title: Developmental changes in hyperexcitability of CA1 pyramidal neurons induced by repeated brief episodes of hypoxia in the rat hippocampal slices.
abstract: We have previously demonstrated that repeated exposure of adult rat hippocampal slices to brief episodes of hypoxia induce a sustained decrease in the threshold of stimulus-evoked population spike discharges in CA1 pyramidal neurons [O. Godukhin, A. Savin, S. Kalemenev, S. Levin, Neuronal hyperexcitability induced by repeated brief episodes of hypoxia in rat hippocampal slices: involvement of ionotropic glutamate receptors and L-type Ca2+ channels, Neuropharmacology 42 (2002) 459-466, S.V. Kalemenev, A.V. Savin, S.G. Levin, O.V. Godukhin, Long-term potentiation and epileptiform activity induced by brief hypoxic episodes in CA1 area of the rat hippocampal slices. Russ. Physiol. J. 86 (2000) 1676-1681]. In the present study, using the above-mentioned in vitro model of epileptogenesis, we compared the developmental changes in hypoxia-induced hyperexcitability of CA1 neuronal network in the rat hippocampal slices prepared from three age rat groups: postnatal days (P) 13-14 (young), P60-70 (adult) and P600-650 (old). Furthermore, we were interested in learning about an age dependence of the hypoxia-induced changes in the efficacies of glutamatergic transmission and paired-pulse inhibition in CA3-CA1 synapses that may underlie ontogenetic differences in seizure susceptibility in hippocampal network. The principal results of this work are summarized as follow. In comparison with P60-70 hippocampal slices, CA1 pyramidal neurons in P13-14 and P600-650 slices showed intrinsically (without repeated brief hypoxa) an increased propensity to generate epileptiform stimulus-evoked population spike discharges. However, in contrast to adult and old animals, repeated brief episodes of hypoxia are incapable to induce a sustained decrease in the threshold of stimulus-evoked population spike discharges in CA1 pyramidal neurons of hippocampal slices prepared from of P13-14 rats, though they transform paired-pulse inhibition to paired-pulse facilitation and induce hypoxic LTP in CA3-CA1 synapses. The role of some other factors in the developmental changes in hyperexcitability of CA1 pyramidal neurons in response to repeated brief episodes of hypoxia is discussed.
authors.affiliation: Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences, Group of Synaptic Transmission Study, Institutskaja 3, 142290 Pushchino, Moscow Region 142290, Russia.
authors.forename: Sergei
authors.initials: S
authors.lastname: Levin
authors.forename: Oleg
authors.initials: O
authors.lastname: Godukhin
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D015687:Cell Hypoxia / Q000502:physiology; D006624:Hippocampus / Q000254:growth & development / Q000378:metabolism; D066298:In Vitro Techniques; D009474:Neurons / Q000378:metabolism*; D017966:Pyramidal Cells / Q000254:growth & development* / Q000378:metabolism*; D051381:Rats