TY - JOUR
T1 - Neuronal networks and synaptic plasticity in Parkinson's disease
T2 - beyond motor deficits
AU - Calabresi, Paolo
AU - Galletti, Francesca
AU - Saggese, Emanuele
AU - Ghiglieri, Veronica
AU - Picconi, Barbara
PY - 2007
Y1 - 2007
N2 - The excitatory corticostriatal pathway, which plays a critical role in the building up and storage of adaptive motor behaviours, can undergo long-lasting, activity-dependent changes in the efficacy of synaptic transmission, named long-term potentiation (LTP) and long- term depression (LTD). Both forms of plasticity are thought to underlie motor learning and depend upon the concomitant activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways. Accordingly, corticostriatal LTP and LTD are altered in Parkinson's Disease (PD) models. The dopamine (DA)/acetylcholine(Ach) synaptic unbalance could be responsible of some of the cognitive deficits described in PD patients. The impairment of DA/ACh-dependent cellular learning could lead to the storage of unessential memory traces, as it has been postulated for the induction of L-DOPA-induced dyskinesias. Other non-motor symptoms involve not only the central dopaminergic system, but also in the noradrenergic, serotoninergic and cholinergic transmitter systems.
AB - The excitatory corticostriatal pathway, which plays a critical role in the building up and storage of adaptive motor behaviours, can undergo long-lasting, activity-dependent changes in the efficacy of synaptic transmission, named long-term potentiation (LTP) and long- term depression (LTD). Both forms of plasticity are thought to underlie motor learning and depend upon the concomitant activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways. Accordingly, corticostriatal LTP and LTD are altered in Parkinson's Disease (PD) models. The dopamine (DA)/acetylcholine(Ach) synaptic unbalance could be responsible of some of the cognitive deficits described in PD patients. The impairment of DA/ACh-dependent cellular learning could lead to the storage of unessential memory traces, as it has been postulated for the induction of L-DOPA-induced dyskinesias. Other non-motor symptoms involve not only the central dopaminergic system, but also in the noradrenergic, serotoninergic and cholinergic transmitter systems.
KW - Basal ganglia
KW - Dopamine
KW - Long-term depression
KW - Long-term potentiation
KW - Sleep
KW - Synaptic transmission
UR - http://www.scopus.com/inward/record.url?scp=38949199377&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=38949199377&partnerID=8YFLogxK
U2 - 10.1016/S1353-8020(08)70013-0
DO - 10.1016/S1353-8020(08)70013-0
M3 - Article
C2 - 18267247
AN - SCOPUS:38949199377
VL - 13
JO - Parkinsonism and Related Disorders
JF - Parkinsonism and Related Disorders
SN - 1353-8020
IS - SUPPL. 3
ER -