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 language | English |
|---|---|
| Pages (from-to) | 106-111 |
| Number of pages | 6 |
| Journal | Current Opinion in Pharmacology |
| Volume | 7 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Feb 2007 |
Fingerprint
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 journal › Article
}
TY - JOUR
T1 - Plastic abnormalities in experimental Huntington's disease
AU - Di Filippo, Massimiliano
AU - Tozzi, Alessandro
AU - Picconi, Barbara
AU - Ghiglieri, Veronica
AU - Calabresi, Paolo
PY - 2007/2
Y1 - 2007/2
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=33846924382&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33846924382&partnerID=8YFLogxK
U2 - 10.1016/j.coph.2006.08.010
DO - 10.1016/j.coph.2006.08.010
M3 - Article
C2 - 17071137
AN - SCOPUS:33846924382
VL - 7
SP - 106
EP - 111
JO - Current Opinion in Pharmacology
JF - Current Opinion in Pharmacology
SN - 1471-4892
IS - 1
ER -