Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (9): 1418-1420.doi: 10.4103/1673-5374.165509

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Piroxicam-mediated modulatory action of 5-hydroxytryptamine serves as a “brake” on neuronal excitability in ischemic stroke

Pallab Bhattacharya1, 2, Anand Kumar Pandey2, Sudip Paul2, 3, Ranjana Patnaik2   

  1. 1 Department of Neurology, Leonard M. Miller School of Medicine, Miami, FL, USA
    2 School of Biomedical Engineering, Indian Institute of Technology, Banaras Hindu University, Varanasi, India
    3 Department of Biomedical Engineering, North Eastern Hill University (NEHU), Shillong, India
  • Received:2015-07-01 Online:2015-09-28 Published:2015-09-28
  • Contact: Pallab Bhattacharya, Ph.D., or Ranjana Patnaik, Ph.D., p.bhattacharya@med.miami.edu or drranjanapatnaik@gmail.com.

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Abstract:

Our previous studies indicated an increase in extracellular γ-aminobutyric acid (GABA) in rodent’s ischemic brain after Piroxicam administration, leading to alleviation of glutamate mediated excitotoxicity through activation of type A GABA receptor (GABAA). This study was to investigate if GABAA activation by Piroxicam affects extracellular 5-hydroxytryptamine or not. High performance liquid chromatography revealed that there was a significant decrease in extracellular 5-hydroxytryptamine release in ischemic cerebral cortex and striatum in Piroxicam pre-treated rat brains. This suggests a probable role of Piroxicam in reducing extracellular 5-hydroxytryptamine release in ischemic cerebral cortex and striatum possibly due to the GABAA activation by Piroxicam.