An abnormal striatal synaptic plasticity may account for the selective neuronal vulnerability in Huntington's disease

D. Centonze, P. Gubellini, B. Picconi, E. Saulle, M. Tolu, P. Bonsi, P. Giacomini, P. Calabresi

Research output: Contribution to journalArticlepeer-review

Abstract

A marked decrease in the activity of mitochondrial complex II (succinate dehydrogenase, SD) has been found in the brains of Huntington's disease (HD) patients. Here we have examined the possibility that SD inhibitors might produce their toxic action by increasing corticostriatal glutamatergic transmission. We report that SD inhibitors produce a durable augmentation of NMDA-mediated corticostriatal excitation (DANCE) in striatal spiny neurons, but not in striatal cholinergic interneurons. DANCE involves increased intracellular calcium, activation of MAP kinase ERK and is critically dependent upon endogenous dopamine (DA) acting via D2-like receptors. This pathological form of corticostriatal synaptic plasticity might play a key role in the regional and cell-type specific neuronal death observed in HD.

Original languageEnglish
Pages (from-to)61-62
Number of pages2
JournalNeurological Sciences
Volume22
Issue number1
DOIs
Publication statusPublished - Feb 2001

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

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