes, a type of [[glia]]l cell in the brain, actively contribute to synaptic communication through astrocytic diffusion or [[Gliotransmitter|gliotransmission]]. Neuronal activity triggers an increase in astrocytic calcium levels, prompting the release of gliotransmitters, such as [[Glutamate (neurotransmitter)|glutamate]], ATP, and D-serine. These gliotransmitters diffuse into the [[Extracellular fluid|extracellular]] space, interacting with nearby neurons and influencing synaptic transmission. By regulating extracellular neurotransmitter levels, astrocytes help maintain proper synaptic function. This bidirectional communication between astrocytes and neurons add complexity to brain signaling, with implications for brain function and neurological disorders.<ref>{{Cite journal |last1=Mustafa |first1=Asif K. |last2=Kim |first2=Paul M. |last3=Snyder |first3=Solomon H. |date=August 2004 |title=D-Serine as a putative glial neurotransmitter |journal=Neuron Glia Biology |language=en |volume=1 |issue=3 |pages=275–281 |doi=10.1017/S1740925X05000141 |pmid=16543946 |pmc=1403160 |issn=1741-0533}}</ref><ref>{{Cite journal |last1=Wolosker |first1=Herman |last2=Dumin |first2=Elena |last3=Balan |first3=Livia |last4=Foltyn |first4=Veronika N. |date=July 2008 |title=d-Amino acids in the brain: d-serine in neurotransmission and neurodegeneration: d-Serine in neurotransmission and neurodegeneration |journal=FEBS Journal |language=en |volume=275 |issue=14 |pages=3514–3526 |doi=10.1111/j.1742-4658.2008.06515.x|pmid=18564180 |s2cid=25735605 |doi-access=free }}</ref>
# Enzyme degradation – proteins called [[enzymes]] break the neurotransmitters down.
# [[Reuptake]] – neurotransmitters are reabsorbed into the pre-synaptic 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 for reuse.

For example, [[acetylcholine]] is eliminated by having its acetyl group cleaved by the enzyme [[acetylcholinesterase]]; the remaining [[choline]] is then taken in and recycled by the pre-synaptic neuron to synthesize more [[acetylcholine]].<ref>{{cite journal | vauthors = Thapa S, Lv M, Xu H | title = Acetylcholinesterase: A Primary Target for Drugs and Insecticides | journal = Mini Reviews in Medicinal Chemistry | volume = 17 | issue = 17 | pages = 1665–1676 | date = 2017-11-30 | pmid = 28117022 | doi = 10.2174/1389557517666170120153930 }}</ref> Other neurotransmitters 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 medication. [[Cocaine]] blocks a dopamine transporter responsible for the reuptake of dopamine. Without the transporter, dopamine diffuses much more slowly from the synaptic cleft and continues to activate the dopamine receptors on the target cell.<ref>{{cite journal | vauthors = Vasica G, Tennant CC | title = Cocaine use and cardiovascular complications | journal = The Medical Journal of Australia | volume = 177 | issue = 5 | pages = 260–262 | date = September 2002 | pmid = 12197823 | doi = 10.5694/j.1326-5377.2002.tb04761.x | s2cid = 18572638 }}</ref>