Metabotropic glutamate receptors and striatal synaptic plasticity: implications for neurological diseases.
Long- and short-term changes in the efficacy of synaptic transmission are known as synaptic plasticity. Phenomena such as long-term depression (LTD) and long-term potentiation (LTP) are two classical forms of synaptic plasticity that are expressed in several brain areas, including the striatum. Bi-directional changes in corticostriatal synaptic transmission, i.e. LTD and LTP, have been proposed to represent the cellular mechanisms underlying the physiological processes of motor learning and behavior. In parallel, other forms of synaptic plasticity induced by different experimental pathological conditions have been described in the striatum; these changes are presumed to represent the cellular processes underlying several neurological disorders, including Parkinson's disease and Huntington's chorea. A considerable number of receptor and post-receptor systems participate in the mechanisms of synaptic plasticity in the striatum, where glutamate plays a primary role through its ionotropic and metabotropic receptors (mGluRs). These latter constitute a group of recently characterized molecules, which have been shown to modulate synaptic transmission by acting on cellular excitability, ionic conductances and neurotransmitter release. These receptors have also been involved in several neuronal pathophysiological processes. The role of mGluRs in synaptic transmission and synaptic plasticity has been recently deeply studied and characterized in the striatum, in both physiological and pathological conditions. These findings open new and interesting perspectives in the study of basal ganglia function, and introduce new possible pharmacological approaches for the treatment of neurological disorders in which mGluRs have been experimentally involved.
Gubellini
Paolo
P
Interactions Cellulaires, Neurodégénérescence et Neuroplasticité (IC2N-UMR6186), Centre National de la Recherche Scientifique (CNRS), 31 Chemin Joseph Aiguier, 13402 Marseille Cedex 20, France. paolo.gubellini@lncf.cnrs-mrs.fr
Pisani
Antonio
A
Centonze
Diego
D
Bernardi
Giorgio
G
Calabresi
Paolo
P
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D003342:Corpus Striatum / Q000502:physiology* / Q000503:physiopathology; D004195:Disease Models, Animal; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D009422:Nervous System Diseases / Q000209:etiology / Q000503:physiopathology*; D016571:Neural Networks, Computer; D009434:Neural Pathways / Q000502:physiology / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D018091:Receptors, AMPA / Q000502:physiology; D018094:Receptors, Metabotropic Glutamate / Q000502:physiology*
D018091:Receptors, AMPA; D018094:Receptors, Metabotropic Glutamate; D018698:Glutamic Acid; D000109:Acetylcholine