Carrier-mediated GABA Release: Is There a Functional Role?

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Abstract
Neurotransmitters are normally released from neurons via calcium-dependent exocytosis of synaptic vesicles. However, after blockade of vesicular release by removal of calcium, or treatment with tetanus toxin, neurotransmitter release can still occur. In the case of GABA, nonvesicular release results from reversal of its uptake transporter, found on both neurons and glia. These GABA transporters are sodium-dependent and electrogenic, and therefore can be induced to operate in reverse by cell depolarization or by breakdown of the sodium gradient. Although demonstrated biochemically, less is known about whether this form of release occurs in vivo or whether it results in electrophysiological effects. Because conditions that favor reversal of the GABA transporter occur during high-frequency firing, nonvesicular GABA release may occur with excessive neuronal activity, such as during seizures. NEUROSCIENTIST 3:151-157, 1997