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Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
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Protease-activated receptor 1-dependent neuronal damage involves NMDA receptor function.

Cecily E Hamill1, Guido Mannaioni, Polina Lyuboslavsky

  • 1Department of Pharmacology, Emory University School of Medicine, Rollins Research Center, Atlanta, GA 30322-3090, USA.

Experimental Neurology
|May 7, 2009
PubMed
Summary

Removing Protease-activated receptor 1 (PAR1) reduces brain damage from stroke and NMDA excitotoxicity. PAR1 potentiation of NMDA receptors contributes to these harmful effects in the central nervous system.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Cellular Biology

Background:

  • Protease-activated receptor 1 (PAR1) is a G-protein coupled receptor found in the central nervous system.
  • PAR1 activation by proteases has complex effects on neuronal injury and inflammation in animal models.

Purpose of the Study:

  • To evaluate the role of PAR1 in lesion volume following ischemic stroke and NMDA-induced neurotoxicity.
  • To investigate if PAR1 potentiation of NMDA receptors contributes to neurotoxicity.

Main Methods:

  • Utilized wild-type and PAR1 knockout mice subjected to transient middle cerebral artery occlusion (stroke model).
  • Administered NMDA intrastriatally to induce excitotoxicity in wild-type and PAR1 knockout mice.
  • Tested the effects of NMDA receptor antagonists (MK801, ketamine) in PAR1 knockout and wild-type mice.

Main Results:

  • PAR1 knockout mice exhibited reduced infarct volume (57%) after focal ischemia.
  • PAR1 knockout or antagonism reduced NMDA-induced neuronal injury by 60%.
  • NMDA receptor antagonists did not significantly alter lesion volumes in PAR1 knockout mice, suggesting PAR1's primary role is NMDA potentiation.

Conclusions:

  • PAR1 activation exacerbates neuronal injury, potentially by potentiating NMDA receptor function.
  • Targeting PAR1 may offer a therapeutic strategy for reducing brain damage in stroke and excitotoxicity.