Paras Kumar Mishra, PhD

Associate Professor at University of Nebraska Medical Center


Curriculum vitae



Cellular and Integrative Physiology

University of Nebraska Medical Center



Activation of GABA¬A receptor Protects Mitochondria and Reduces Cerebral ischemia.


Journal article


N. Tyagi, S. Givvimani, Munish Kumar, Soumi Kundu, W. M. Gillespie, P. Mishra, Pushpa Kumar Sathnur, D. Lominadze, U. Sen, Suresh Tyagi
2009

Semantic Scholar DOI
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APA   Click to copy
Tyagi, N., Givvimani, S., Kumar, M., Kundu, S., Gillespie, W. M., Mishra, P., … Tyagi, S. (2009). Activation of GABA¬A receptor Protects Mitochondria and Reduces Cerebral ischemia.


Chicago/Turabian   Click to copy
Tyagi, N., S. Givvimani, Munish Kumar, Soumi Kundu, W. M. Gillespie, P. Mishra, Pushpa Kumar Sathnur, D. Lominadze, U. Sen, and Suresh Tyagi. “Activation of GABA¬A Receptor Protects Mitochondria and Reduces Cerebral Ischemia.” (2009).


MLA   Click to copy
Tyagi, N., et al. Activation of GABA¬A Receptor Protects Mitochondria and Reduces Cerebral Ischemia. 2009.


BibTeX   Click to copy

@article{n2009a,
  title = {Activation of GABA¬A receptor Protects Mitochondria and Reduces Cerebral ischemia.},
  year = {2009},
  author = {Tyagi, N. and Givvimani, S. and Kumar, Munish and Kundu, Soumi and Gillespie, W. M. and Mishra, P. and Sathnur, Pushpa Kumar and Lominadze, D. and Sen, U. and Tyagi, Suresh}
}

Abstract

Gamma‐aminobutyric acid is the inhibitory neurotransmitter and has been identified in mitochondria. Because the release of mitochondrial factors is known to correlate with acute neurological damage, we proposed to investigate the possible neuroprotective effects of GABA‐A receptors in cerebral ischemia. In this study transient ischemia was induced in mice by occlusion in the middle of the carotid artery (MACO). Effects of GABA‐A receptor agonist (muscimol) were first studied in oxygen/glucose deprivation‐induced death of neuronal cells. Mitochondrial membrane potential, cytochrome‐c release, caspase 3 activation, the infarct volume and neurological function were examined in the absence or presence of muscimol. Our results shows that GABA‐A receptor agonist inhibits oxygen/glucose deprivation‐induced cell death, loss of mitochondrial membrane potential, downstream release of cytochrome‐C, which activates the caspase apoptotic signaling cascade. Furthermore, it decreases infarct size and improves neurological scores after MACO in mice. This study indicated that GABA‐A receptor is neuroprotective against cerebral ischemia. It also suggested mitochondrial permeability transition might be a valuable therapeutic target for acute neurodegeneration.


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