Chloride-dependent inhibitory postsynaptic potentials recorded in amygdalar slices of rat

The physiological and pharmacological properties of inhibitory postsynaptic potentials (IPSPs) were studied in rat amygdalar slices using intracellular recording techniques. Stimulation of the ventral endopyriform nucleus evoked an excitatory postsynaptic potential (EPSP)-IPSP sequence. Depolarization of the membrane potential increased the amplitude of IPSPs, whereas hyperpolarization of the membrane potential decreased the amplitude of IPSPs. The IPSP reversed polarity (E(IPSP)) at -72 mV which is close to the equilibrium potential for chloride ions. Application of bicuculline or picrotoxin blocked the IPSP leading to the development of bursting discharges. Impalement with electrode containing 3 M KCl revealed spontaneous reversed IPSPs and caused a 10 mV depolarizing shift in E(IPSP), corresponding to an increase in intracellular Cl^- concentration from 8.7 mM to 13.6 mM. It is concluded that the IPSP is mediated by the activation of GABA(A) receptors through the opening of chloride channels and that GABAergic IPSPs play an important role in controlling the excitability of amygdalar neurons.