Excitatory GABA goes to the striatum

In textbooks, GABA (gamma-aminobutyric acid) is an inhibitory neurotransmitter. Some investigators have found, however, that GABA_A can mediate excitatory responses (Owens and Kriegstein, 2002). The reason for this curious phenomenon is that in some immature neurones, the chloride gradients are not yet established, setting the reversal potential for chloride above threshold. Now, excitatory responses, mediated by GABA_A receptors have been found in the medium-spiny neurones of the striatum.

Beside the chloride ionic gradient, another mechanism, by which GABAergic responses can be excitatory, is the co-release of GABA and glutamate. The experiments of Bracci and Panzeri (2006) published in the Journal of Neurophysiology are pristine. They recorded from striatal slices of older animals (18–28 postnatal), where the chloride gradients should have been established. They recorded from striatal medium-spiny neurones (the projection neurones) using perforated patch. In presence of NBQX and DAP-5, they found post-synaptic potentials that reversed at -64 mV, and were sensitive to bicuculline.

It is unlikely that another neurotransmitter mediate the responses, because, they were sensitive to a GABAA receptor antagonist (bicuculine). Other possibility would be that the chloride gradients are different for medium-spiny neurones that have reached a mature state. This is an adventurous hypothesis that would need to be tested, and confirmed. Another alternative would be another, yet to be discovered, GABA receptor with poor chloride selectivity.