GABAa receptor-mediated field potentials are enhanced in area CA1 following prenatal cocaine exposure

Prenatal cocaine exposure results in several documented changes in neurotransmitter receptor number and structure. Increases have been reported for cortical catecholamine and indoleamine receptor number and binding affinity, in the subunit expression of glutamatergic NMDA and AMPA receptors in the striatum, and in GABA immunoreactivity in the anterior cingulate cortex. We sought information on the functional consequences of cocaine-induced alterations in receptor structure/number. Since hippocampal amino acid neurotransmitters are of critical importance and have been shown to be affected by cocaine, we studied field potentials produced by synaptic activation of isolated glutamatergic NMDA and AMPA receptors and GABAa and GABAb responsive receptors in area CA1 of rabbit hippocampal slices. We found the GABAa receptor population produced significantly larger field potentials in cocaine-exposed offspring compared to controls, while other receptors produced responses similar to controls.