Glial strategy for metabolic shuttling and neuronal function.
Glial cells serve a variety of functions in nervous systems, some of which are activated by neurotransmitters released from neurons. Glial cells respond to these neurotransmitters via receptors, but also take up some of the transmitters to help terminate the synaptic process. Among these, glutamate uptake by glial cells is pivotal to avoid transmitter-mediated excitotoxicity. Here, a new model is proposed in which glutamate uptake via the excitatory amino acid transporter (EAAT) is functionally coupled to other glial transporters, in particular the sodium-bicarbonate cotransporter ( NBC) and the monocarboxylate transporter ( MCT), as well as other glial functions, such as calcium signalling, a high potassium conductance and CO(2) consumption. The central issue of this hypothesis is that the shuttling of sodium ions and acid/base equivalents, which drive the metabolite transport across the glial membrane, co-operate with each other, and hence save energy. As a result, glutamate removal from synaptic domains and lactate secretion serving the energy supply to neurons would be facilitated and could operate with greater capacity.[1]References
- Glial strategy for metabolic shuttling and neuronal function. Deitmer, J.W. Bioessays (2000) [Pubmed]
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