Abstract
Impaired inhibition is thought to be important in temporal lobe epilepsy (TLE), the most common form of epilepsy in adult patients. We report that, in experimental TLE, spontaneous GABAergic inhibition was increased in the soma but reduced in the dendrites of pyramidal neurons. The former resulted from the hyperactivity of somatic projecting interneurons, whereas the latter was probably due to the degeneration of a subpopulation of dendritic projecting interneurons. A deficit in dendritic inhibition could reduce seizure threshold, whereas enhanced somatic inhibition would prevent the continuous occurrence of epileptiform activity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Action Potentials / physiology
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Animals
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Calbindins
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Dendrites / metabolism*
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Dendrites / ultrastructure
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Epilepsy, Temporal Lobe / chemically induced
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Epilepsy, Temporal Lobe / metabolism*
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Excitatory Amino Acid Antagonists / pharmacology
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Excitatory Postsynaptic Potentials / physiology
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Glutamate Decarboxylase / genetics
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Glutamate Decarboxylase / metabolism
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Hippocampus / cytology
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Hippocampus / drug effects
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Hippocampus / metabolism
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In Vitro Techniques
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Interneurons / cytology
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Interneurons / drug effects
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Interneurons / metabolism
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Isoenzymes / genetics
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Isoenzymes / metabolism
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Kainic Acid
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Muscarinic Agonists / pharmacology
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Neural Inhibition*
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Neurons / cytology
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Neurons / drug effects
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Neurons / metabolism*
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Patch-Clamp Techniques
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Pyramidal Cells / cytology
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Pyramidal Cells / metabolism
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RNA, Messenger / metabolism
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Rats
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S100 Calcium Binding Protein G / metabolism
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Somatostatin / metabolism
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gamma-Aminobutyric Acid / metabolism*
Substances
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Calbindins
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Excitatory Amino Acid Antagonists
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Isoenzymes
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Muscarinic Agonists
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RNA, Messenger
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S100 Calcium Binding Protein G
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Somatostatin
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gamma-Aminobutyric Acid
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Glutamate Decarboxylase
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glutamate decarboxylase 1
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Kainic Acid