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Related Experiment Video

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Guanfacine ameliorates hypobaric hypoxia induced spatial working memory deficits.

H Kauser1, S Sahu, S Kumar

  • 1Defence Institute of Physiology and Allied Sciences (DIPAS), Defence Research and Development Organization (DRDO), Lucknow Road, Timarpur, Delhi 110054, India.

Physiology & Behavior
|November 5, 2013
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Summary

High altitude exposure causes cognitive deficits, but Guanfacine (GFC) effectively restores spatial working memory and reduces neuronal damage in the prefrontal cortex. This suggests GFC as a potential countermeasure for hypobaric hypoxia effects.

Keywords:
ApoptosisDATGFCGuanfacineHHHypobaric hypoxiaNeurodegenerationPFCPrefrontal cortexSWMSpatial working memorydelayed alternation taskhypobaric hypoxiaprefrontal cortexspatial working memory

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Area of Science:

  • Neuroscience
  • Altitude Medicine
  • Pharmacology

Background:

  • Hypobaric hypoxia (HH) at high altitudes impairs cognitive functions, particularly attention and working memory.
  • Adrenergic dysregulation and prefrontal cortex (PFC) neuronal damage are implicated in hypoxia-induced memory deficits.
  • Alpha 2A adrenergic receptor stimulation in the PFC is crucial for spatial working memory (SWM) under stress.

Purpose of the Study:

  • To evaluate the efficacy of Guanfacine (GFC), an alpha 2A adrenergic agonist, in reversing HH-induced SWM deficits.
  • To assess GFC's ability to mitigate neuronal damage in the PFC caused by chronic HH exposure.

Main Methods:

  • Rats were exposed to chronic HH (25,000ft for 7 days) in a decompression chamber.
  • Daily intramuscular administration of GFC (1mg/kg) was given during HH exposure.
  • Cognitive function was assessed using the Delayed Alternation Task (DAT) in a T-maze.
  • PFC neuronal damage was evaluated through apoptotic and neurodegenerative markers.

Main Results:

  • HH exposure significantly decreased correct choices and increased perseverative errors in the DAT.
  • GFC treatment significantly ameliorated SWM deficits and reduced perseveration.
  • HH exposure led to increased chromatin condensation, DNA fragmentation, neuronal pyknosis, and Fluoro-Jade positive cells in the medial PFC.
  • GFC administration significantly reduced the severity of these neurodegenerative changes.

Conclusions:

  • GFC effectively restores spatial working memory and ameliorates perseveration in rats exposed to hypobaric hypoxia.
  • GFC significantly mitigates HH-induced neuronal damage, including apoptosis and neurodegeneration, in the medial prefrontal cortex.
  • Modulating adrenergic mechanisms with GFC shows promise as a countermeasure against cognitive and neurodegenerative deficits associated with hypobaric hypoxia.