Editing Glutamic acid (section)

=== Brain nonsynaptic glutamatergic signaling circuits ===
Extracellular glutamate in ''[[Drosophila]]'' brains has been found to regulate postsynaptic glutamate receptor clustering, via a process involving receptor desensitization.<ref name = augustin>{{cite journal |vauthors=Augustin H, Grosjean Y, Chen K, Sheng Q, Featherstone DE | title=Nonvesicular Release of Glutamate by Glial xCT Transporters Suppresses Glutamate Receptor Clustering In Vivo | journal=Journal of Neuroscience | volume=27 | issue=1 | year=2007 | pages=111–123 | pmid=17202478 | doi = 10.1523/JNEUROSCI.4770-06.2007 | pmc=2193629}}</ref> A gene expressed in [[glial cell]]s actively transports glutamate into the [[extracellular space]],<ref name = augustin/> while, in the [[nucleus accumbens]]-stimulating group II [[metabotropic glutamate receptor]]s, this gene was found to reduce extracellular glutamate levels.<ref>{{cite journal |author1=Zheng Xi |author2=Baker DA |author3=Shen H |author4=Carson DS |author5=Kalivas PW | title=Group II metabotropic glutamate receptors modulate extracellular glutamate in the nucleus accumbens | journal=Journal of Pharmacology and Experimental Therapeutics | volume=300 | issue=1 | year=2002 | pages=162–171 | pmid=11752112 | doi=10.1124/jpet.300.1.162}}</ref> This raises the possibility that this extracellular glutamate plays an "endocrine-like" role as part of a larger homeostatic system.

==== GABA precursor ====
Glutamate also serves as the precursor for the synthesis of the inhibitory [[gamma-aminobutyric acid]] (GABA) in GABA-ergic neurons. This reaction is catalyzed by [[glutamate decarboxylase]] (GAD).<ref>{{Cite journal |last1=Bak |first1=Lasse K. |last2=Schousboe |first2=Arne |last3=Waagepetersen |first3=Helle S. |date=August 2006 |title=The glutamate/GABA-glutamine cycle: aspects of transport, neurotransmitter homeostasis and ammonia transfer |url=https://pubmed.ncbi.nlm.nih.gov/16787421/ |journal=Journal of Neurochemistry |volume=98 |issue=3 |pages=641–653 |doi=10.1111/j.1471-4159.2006.03913.x |issn=0022-3042 |pmid=16787421}}</ref> GABA-ergic neurons are identified (for research purposes) by revealing its activity (with the [[autoradiograph]]y and [[immunohistochemistry]] methods)<ref>{{Cite journal |last1=Kerr |first1=D.I.B. |last2=Ong |first2=J. |date=January 1995 |title=GABA<sub>B</sub> receptors |url=https://linkinghub.elsevier.com/retrieve/pii/016372589500016A |journal=Pharmacology & Therapeutics |language=en |volume=67 |issue=2 |pages=187–246 |doi=10.1016/0163-7258(95)00016-A |pmid=7494864 |url-access=subscription}}</ref> which is most abundant in the [[cerebellum]] and [[pancreas]].<ref>{{Cite book |last1=Krueger |first1=Christian |title=Autoantibodies |last2=Stöker |first2=Winfried |last3=Schlosser |first3=Michael |year=2007 |edition=2nd |publication-date=2007 |pages=369–378 |language=en |chapter=GLUTAMIC ACID DECARBOXYLASE AUTOANTIBODIES |doi=10.1016/B978-044452763-9/50052-4 |isbn=978-0-444-52763-9 |chapter-url=https://www.sciencedirect.com/science/article/pii/B9780444527639500524 |chapter-url-access=subscription}}</ref>

[[Stiff person syndrome]] is a neurologic disorder caused by anti-GAD antibodies, leading to a decrease in GABA synthesis and, therefore, impaired motor function such as muscle stiffness and spasm. Since the pancreas has abundant GAD, a direct immunological destruction occurs in the pancreas and the patients will have [[diabetes mellitus]].<ref>{{Cite journal |last1=Newsome |first1=Scott D. |last2=Johnson |first2=Tory |date=2022-08-15 |title=Stiff Person Syndrome Spectrum Disorders; More Than Meets the Eye |journal=Journal of Neuroimmunology |volume=369 |pages=577915 |doi=10.1016/j.jneuroim.2022.577915 |issn=0165-5728 |pmc=9274902 |pmid=35717735}}</ref>