Plastic abnormalities in experimental Huntington's disease.
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.
Di Filippo
Massimiliano
M
Clinica Neurologica, Università degli Studi di Perugia, Ospedale S. Maria della Misericordia, Via S Andrea delle Fratte, 06156, Perugia, Italy; IRCCS Fondazione Santa Lucia, Rome, Italy.
Tozzi
Alessandro
A
Picconi
Barbara
B
Ghiglieri
Veronica
V
Calabresi
Paolo
P
D000818:Animals; D001479:Basal Ganglia / Q000503:physiopathology; D019208:Brain-Derived Neurotrophic Factor; D006624:Hippocampus / Q000503:physiopathology; D006801:Humans; D006816:Huntington Disease / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology*; D013569:Synapses / Q000502:physiology
D019208:Brain-Derived Neurotrophic Factor