Unbound MEDLINE

Acetylcholinesterase inhibitors enhance cognitive functions in rats following hypobaric hypoxia. Behavioural brain research [Behav Brain Res] Journal article

 
TitleAcetylcholinesterase inhibitors enhance cognitive functions in rats following hypobaric hypoxia.
Author(s)Muthuraju S, Maiti P, Solanki P, Sharma AK, Amitabh , Singh SB, Prasad D, Ilavazhagan G 
InstitutionNeurobiology Division, Defence Institute of Physiology and Allied Sciences, Defence Research and Development Organization, Ministry of Defence, Govt. of India, Lucknow Road, Timarpur, Delhi, India.
SourceBehav Brain Res 2009 Mar 28.
AbstractHypobaric hypoxia (HBH) can produce neuropsychological disorders such as insomnia, dizziness, memory deficiencies, headache and nausea. It is well known that exposure to HBH cause alterations of neurotransmitters and cognitive impairment in terms of learning and memory. But the mechanisms are poorly understood. The present study aimed to investigate the cholinergic system alterations associated with simulated HBH induced cognitive impairment. Male Sprague-Dawley rats were exposed to HBH equivalent to 6100m for 7 days in a simulation chamber. The cognitive performance was assessed using Morris Water Maze (MWM) task. Cholinergic markers like acetylcholine (ACh) and acetylcholinesterase (AChE) were evaluated in hippocampus and cortex of rats. Neuronal damage was also studied through morphological changes. Exposure to HBH led to impairment in relearning ability and memory retrieval and it was accompanied by decrease in ACh level and increase in AChE and led to morphological damage. Administration of AChE inhibitor (AChEI), physostigmine (PHY) and galantamine (GAL) to rats during HBH exposure resulted in amelioration of the deleterious effects induced by HBH. The AChEIs were able to improve the cholinergic activity by restoring the level of ACh by blocking the AChE activity. In addition, the AChEIs also prevented neurodegeneration by reducing the AChE level in cortical and hippocampal neurons.
LanguageENG
Pub Type(s)JOURNAL ARTICLE
PubMed ID19446892
  
Advertise on this site.