TY - JOUR
T1 - Maladaptive plasticity in levodopa-induced dyskinesias and tardive dyskinesias
T2 - Old and new insights on the effects of dopamine receptor pharmacology
AU - Cerasa, Antonio
AU - Fasano, Alfonso
AU - Morgante, Francesca
AU - Koch, Giacomo
AU - Quattrone, Aldo
PY - 2014
Y1 - 2014
N2 - Maladaptive plasticity can be defined as behavioral loss or even development of disease symptoms resulting from aberrant plasticity changes in the human brain. Hyperkinetic movement disorders, in the neurological or psychiatric realms, have been associated with maladaptive neural plasticity that can be expressed by functional changes such as an increase in transmitter release, receptor regulation, and synaptic plasticity or anatomical modifications such as axonal regeneration, sprouting, synaptogenesis, and neurogenesis. Recent evidence from human and animal models provided support to the hypothesis that these phenomena likely depend on altered dopamine turnover induced by long-term drug treatment. However, it is still unclear how and where these altered mechanisms of cortical plasticity may be localized. This study provides an up-to-date overview of these issues together with some reflections on future studies in the field, particularly focusing on two specific disorders (levodopa-induced dyskinesias in Parkinson's disease patients and tardive dyskinesias in schizophrenic patients) where the modern neuroimaging approaches have recently provided new fundamental insights.
AB - Maladaptive plasticity can be defined as behavioral loss or even development of disease symptoms resulting from aberrant plasticity changes in the human brain. Hyperkinetic movement disorders, in the neurological or psychiatric realms, have been associated with maladaptive neural plasticity that can be expressed by functional changes such as an increase in transmitter release, receptor regulation, and synaptic plasticity or anatomical modifications such as axonal regeneration, sprouting, synaptogenesis, and neurogenesis. Recent evidence from human and animal models provided support to the hypothesis that these phenomena likely depend on altered dopamine turnover induced by long-term drug treatment. However, it is still unclear how and where these altered mechanisms of cortical plasticity may be localized. This study provides an up-to-date overview of these issues together with some reflections on future studies in the field, particularly focusing on two specific disorders (levodopa-induced dyskinesias in Parkinson's disease patients and tardive dyskinesias in schizophrenic patients) where the modern neuroimaging approaches have recently provided new fundamental insights.
KW - Dopaminergic treatment
KW - Hyperkinetic movement disorders
KW - Inferior frontal cortex
KW - Levodopa-induced dyskinesias
KW - Tardive dyskinesias
UR - http://www.scopus.com/inward/record.url?scp=84901035168&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84901035168&partnerID=8YFLogxK
U2 - 10.3389/fneur.2014.00049
DO - 10.3389/fneur.2014.00049
M3 - Article
AN - SCOPUS:84901035168
VL - 5 APR
JO - Frontiers in Neurology
JF - Frontiers in Neurology
SN - 1664-2295
M1 - Article 49
ER -