Abstract
Altered glutamate transmission in the striatum has been proposed to play a critical role in the pathophysiology of Huntington's disease (HD), a genetic disorder associated with impaired activity of the mitochondrial complex II (succinate dehydrogenase, SD). In the present study, we recorded spontaneous (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) from striatal neurons of both toxic (systemic administration of 3-nitropropionic acid in rats) and genetic models of HD (R6/2 transgenic mice). In both models, we found a significant down-regulation of glutamate transmission, suggesting that reduced synaptic excitation of the input structure of the basal ganglia represents a physiological correlate of HD.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Corpus Striatum / drug effects
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Corpus Striatum / pathology
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Corpus Striatum / physiopathology*
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Disease Models, Animal
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Excitatory Postsynaptic Potentials / drug effects
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Excitatory Postsynaptic Potentials / radiation effects
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Glutamic Acid / metabolism*
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Huntington Disease / chemically induced
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Huntington Disease / genetics*
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Huntington Disease / pathology
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Huntington Disease / physiopathology*
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In Vitro Techniques
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Male
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Mice
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Mice, Transgenic
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Neurons / drug effects
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Neurons / physiology
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Nitro Compounds
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Patch-Clamp Techniques / methods
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Propionates
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Rats
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Rats, Sprague-Dawley
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology
Substances
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Nitro Compounds
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Propionates
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Glutamic Acid
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3-nitropropionic acid