|
|
|
|
|
|
|
|
|
|
Expert
Reviews in Molecular Medicine: http://www.expertreviews.org/
Accession information: Vol. 8; Issue 11; 24 May 2006 Abstract
PDF
Glutamatergic transmission in the central nervous system
Emily F. Goodall and Karen E. Morrison
Figure 4. Glutamatergic transmission in the central nervous system. (a) A glutamatergic synapse under normal physiological conditions. Glutamate is released from the presynaptic nerve terminal and diffuses into the synaptic cleft. It acts on several glutamate receptors on the postsynaptic neuron. The action of glutamate in the cleft is terminated by its rapid reuptake via glutamate transporter proteins. EAAT1 and EAAT2 are expressed on glial cells; EAAT3 is mainly on presynaptic motor neurons. EAAT2 is responsible for most glutamate reuptake in the human brain. Under normal physiological conditions postsynaptic activation of glutamate receptors results in a small rise in intracellular calcium that can be buffered in the cell. (b) A glutamatergic synapse under conditions of excitotoxicity. When excess glutamate is present, there is a greater elevation in intracellular calcium postsynaptically. This triggers mitochondrial production of reactive oxygen species (ROS), which then inhibit glial EAAT2 function. This leads to further increases in glutamate concentrations in the synapse and further rises in postsynaptic calcium levels.
| home
| search | glossary
| links | sitemap
| contact |
Expert Reviews in Molecular Medicine © Cambridge
University Press ISSN 1462-3994 (Disclaimer and copyright)
Editorial Office: Centre for Applied Research
in Educational Technologies (CARET), 1st Floor, 16 Mill Lane, Cambridge,
CB2 1SB, UK. Tel: +44 (0)1223 765 375; Fax: +44(0)1223 765 505; E-mail: ermm@caret.cam.ac.uk