Abstract
Glutamate transporters in neurones and glia, four of which have been cloned from mammals, play a crucial rule in controlling the extracellular glutamate concentration in the brain. In normal conditions, they remove glutamate from the extracellular space and thereby help to terminate glutamatergic synaptic transmission and to prevent the extracellular glutamate concentration from rising to neurotoxic values. Glutamate transport on these carriers is thought to be driven by the cotransport of Na+, the countertransport of K+, and either the cotransport of H+ or the counter-transport of OH-. Activating the transporters also activates an anion conductance in their structure, the anion flux through which is not coupled to glutamate movement and varies widely for the different transporters. During hypoxia or ischaemia, glutamate transporters can run backwards, releasing glutamate into the extracellular space, triggering the death of neurones and thus causing mental and physical handicap. The rate of glutamate release by this process is slowed by the acid pH occurring in hypoxia/ischaemia, which may help protect the brain during transient, but not sustained, ischaemia.
Original language | English (US) |
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Pages (from-to) | 401-409 |
Number of pages | 9 |
Journal | Journal of Experimental Biology |
Volume | 200 |
Issue number | 2 |
State | Published - Jan 1997 |
Externally published | Yes |
Keywords
- anion conductance
- cloning
- epilepsy
- glial cell
- glutamate transporter
- hypoxia
- ischaemia
- neurone
- pH
- postsynaptic uptake
- stoichiometry
- synaptic transmission
ASJC Scopus subject areas
- Ecology, Evolution, Behavior and Systematics
- Physiology
- Aquatic Science
- Animal Science and Zoology
- Molecular Biology
- Insect Science