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Titolo:
Levodopa-induced dyskinesia: A pathological form of striatal synaptic plasticity?
Autore:
Calabresi, P; Giacomini, P; Centonze, D; Bernardi, G;
Indirizzi:
Univ Roma Tor Vergata, Dipartimento Neurosci, Neurol Clin, I-00133 Rome, Italy Univ Roma Tor Vergata Rome Italy I-00133 eurol Clin, I-00133 Rome, Italy IRCCS Osped S Lucia, Rome, Italy IRCCS Osped S Lucia Rome ItalyIRCCS Osped S Lucia, Rome, Italy Univ Rome La Sapienza, Neurol Clin, Rome, Italy Univ Rome La Sapienza Rome Italy La Sapienza, Neurol Clin, Rome, Italy
Titolo Testata:
ANNALS OF NEUROLOGY
fascicolo: 4, volume: 47, anno: 2000, supplemento:, 1
pagine: S60 - S69
SICI:
0364-5134(200004)47:4<S60:LDAPFO>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; DOPAMINE D2 RECEPTORS; PARKINSONS-DISEASE; NEOSTRIATAL NEURONS; GENE-EXPRESSION; NMDA RECEPTOR; SUBTHALAMIC NUCLEUS; MOTOR FLUCTUATIONS; BASAL GANGLIA; MESSENGER-RNA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Calabresi, P Univ Roma Tor Vergata, Dipartimento Neurosci, Neurol Clin, Via Tor Vergata135, I-00133 Rome, Italy Univ Roma Tor Vergata Via Tor Vergata135 Rome Italy I-00133
Citazione:
P. Calabresi et al., "Levodopa-induced dyskinesia: A pathological form of striatal synaptic plasticity?", ANN NEUROL, 47(4), 2000, pp. S60-S69

Abstract

The pathogenesis of the alterations in motor response that complicate levodopa therapy of Parkinson's disease remains obscure. Several experimental and clinical observations strongly suggest that changes in striatal activitymay be crucial for this physiopathological condition. Accordingly, it has been postulated that dyskinesia might be due to abnormal activity of the corticostriatal pathway. Here, we review the physiological and pharmacological mechanisms underlying glutamatergic regulation of striatal neurons by thecorticostriatal projection. In particular, we discuss the role of both (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) glutamate receptors in the control of the short- andlong-term efficacy of corticostriatal transmission. Indeed, repetitive cortical activation can generate either long-term depression or long-term potentiation (LTP) at corticostriatal synapses depending on the subtype of glutamate receptor activated during the induction phase of these forms of synaptic plasticity. Dopamine plays an important function in the regulation of both forms of synaptic plasticity. Dopamine denervation abolishes the physiological corticostriatal plasticity by producing biochemical and morphological changes within the striatum. We have recently observed a 'pathological' form of LTP at the corticostriatal synapse during energy deprivation. We speculate that this 'pathological' LTP, depending on the activation of NMDA glutamate receptors located on spiny striatal neurons, might play a role in the generation of levodopa-induced dyskinesia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 04:40:11