title: Pathological synaptic plasticity in the striatum: implications for Parkinson's disease.
abstract: 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 (LTD), both requiring a complex sequence of biochemical events. Once established, LTP can be reversed to control levels by a low-frequency stimulation (LFS) protocol, an active phenomenon defined "synaptic depotentiation", required to erase redundant information. In the 6-hydroxydopamine (6-OHDA) rat model of Parkinson's disease (PD), striatal synaptic plasticity has been shown to be impaired, though chronic treatment with l-dopa was able to restore it. Interestingly, 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 Parkinson's disease 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., Via di Tor Vergata 135, Roma, Italy.
authors.forename: Barbara
authors.initials: B
authors.lastname: Picconi
authors.forename: Antonio
authors.initials: A
authors.lastname: Pisani
authors.forename: Ilaria
authors.initials: I
authors.lastname: Barone
authors.forename: Paola
authors.initials: P
authors.lastname: Bonsi
authors.forename: Diego
authors.initials: D
authors.lastname: Centonze
authors.forename: Giorgio
authors.initials: G
authors.lastname: Bernardi
authors.forename: Paolo
authors.initials: P
authors.lastname: Calabresi
mesh_terms: D000818:Animals; D000978:Antiparkinson Agents / Q000009:adverse effects / Q000627:therapeutic use; D002540:Cerebral Cortex / Q000503:physiopathology; D003714:Denervation; D004409:Dyskinesia, Drug-Induced / Q000503:physiopathology; D006801:Humans; D007980:Levodopa / Q000009:adverse effects / Q000627:therapeutic use; D017774:Long-Term Potentiation / Q000502:physiology; D017072:Neostriatum / Q000502:physiology* / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology*; D010300:Parkinson Disease / Q000188:drug therapy / Q000503:physiopathology*; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000503:physiopathology; D051381:Rats; D013569:Synapses / Q000502:physiology*
chemical_list: D000978:Antiparkinson Agents; D007980:Levodopa