Bogdan A Stoica

Publication Detail

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MGLuR5 activation reduces beta-amyloid-induced cell death in primary neuronal cultures and attenuates translocation of cytochrome c and apoptosis-inducing factor.

Vilen A Movsesyan; Bogdan A Stoica; Alan I Faden (Profiled Authors: Alan I Faden; Bogdan A Stoica)

Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057, USA.
Journal of neurochemistry 2004;89(6):1528-36.

Activation of metabotropic glutamate receptor 5 (mGluR5) has been shown to reduce caspase-dependent apoptosis in primary neuronal cultures induced by staurosporine and etoposide. beta-Amyloid (Abeta)-induced neurotoxicity in culture appears to be in part caspase mediated. In the present studies the effects of treatment with an mGluR5 agonist or antagonist on Abeta-induced neuronal apoptosis were examined in rat cortical neuronal cultures. Pretreatment with the selective mGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG) markedly reduced the number of apoptotic cells after exposure to Abeta (25-35), as well as associated LDH release. Blockade of mGluR5 by the selective antagonist, 2-methyl-6-(phenylethynyl)pyridine (MPEP) attenuated these effects of CHPG. A similar neuroprotective effect of mGluR5 activation by CHPG was observed in cultures treated with full-length Abeta peptide (1-42). CHPG attenuated Abeta (25-35)-induced cytochrome c release and decreased levels of active caspase-3 protein. CHPG also reduced translocation of apoptosis-inducing factor (AIF) induced by Abeta (25-35). Thus, mGluR5 activation limits the release of mitochondrial proteins associated with induction of both caspase-dependent and -independent apoptosis.

2 Originating Grant

• 1.

  FADEN, ALAN IRA

  mGluR5 inhibits microglial activation and neuronal cell death after TBI

  3 February 1999 - 31 January 2014

  NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

• 2.

  Faden, Alan I

  Apoptosis Induced by Traumatic Brain Injury

  15 May 1998 - 28 February 2007

  NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

Scientific Context

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