Abstracts

RATIONALE: Periodic repetition (kindling) of audiogenic seizures (AGS) in rats results in seizure severity increases, characterized by additional convulsive behaviors and the appearance of epileptiform activity in the cortex. The AGS neuronal network expands as a result of AGS kindling, and there is suggestive evidence that the amygdala (AMG) becomes a major component of the expanded network. The present study examined the neuronal firing pattern changes in the lateral nucleus of AMG (LAMG) in genetically epilepsy-prone rats (GEPR-9s) after AGS kindling. METHODS: AGS kindling (14 AGS) involved 2 daily presentations of an electrical bell (122 dB SPL). Microwire (13 ?m) electrodes were implanted in the LAMG of GEPR-9s, and neuronal responses were evaluated before and after kindling. Acoustic stimuli consisted of pure tone bursts (12 kHz, 100 ms duration) presented at rates of 0.5, 1 and 2 Hz. LAMG action potentials (APs) were evaluated using post stimulus time histograms (PSTH). RESULTS: Before AGS kindling, onset-only responses (13/36) with a <20 ms latency from stimulus onset, onset-delayed response patterns (18/36) with a response peak with a latency of 60-300 ms, and delayed-only response patterns (5/36) were observed. The incidence of these neuronal firing patterns was significantly altered after AGS kindling (p<0.01), and most (28/30) LAMG neurons displayed onset-only patterns with two neurons exhibiting onset-delayed patterns. The number of APs/peak was significantly (p<0.01) elevated after AGS kindling at 0.5 and 1 Hz. The mean number of APs/peak at 100 dB (@ 0.5 Hz) was 31.4?4.9 (?SEM) before kindling and 162.1?11.8 after kindling. The mean number of APs/peak at 100 dB (@ 1 Hz) was 6.3?1.5 before kindling and 30.1?5.7 after kindling. CONCLUSIONS: These findings indicate that AGS kindling results in enhancement of LAMG neuronal responses to acoustic stimuli. The pathophysiological mechanisms subserving the seizure severity increases induced by AGS kindling could involve upregulation of glutamate receptor-mediated excitation and/or downregulation of GABA receptor-mediated inhibition, which are reported to occur in AMG neurons in electric kindling. (Support NS 21281).