Altered hippocampal network excitability in the hypernoradrenergic mutant mousetottering
JL Noebels, PA Rutecki - Brain Research, 1990 - Elsevier
Brain Research, 1990•Elsevier
A latent, gene-linked alteration of hippocampal network excitability intg/tg mutant mice was
unmasked in vitro by convulsant-activated synchronous neuronal discharges. Exposure to
elevated extracellular potassium ions or 4-aminopyridine, but not picrotoxin, revealed an
abnormally prolonged network discharge duration in the mutant CA3 pyramidal cell region.
In both phenotypes, noradrenaline, and a selective β-noradrenergic receptor agonist,
isoproterenol, reversibly accelerated the frequency of the discharges. These findings identify …
unmasked in vitro by convulsant-activated synchronous neuronal discharges. Exposure to
elevated extracellular potassium ions or 4-aminopyridine, but not picrotoxin, revealed an
abnormally prolonged network discharge duration in the mutant CA3 pyramidal cell region.
In both phenotypes, noradrenaline, and a selective β-noradrenergic receptor agonist,
isoproterenol, reversibly accelerated the frequency of the discharges. These findings identify …
Abstract
A latent, gene-linked alteration of hippocampal network excitability intg/tg mutant mice was unmasked in vitro by convulsant-activated synchronous neuronal discharges. Exposure to elevated extracellular potassium ions or 4-aminopyridine, but not picrotoxin, revealed an abnormally prolonged network discharge duration in the mutant CA3 pyramidal cell region. In both phenotypes, noradrenaline, and a selective β-noradrenergic receptor agonist, isoproterenol, reversibly accelerated the frequency of the discharges. These findings identify an intrinsic alteration in the excitability of an isolated neuronal network in a model of inherited generalized spike-wave epilepsy, and further implicate noradrenergic mechanisms in the temporal modulation of hippocampal synchronization and epileptogenesis.
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