title: Striatal synaptic plasticity: implications for motor learning and Parkinson's disease.
abstract: Changing the strength of synaptic connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. Plastic changes appear to follow a regional specialization and underlie the specific type of memory mediated by the brain area in which plasticity occurs. Thus, long-term changes occurring at excitatory corticostriatal synapses should be critically involved in motor learning. Indeed, repetitive stimulation of the corticostriatal pathway can cause either a long-lasting increase or an enduring decrease in synaptic strength, respectively referred to as long-term potentiation (LTP), and long-term depression, both requiring a complex sequence of biochemical events. Once established, LTP can be reversed to control levels by a low-frequency stimulation protocol, an active phenomenon defined "synaptic depotentiation," required to erase redundant information. In the 6-hydroxydopamine rat model of Parkinson's disease (PD), striatal synaptic plasticity has been shown to be impaired, although chronic treatment with levodopa was able to restore it. Of interest, a consistent number of L-dopa-treated animals developed involuntary movements, resembling human dyskinesias. Strikingly, electrophysiological recordings from the dyskinetic group of rats demonstrated a selective impairment of synaptic depotentiation. This survey will provide an overview of plastic changes occurring at striatal synapses. The potential relevance of these findings in the control of motor function and in the pathogenesis both of PD and L-dopa-induced motor complications will be discussed.
authors.affiliation: Clinica Neurologica, Dipartimento di Neuroscienze, Università di Roma "Tor Vergata" and Fondazione Santa Lucia, I.R.C.C.S., Roma, Italy.
authors.forename: Antonio
authors.initials: A
authors.lastname: Pisani
authors.affiliation: Clinica Neurologica, Dipartimento di Neuroscienze, Università di Roma "Tor Vergata" and Fondazione Santa Lucia, I.R.C.C.S., Roma, Italy.
authors.forename: Diego
authors.initials: D
authors.lastname: Centonze
authors.affiliation: Clinica Neurologica, Dipartimento di Neuroscienze, Università di Roma "Tor Vergata" and Fondazione Santa Lucia, I.R.C.C.S., Roma, Italy.
authors.forename: Giorgio
authors.initials: G
authors.lastname: Bernardi
authors.affiliation: Clinica Neurologica, Dipartimento di Neuroscienze, Università di Roma "Tor Vergata" and Fondazione Santa Lucia, I.R.C.C.S., Roma, Italy.
authors.forename: Paolo
authors.initials: P
authors.lastname: Calabresi
mesh_terms: D000818:Animals; D000978:Antiparkinson Agents / Q000009:adverse effects; D003342:Corpus Striatum / Q000473:pathology* / Q000503:physiopathology*; D004195:Disease Models, Animal; D004409:Dyskinesia, Drug-Induced / Q000209:etiology; D006801:Humans; D007858:Learning; D007980:Levodopa / Q000009:adverse effects; D009048:Motor Skills / Q000502:physiology*; D009434:Neural Pathways / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology*; D010300:Parkinson Disease / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D051381:Rats; D013569:Synapses / Q000473:pathology*
chemical_list: D000978:Antiparkinson Agents; D007980:Levodopa
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