Abstract
Parvalbumin- and cholecystokinin (CCK)-expressing basket cells provide two parallel, functionally distinct sources of perisomatic inhibition to postsynaptic cells. We show that exogenously applied CCK enhances the output from rat parvalbumin-expressing basket cells, while concurrently suppressing GABA release from CCK-expressing neurons through retrograde endocannabinoid action. These results indicate that CCK may act as a molecular switch that determines the source of perisomatic inhibition for hippocampal principal cells.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Benzodiazepines / pharmacology
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Calcium Channel Blockers / pharmacology
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Cholecystokinin / metabolism
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Cholecystokinin / pharmacology*
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Dose-Response Relationship, Drug
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Drug Interactions
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Hippocampus / cytology
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Hormone Antagonists / pharmacology
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In Vitro Techniques
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Ion Channel Gating / drug effects*
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Ion Channel Gating / physiology
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Membrane Potentials / drug effects
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Membrane Potentials / radiation effects
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Neural Inhibition / drug effects*
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Neural Inhibition / physiology
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Neurons / classification*
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Neurons / drug effects*
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Neurons / metabolism
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Parvalbumins / metabolism
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Patch-Clamp Techniques / methods
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Rats
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gamma-Aminobutyric Acid / metabolism
Substances
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Calcium Channel Blockers
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Hormone Antagonists
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Parvalbumins
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Benzodiazepines
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YM 022
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gamma-Aminobutyric Acid
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Cholecystokinin