GAT-3 Dysfunction Generates Tonic Inhibition in Exter nal Globus Pallidus Neurons in Parkinsonian Rodents

The external globus pallidus (GP) is a key GABAergic hub in the basal ganglia (BG) circuitry, a neuronal network involved in motor control. In Parkinson's disease (PD), the rate and pattern of activity of GP neurons are profoundly altered and contribute to the motor symptoms of the disease. In...

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Detalhes bibliográficos
Autores: Chazalon, Marine, Paredes Rodríguez, Elena, Morin, Stéphanie, Martinez, Audrey, Cristóvão-Ferreira, Sofia, Vaz, Sandra, Sebastiao, Ana, Panatier, Aude, Boué-Grabot, Eric, Miguélez Palomo, Cristina, Baufreton, Jérôme
Tipo de documento: artigo
Data de publicação:2018
País:España
Recursos:Universidad del País Vasco
Repositório:Addi. Archivo Digital para la Docencia y la Investigación
OAI Identifier:oai:addi.ehu.eus:10810/29869
Acesso em linha:http://hdl.handle.net/10810/29869
Access Level:Acceso aberto
Palavra-chave:extrasynaptic gaba(a) receptors
monkey basal ganglia
synaptic-transmission
subthalamic nucleus
projection neurons
transporter gat-1
beta oscillations
adult-rat
in-vitro
plasticity
Descrição
Resumo:The external globus pallidus (GP) is a key GABAergic hub in the basal ganglia (BG) circuitry, a neuronal network involved in motor control. In Parkinson's disease (PD), the rate and pattern of activity of GP neurons are profoundly altered and contribute to the motor symptoms of the disease. In rodent models of PD, the striato-pallidal pathway is hyperactive, and extracellular GABA concentrations are abnormally elevated in the GP, supporting the hypothesis of an alteration of neuronal and/or glial clearance of GABA. Here, we discovered the existence of persistent GABAergic tonic inhibition in GP neurons of dopamine-depleted (DD) rodent models. We showed that glial GAT-3 transporters are down-regulated while neuronal GAT-1 function remains normal in DD rodents. Finally, we showed that blocking GAT-3 activity in vivo alters the motor coordination of control rodents, suggesting that GABAergic tonic inhibition in the GP contributes to the pathophysiology of PD.