Abstract
Introduction: Sleep has been found to influence both acquisition and consolidation of memory; therefore, sleep deprivation is often linked to multiple anomalies in cognitive paradigms giving rise cognitive dysfunctions. Objective: The present study has been designed with an aim to decipher plausible mechanistic interplays involved in the induction of cognitive dysfunction as a direct consequence of sleep deprivation. Methods: Male laca mice were sleep deprived for 24-hours using grid suspended over water method on alternate days extended over the total protocol duration of 21 days. Various neurobehavioral memory evaluating parameters followed by biochemical, acetylcholinesterase (AChE) activity, mitochondrial respiratory enzyme complex activities (I-IV) and histopathological examinations of the mice brain were monitored. Results: Sleep deprivation of 24-hours on alternate days for 21 days significantly impaired cognitive performance in both memory evaluating paradigms (Morris water maze test and elevated plus maze test) as compared to naive animals. Additionally animals subjected to sleep deprivation also demonstrated conditions of elevated oxidative stress, impaired mitochondrial enzyme complex activities, increased aceytlcholineestaerase activity, as well as histopathological alterations pertaining to hippocampal and thalamo-cortical regions of mice brain as compared to naive animals. However, chronic piracetam (100 mg/kg) treatment showed significant protective effect against sleep deprivation induced cognitive dysfunction, oxidative damage, mitochondrial respiratory enzyme complex insuffeciencies, increased acetylcholinesterase activity as well as neuromorphological alterations. Conclusion: The present study suggests mechanistic interplay between oxidative stresses; mitochondrial impairment as well as acetylcholineesterase activity may influence hippocampal and cortical neuronal survival and thus lead to precipitation of sleep deprivation induced cognitive deficits.
Highlights
Sleep has been found to influence both acquisition and consolidation of memory; sleep deprivation is often linked to multiple anomalies in cognitive paradigms giving rise cognitive dysfunctions
The present study suggests mechanistic interplay between oxidative stresses; mitochondrial impairment as well as acetylcholineesterase activity may influence hippocampal and cortical neuronal survival and lead to precipitation of sleep deprivation induced cognitive deficits
Mean escape/transfer latency gradually decreased in all groups on subsequent days of training period from day 18 to day 20 in Morris water maze (MWM) test
Summary
Sleep has been found to influence both acquisition and consolidation of memory; sleep deprivation is often linked to multiple anomalies in cognitive paradigms giving rise cognitive dysfunctions. It has been validated that sleep affects almost every individual component of cognition such as stimulus detection, information encoding, working memory, etc. Against this background, sleep deprivation [SD] is entitled to cause cognitive deficits. The significant alterations observed in key characteristics of single and paired TMS techniques (as a consequence of SD) clearly demonstrate significant variations in cortical excitability as well as functionality of interneuronal circuitry in the primary motor cortex brought and aptly explain pathophysiological substrates of SD induced cognitive impairments [8,9,10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
