Whole-cell patch clamp recordings were made from ICC neurons in brain slices of 9-16 day old rats. Postsynaptic currents were evoked by electrical stimulation of the lemniscal inputs. Excitatory postsynaptic currents (EPSCs) were isolated pharmacologically by blocking GABAA and glycine receptors. EPSCs were further dissected into AMPA and NMDA receptor-mediated responses by adding the receptor antagonists, APV and CNQX, respectively. The internal solution in the recording electrodes contained CsF and TEA to block K+ channels that might be activated by postsynaptic GABAB receptors. The modulatory effects of GABAB receptors on EPSCs in ICC neurons were examined by bath application of the GABAB receptor agonist, baclofen, and the antagonist, CGP 35348. The amplitudes of EPSCs in ICC neurons were reduced to 34.4 ± 3.2% of the control by baclofen (5-10 μM). The suppressive effect by baclofen was concentration-dependent. The reduction of the EPSC amplitude was reversed by CGP35348. The ratio of the 2nd to 1st EPSCs evoked by paired-pulse stimulation was significantly increased after application of baclofen. These results suggest that glutamatergic excitation in the ICC can be modulated by presynaptic GABAB receptors. In addition, baclofen reduced NMDA EPSCs more than AMPA EPSCs. The GABAB receptor-mediated modulation of glutamatergic excitation in the ICC provides a likely mechanism for preventing overstimulation and/or regulating the balance of excitation and inhibition involved in processing auditory information.

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Neuroscience Letters
Department of Neuroscience

Sun, H, Ma, C.L. (Chun Lei), Kelly, J.B. (Jack B.), & Wu, S.H. (Shu Hui). (2006). GABAB receptor-mediated presynaptic inhibition of glutamatergic transmission in the inferior colliculus. Neuroscience Letters, 399(1-2), 151–156. doi:10.1016/j.neulet.2006.01.049