Glutamate differently modulates metabotropic glutamate receptors in neuronal and glial cells.

Neurochem Res

Area de Bioquímica, Departamento de Química Inorgánica, Orgánica y Bioquímica, Facultad de Ciencias Químicas, Centro Regional de Investigaciones Biomédicas (CRIB), Universidad de Castilla-La Mancha (UCLM), Avenida Camilo José Cela, 10, 13071, Ciudad Real, Spain.

Published: July 2010

AI Article Synopsis

  • Glutamate is essential for learning and memory but can be toxic in high amounts, leading to neuronal death.
  • The study investigates how glutamate affects neurons and C6 glioma cells, revealing that neuronal damage is dependent on the concentration and duration of exposure.
  • In neurons, total levels of metabotropic glutamate receptors (mGluR) decrease with glutamate exposure, while in C6 cells, mGluR levels initially drop and then rise after longer exposure, indicating a complex, cell-specific response to glutamate.

Article Abstract

Glutamate is an excitatory neurotransmitter implicated in learning and memory processes, but at high concentrations it acts as an excitotoxin causing degeneration and neuronal death. The aim of this work was to determine the excitotoxic effect of glutamate and the regulation of metabotropic glutamate receptors (mGluR) during excitotoxicity in neurons and C6 glioma cells. Results show that glutamate causes excitotoxic damage only in cortical neurons. Loss of cell viability in neurons was glutamate concentration- and time-dependent. Total mGluR levels were significantly reduced in these cells when exposed to glutamate. However, in C6 cells, which have been used as a model of glial cells, these receptors were regulated in a biphasic manner, decreased after 6 h, and increased after 24/48 h of treatment. Results show a cell dependent mGluR regulation by glutamate exposure which could mediate the vulnerability or not to glutamate mediated excitotoxicity.

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Source
http://dx.doi.org/10.1007/s11064-010-0154-yDOI Listing

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