Abstract
Although experience-dependent changes in neural circuits are commonly assumed to be mediated by synaptic plasticity, modifications of intrinsic excitability may serve as a complementary mechanism. In whole-cell recordings from spontaneously firing vestibular nucleus neurons, brief periods of inhibitory synaptic stimulation or direct membrane hyperpolarization triggered long-lasting increases in spontaneous firing rates and firing responses to intracellular depolarization. These increases in excitability, termed firing rate potentiation, were induced by decreases in intracellular calcium and expressed as reductions in the sensitivity to the BK-type calcium-activated potassium channel blocker iberiotoxin. Firing rate potentiation is a novel form of cellular plasticity that could contribute to motor learning in the vestibulo-ocular reflex.
Publication types
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Comparative Study
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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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Animals, Newborn
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Apamin / pharmacology
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Cadmium / pharmacology
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Calcium / metabolism
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Dose-Response Relationship, Radiation
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Egtazic Acid / analogs & derivatives*
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Egtazic Acid / metabolism
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Electric Impedance
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Electric Stimulation
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Electrophysiology
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In Vitro Techniques
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Membrane Potentials / drug effects
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Membrane Potentials / physiology
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Mice
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Mice, Inbred C57BL
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Neural Inhibition / drug effects
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Neural Inhibition / physiology*
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Neuronal Plasticity / drug effects
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Neuronal Plasticity / physiology*
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Neurons / drug effects
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Neurons / physiology*
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Neurotoxins / pharmacology
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Peptides / pharmacology
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Synapses / physiology
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Time Factors
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Vestibular Nuclei / cytology
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Vestibular Nuclei / drug effects
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Vestibular Nuclei / physiology*
Substances
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Neurotoxins
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Peptides
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Cadmium
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Apamin
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Egtazic Acid
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iberiotoxin
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1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
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Calcium