Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease

Silvia Rossi, Chiara Prosperetti, Barbara Picconi, Valentina De Chiara, Giorgia Mataluni, Giorgio Bernardi, Paolo Calabresi, Diego Centonze

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)6-10
Number of pages5
JournalNeuroscience Letters
Volume410
Issue number1
DOIs
Publication statusPublished - Dec 13 2006

Keywords

  • Corticostriatal transmission
  • eEPSCs
  • Electrophysiology
  • HD
  • mEPSCs

ASJC Scopus subject areas

  • Neuroscience(all)

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