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The Journal of Neuroscience, October 15, 2001, 21(20):8154-8163
Decreased Glutamate Receptor 2 Expression and Enhanced Epileptogenesis in Immature Rat Hippocampus after Perinatal Hypoxia-Induced Seizures
Russell M. Sanchez1, 2, Sookyong Koh2, Carlos Rio2, Carl Wang2, Ed D. Lamperti2, Deepak Sharma2, Gabriel Corfas1, 2, and Frances E. Jensen1, 2 1 Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, and 2 Division of Neuroscience, Children's Hospital, Boston, Massachusetts 02115
Hypoxic encephalopathy is the most common cause of neonatal seizures and can lead to chronic epilepsy. In rats at postnatal days 10-12 (P10-12), global hypoxia induces spontaneous seizures and chronically decreases seizure threshold, thus mimicking clinical aspects of neonatal hypoxia. We have shown previously that the acute and chronic epileptogenic effects of hypoxia are age-dependent and require AMPA receptor activation. In this study, we aimed to determine whether hypoxia-induced seizures and epileptogenesis are associated with maturational and seizure-induced changes in AMPA receptor composition and function. Northern and Western blots indicated that glutamate receptor 2 (GluR2) mRNA and protein expression were significantly lower in neocortex and hippocampus at P10-12 compared with adult. After hypoxia-induced seizures at P10, GluR2 mRNA was significantly decreased within 48 hr, and GluR2 protein was significantly decreased within 96 hr. AMPA-induced Co2+ uptake by neurons in hippocampal slices indicated higher expression of Ca2+-permeable AMPA receptors in immature pyramidal neurons compared with adult. In slices obtained 96 hr after hypoxia-induced seizures, AMPA-induced Co2+ uptake was significantly increased compared with age-matched controls, and field recordings revealed increased tetanus-induced afterdischarges that could be kindled in the absence of NMDA receptor activation. In situ end labeling showed no acute or delayed cell death after hypoxia-induced seizures. Our results indicate that susceptibility to hypoxia-induced seizures occurs during a developmental stage in which the expression of Ca2+-permeable AMPA receptors is relatively high. Furthermore, perinatal hypoxia-induced seizures induce increased expression of Ca2+-permeable AMPA receptors and an increased capacity for AMPA receptor-mediated epileptogenesis without inducing cell death.
Key words: epilepsy; AMPA receptor; glutamate; neonatal; calcium; hippocampus; cobalt
Copyright © 2001 Society for Neuroscience 0270-6474/01/21208154-10$05.00/0
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