Delay in the development of amygdala kindling following treatment with 3,3'-iminodipropionitrile

A disruption in cognitive function and induction of astrogliosis in the brain have been reported as neurotoxic effects of 3-3'-iminodipropionitrile (IDPN). Kindling is a model of synaptic plasticity that produces functional and structural alterations in brain that may encompass those underlying learning and memory. We examined kindling development in rats exposed to IDPN as neonates (0 or 225 mg/kg on postnatal days 5-7) or as adults (0 or 200 mg/kg/day for 3 days at 2-3 months of age). As adults, animals were electrically kindled in the amygdala with once daily stimulation until fully generalized seizures were evoked. IDPN significantly retarded the rate of development of kindling and shortened the mean afterdischarge (AD) duration with successive stimulations in animals dosed as adults. Neonatally-treated animals were not significantly slower to kindle but did demonstrate protracted AD development. No effect on pentylenetetrazol-induced seizures was seen. IDPN's reported effects on biogenic amines or its olfactory toxicity cannot readily account for the delay in kindling. Alternatively, we propose that disruption of synaptic transmission consequent to IDPN-induced neuronal degeneration in the CNS may contribute to an impairment of kindling.