Abstract

The purpose of this study is to determine whether long-term potentiation (LTP) can be induced in the central nucleus of the inferior colliculus (ICC) by electrical stimulation of the lateral lemniscus. If LTP can be induced, is it mediated by N-methyl-D-aspartate (NMDA) and/or other receptors? Brain slices of the ICC were obtained from 14–35 day old Wistar rats. The field potentials were recorded from the ICC after GABAergic and glycinergic inhibition was suppressed. Following tetanic stimulation (50 Hz, 20 s), the amplitude of the response was increased to about 146% of control response for at least 30 min. LTP was observed in about 78% of the cases tested. Induction of LTP in the ICC required activation of both NMDA and γ-aminobutyric acid (GABA)B receptors. GABAergic inhibitory postsynaptic potentials (IPSPs) were blocked by the GABAA receptor antagonist, but not by the GABAB receptor antagonist. The IPSPs were decreased by the GABAB receptor agonist, baclofen. The intrinsic postsynaptic membrane properties were not affected by baclofen. These results suggest that GABAergic inhibition in the ICC is mediated only by GABAA receptors, but that it is modulated by presynaptic GABAB receptors. The GABAB receptors in the ICC may suppress GABAergic inhibition and promote induction of LTP.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call