Gamma-Aminobutyric acid: Difference between revisions
No edit summary |
Added the references correctly, that is, I added them as explained in the lecture. Cleaned up the text. Removed some stray code. |
||
(One intermediate revision by one other user not shown) | |||
Line 1: | Line 1: | ||
GABA is an inhibitory [[Neurotransmitter|neurotransmitter]] in [[ | GABA is an inhibitory [[Neurotransmitter|neurotransmitter]] in [[Central nervous system|central nervous system]] which is synthesised from [[Glutamate|glutamate]] in brain cells<ref>http://www.denvernaturopathic.com/news/GABA.html</ref>. | ||
When GABA binds to its receptors in the [[ | When GABA binds to its receptors in the [[Synapse|synapse]], it allows the influx of negatively charged [[Chloride|chloride]] [[Ions|ions]] into the [[Neurone|neurone]] which reduces the neurons excitability<ref>http://thebrain.mcgill.ca/flash/d/d_04/d_04_m/d_04_m_peu/d_04_m_peu.html</ref>. | ||
GABA is the main inhibitory neurotransmitter in the brain and Glutamate is the main excitatory neurotransmitter. GABA is formed from glutamate by the enzyme glutamic acid decarboxylase<ref>Petroff OA1.GABA and glutamate in the human brain.2002 Dec;8.Department of Neurology, Yale University, New Haven, Connecticut 06520-8018, USA</ref>. The two receptors for GABA are GABA<sub>A</sub> and GABA<sub>B</sub>, found in the postsynaptic membrane<ref>Ion Channels and Disease. Frances M. Ashcroft. Elsevier. 2000</ref>. GABA<sub>A</sub> receptors are fast-acting, ligand-gated channels which, when open, allows Cl<sup>-</sup> ions to enter the cell, this is inhibitory as the movement of these ions into the cell decreases the membrane potential and so is further away from the threshold to trigger an action potential. GABA can be used to treat various disorders, including anxiety disorders, as it can rectify an imbalance in the amount of glutamate (which is excitatory)<ref>Lydiard RB. The role of GABA in anxiety disorders. Medical University of South Carolina, Charleston, USA. https://www.ncbi.nlm.nih.gov/pubmed/12662130</ref>. | |||
=== References === | === References === | ||
<references /> | <references /> | ||
Latest revision as of 19:30, 29 November 2017
GABA is an inhibitory neurotransmitter in central nervous system which is synthesised from glutamate in brain cells[1].
When GABA binds to its receptors in the synapse, it allows the influx of negatively charged chloride ions into the neurone which reduces the neurons excitability[2].
GABA is the main inhibitory neurotransmitter in the brain and Glutamate is the main excitatory neurotransmitter. GABA is formed from glutamate by the enzyme glutamic acid decarboxylase[3]. The two receptors for GABA are GABAA and GABAB, found in the postsynaptic membrane[4]. GABAA receptors are fast-acting, ligand-gated channels which, when open, allows Cl- ions to enter the cell, this is inhibitory as the movement of these ions into the cell decreases the membrane potential and so is further away from the threshold to trigger an action potential. GABA can be used to treat various disorders, including anxiety disorders, as it can rectify an imbalance in the amount of glutamate (which is excitatory)[5].
References
- ↑ http://www.denvernaturopathic.com/news/GABA.html
- ↑ http://thebrain.mcgill.ca/flash/d/d_04/d_04_m/d_04_m_peu/d_04_m_peu.html
- ↑ Petroff OA1.GABA and glutamate in the human brain.2002 Dec;8.Department of Neurology, Yale University, New Haven, Connecticut 06520-8018, USA
- ↑ Ion Channels and Disease. Frances M. Ashcroft. Elsevier. 2000
- ↑ Lydiard RB. The role of GABA in anxiety disorders. Medical University of South Carolina, Charleston, USA. https://www.ncbi.nlm.nih.gov/pubmed/12662130