PURPOSE: Our previous research indicated that the exposure of rat pups to an hypoxic environment during a discrete developmental period (postnatal days 10-15) produces short-term seizures and confers an enduring increase in susceptibility to pentylenetetrazol- and flurothyl-induced seizures. In this study, we evaluated the effects of hypoxic insult in this neonatal period of susceptibility to electrical kindling and corneal electroconvulsive shock. METHODS: Ten-day-old rat pups were exposed to a 3% O2 environment, as previously described, and were either kindled or exposed to corneal electroshock at adulthood (70 days old). RESULTS: Neither kindled seizure development from the septal nucleus or amygdala nor electroconvulsive shock profiles were significantly altered by hypoxic pretreatment. CONCLUSIONS: Results indicate that hypoxia produces increases in seizure susceptibility that are observable in only some experimental seizure models but not in others. This outcome serves to target some anatomic systems more than others in the mechanisms involved in hypoxia-induced neural reorganization.
PURPOSE: Our previous research indicated that the exposure of rat pups to an hypoxic environment during a discrete developmental period (postnatal days 10-15) produces short-term seizures and confers an enduring increase in susceptibility to pentylenetetrazol- and flurothyl-induced seizures. In this study, we evaluated the effects of hypoxic insult in this neonatal period of susceptibility to electrical kindling and corneal electroconvulsive shock. METHODS: Ten-day-old rat pups were exposed to a 3% O2 environment, as previously described, and were either kindled or exposed to corneal electroshock at adulthood (70 days old). RESULTS: Neither kindled seizure development from the septal nucleus or amygdala nor electroconvulsive shock profiles were significantly altered by hypoxic pretreatment. CONCLUSIONS: Results indicate that hypoxia produces increases in seizure susceptibility that are observable in only some experimental seizure models but not in others. This outcome serves to target some anatomic systems more than others in the mechanisms involved in hypoxia-induced neural reorganization.