Abstract
Correlated pre- and postsynaptic activity that induces long-term potentiation is known to induce a persistent enhancement of the intrinsic excitability of the presynaptic neuron. Here we report that, associated with the induction of long-term depression in hippocampal cultures and in somatosensory cortical slices, there is also a persistent reduction in the excitability of the presynaptic neuron. This reduction requires postsynaptic Ca(2+) elevation and presynaptic PKA- and PKC-dependent modification of slow-inactivating K(+) channels. The bidirectional changes in neuronal excitability and synaptic efficacy exhibit identical requirements for the temporal order of pre- and postsynaptic activation but reflect two distinct aspects of activity-induced modification of neural circuits.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Calcium / physiology
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Calcium Signaling / physiology
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Cells, Cultured
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Cerebral Cortex / cytology
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Cerebral Cortex / physiology
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Cyclic AMP-Dependent Protein Kinases / physiology
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Excitatory Postsynaptic Potentials / physiology
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Hippocampus / cytology
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Hippocampus / physiology
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In Vitro Techniques
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Long-Term Potentiation / physiology
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Membrane Potentials / physiology
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Neuronal Plasticity / physiology*
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Neurons / physiology*
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Patch-Clamp Techniques
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Potassium Channels / physiology
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Protein Kinase C / physiology
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Rats
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Rats, Sprague-Dawley
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Receptors, Presynaptic / physiology*
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Somatosensory Cortex / cytology
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Somatosensory Cortex / physiology
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Synapses / physiology*
Substances
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Potassium Channels
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Receptors, Presynaptic
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Cyclic AMP-Dependent Protein Kinases
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Protein Kinase C
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Calcium