Plastic abnormalities in experimental Huntington's disease

Massimiliano Di Filippo, Alessandro Tozzi, Barbara Picconi, Veronica Ghiglieri, Paolo Calabresi

Research output: Contribution to journalArticlepeer-review


Huntington's disease (HD) is a late-onset neurodegenerative disorder that follows an autosomal-dominant pattern of inheritance. In human cases of HD and experimental models of the disease, multiple alterations in neurotransmitters and post-receptor machineries have been described. Dopamine, acetylcholine and glutamate signalling, which usually cooperate in the induction of physiological synaptic plasticity, are all disrupted. Impairment of the induction and reversal of the main forms of neuronal synaptic plasticity influences the computational function of complex neural circuits that mediate essential cognitive and motor functions. As long-term potentiation and long-term depression represent the accepted model for neuronal learning processes, their impairment could account for the onset and progression of both motor and cognitive symptoms of HD.

Original languageEnglish
Pages (from-to)106-111
Number of pages6
JournalCurrent Opinion in Pharmacology
Issue number1
Publication statusPublished - Feb 2007

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology


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