Abstract
In the immature brain, GABA (gamma-aminobutyric acid) is excitatory, and GABA-releasing synapses are formed before glutamatergic contacts in a wide range of species and structures. GABA becomes inhibitory by the delayed expression of a chloride exporter, leading to a negative shift in the reversal potential for choride ions. I propose that this mechanism provides a solution to the problem of how to excite developing neurons to promote growth and synapse formation while avoiding the potentially toxic effects of a mismatch between GABA-mediated inhibition and glutamatergic excitation. As key elements of this cascade are activity dependent, the formation of inhibition adds an element of nurture to the construction of cortical networks.
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Publication Info
- Year
- 2002
- Type
- review
- Volume
- 3
- Issue
- 9
- Pages
- 728-739
- Citations
- 2382
- Access
- Closed
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Identifiers
- DOI
- 10.1038/nrn920
- PMID
- 12209121