Abstract
Chronic blockade of actively excitatory glutamatergic synaptic receptors in co-cultured organotypic rodent neocortex explants rapidly leads to a compensatory sensitization of otherwise inactive input channels so as to maintain ongoing action potential bursts. We report here that the homeostatic return of spontaneous, kainate receptor driven, spike discharges is followed by a reciprocal desensitization of blocked AMPA and NMDA receptors, such that the developing network is protected against becoming hyperactive once full synaptic drive is restored.
MeSH terms
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Action Potentials / drug effects
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Action Potentials / physiology
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Animals
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Animals, Newborn
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Drug Interactions
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Excitatory Amino Acid Antagonists / pharmacology
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Homeostasis / drug effects
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Homeostasis / physiology*
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Nerve Net / drug effects
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Nerve Net / physiology*
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Organ Culture Techniques
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Periodicity
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Rats
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Receptors, Glutamate / classification
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Receptors, Glutamate / physiology*
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Statistics, Nonparametric
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Time Factors
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Visual Cortex / drug effects
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Visual Cortex / physiology*
Substances
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Excitatory Amino Acid Antagonists
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Receptors, Glutamate