RT info:eu-repo/semantics/article
T1 Glycine release in the substantia nigra: Interaction with glutamate and GABA.
A1 Morales Pérez, Ingrid
A1 García Dopico, José
A1 González Hernández, Tomás
A1 Gómez García, Isabel
A1 Milena Abril, Antonio
A1 Obeso Inchausti, José
A1 Rodríguez Díaz, Manuel
A2 Ciencias Médicas Básicas
A2 Grupo de Neurobiología y Neurología Experimental.
K1 Glycine
K1 Glutamate
K1 GABA
K1 Zinc
K1 Substantia nigra
K1 Parkinson’s disease
AB Previous studies have reported a high number of glycine (GLY) receptors in the substantia nigra (SN) but a low number of GLY-neurons, suggesting that taurine, a partial agonist of GLY-receptors, is the natural substrate for SN GLY-receptors. By using microdialysis to quantify amino acids in the extracellular space of the SN, we observed an extracellular pool of GLY in the rat that increased after depolarizing with high-Kþ in a Ca2þ-dependent manner and that diffuses through the extracellular space. GLY markedly increased after blocking either the tricarboxylic cycle with fluorocitrate or the glutamine synthetase activity with MSO. Because these products act selectively on glial cells, their effects show glia as a key cell in maintaining the extracellular pool of GLY in the SN. Extracellular GLY was modified by glutamate and glutamate receptor agonists. The local administration of GLY modified the extracellular concentration of GABA. Taken together, the complex regulation of the extracellular level of GLY, its possible glial origin and interaction with glutamate and GABA suggest a volume transmitter role for GLY in the SN, a possibility which also agrees with the recent finding of GLY-transporters in this centre.
YR 2006
FD 2006
LK http://riull.ull.es/xmlui/handle/915/38598
UL http://riull.ull.es/xmlui/handle/915/38598
LA en
DS Repositorio institucional de la Universidad de La Laguna
RD 18-oct-2024