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Updated: Aug 16, 2026

Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration
09:07

Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration

Published on: March 18, 2014

N-methyl-D-aspartate receptor agonists decrease protooncogene bcl-2 mRNA expression in cultured rat cerebellar

P Montpied1, M Weller, S M Paul

  • 1Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, Maryland.

Biochemical and Biophysical Research Communications
|September 15, 1993
PubMed

Insights

N-methyl-D-aspartate (NMDA) protects cerebellar neurons from glutamate toxicity, but this effect does not involve changes in bcl-2 messenger RNA (mRNA) levels. Glutamate toxicity in these neurons differs from typical programmed cell death.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • The protooncogene bcl-2 plays a role in neuronal survival.
  • N-methyl-D-aspartate (NMDA) can induce excitoprotection in neurons.
  • Glutamate excitotoxicity is a significant factor in neuronal damage.

Purpose of the Study:

  • To investigate the role of bcl-2 messenger RNA (mRNA) levels in NMDA-induced excitoprotection of cerebellar granule neurons.
  • To determine if changes in bcl-2 mRNA are involved in glutamate toxicity pathways.

Main Methods:

  • Cerebellar granule neurons were exposed to NMDA and glutamate.
  • bcl-2 mRNA levels were measured using quantitative techniques.
  • Neuronal survival rates were assessed.
  • DNA fragmentation was analyzed to identify cell death mechanisms.

Main Results:

  • Both NMDA and glutamate exposure decreased bcl-2 mRNA levels.
  • Pre-exposure to NMDA did not alter the glutamate-evoked decrease in bcl-2 mRNA.
  • NMDA pre-exposure significantly increased neuronal survival despite unchanged bcl-2 mRNA levels.
  • Glutamate toxicity did not induce nucleosomal DNA fragmentation and was inhibited by aurintricarboxylic acid.

Conclusions:

  • NMDA-induced excitoprotection of cerebellar granule neurons does not appear to be mediated by changes in bcl-2 mRNA levels.
  • Glutamate toxicity in these neurons exhibits characteristics distinct from classical programmed cell death.
  • The intracellular mechanisms of NMDA excitoprotection and glutamate toxicity warrant further investigation beyond bcl-2 mRNA regulation.

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