RT info:eu-repo/semantics/article
T1 Striatal Glutamate Degenerates Thalamic Neurons
A1 Morales Pérez, Ingrid
A1 Yanos, Catalina
A1 Rodríguez Sabaté, Clara
A1 Sánchez, Alberto
A1 Rodríguez, Manuel
A2 Ciencias Médicas Básicas
A2 Grupo de Neurobiología y Neurología Experimental
K1 Astrocyte
K1 Excitotoxicity
K1 Glutamate
K1 Self-induced glutamate accumulation
K1 Striatum
K1 Thalamus
AB Glutamate (GLU)-induced excitotoxicity is considered to be a frequent cause of cell degeneration in basal ganglia disorders; it is normally prevented by uptake of GLU by astrocytes. We recently found that transient perfusion of GLU in the striatum induces persistent accumulation of GLU in striatal astrocytes that could be from the initial administration or caused by the slow release from neurons or astrocytes in response to it. Endogenous production of GLU, that is, ‘‘self-induced GLU accumulation’’ (SIGA), may occur under physiological and pathological conditions. Here we studied the possible induction of SIGA after injury induced by perfusion of GLU receptor agonists into the striatum of rats. The agonists induced local degeneration in neurons and myelinated axons and microgliosis and astrocytosis; there was also gliosis and remote degeneration of neurons in the ventral-posterior complex of the thalamus that project to the cerebral cortex across the striatum. Reactive astrocytes showed persistent GLU accumulation in the striatum (local SIGA) and thalamus (remote SIGA) that persisted for at least 6 weeks after the injury. Thus, SIGA can be induced by neuronal degeneration retrogradely triggered from a remote brain region after excessive release of endogenous GLU from astrocytes. This may be an additional factor to be considered in basal ganglia disorders with glutamatergic excitotoxicity.
YR 2013
FD 2013
LK http://riull.ull.es/xmlui/handle/915/38591
UL http://riull.ull.es/xmlui/handle/915/38591
LA en
NO Plan Nacional I+D+I del Ministerio de Ciencia y Tecnología (SAF2008-03746)
DS Repositorio institucional de la Universidad de La Laguna
RD 25-nov-2024