Picrotoxin induced epileptiform activity in amygdaloid neurons.

The effects of the epileptogenic agent, picrotoxin, on inhibitory postsynaptic potentials (IPSPs) were studied in the amygdala in vitro slice preparation. Picrotoxin was superfused onto the tissue and intracellular recordings were obtained from basolateral amygdaloid neurons (BLANs). Stimulation of the stria terminalis pathway evoked an excitatory postsynaptic potential (EPSP)--IPSP sequence. Depolarization of the membrane potential increased the amplitude of the IPSP, whereas hyperpolarization of the membrane potential decreased the amplitude of the IPSP. The IPSP reversed polarity at -74 mV. Application of picrotoxin reduced the IPSP and resulted in the development of paroxysmal depolarizing shifts. Picrotoxin itself had no apparent effect on the resting membrane potential or input resistance. These results indicate that epileptiform activity induced by picrotoxin in the basolateral amygdaloid neuron is of synaptic origin.