Plastic abnormalities in experimental Huntington's disease

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

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

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
Volume7
Issue number1
DOIs
Publication statusPublished - Feb 2007

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Neuronal Plasticity
Huntington Disease
Plastics
Inheritance Patterns
Neurobehavioral Manifestations
Neurotransmitter Receptor
Long-Term Potentiation
Neurodegenerative Diseases
Cognition
Acetylcholine
Glutamic Acid
Dopamine
Theoretical Models
Learning
Depression

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

Plastic abnormalities in experimental Huntington's disease. / Di Filippo, Massimiliano; Tozzi, Alessandro; Picconi, Barbara; Ghiglieri, Veronica; Calabresi, Paolo.

In: Current Opinion in Pharmacology, Vol. 7, No. 1, 02.2007, p. 106-111.

Research output: Contribution to journalArticle

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