Effect of Ang II Receptor Inhibition on GSK-3β/CREB/BDNF Signalling in REM Sleep Deprivation-Induced Memory...

Area of Science:

• Neuroscience
• Pharmacology
• Sleep Science

Background:

• REM sleep deprivation significantly impairs hippocampus-dependent learning and memory.
• Cognitive deficits are linked to molecular pathway disruptions and oxidative stress.

Purpose of the Study:

• To investigate the neuroprotective effects of telmisartan against REM sleep deprivation-induced cognitive impairments.
• To examine telmisartan's impact on molecular pathways and oxidative stress markers in the hippocampus and prefrontal cortex.

Main Methods:

• Chronic REM sleep deprivation was induced in Wistar-Albino rats using the modified multiple platform method for 21 days.
• Telmisartan (1 mg/kg and 3 mg/kg) or placebo was administered orally daily.
• Cognitive function was assessed using the Morris water maze; molecular markers (BDNF, CREB, GSK-3β) and oxidative stress markers were analyzed.

Main Results:

• REM sleep deprivation led to impaired learning, memory deficits, altered molecular signaling (reduced BDNF/CREB, increased GSK-3β), and oxidative stress.
• Telmisartan treatment significantly improved cognitive performance in sleep-deprived rats.
• Telmisartan administration increased BDNF and CREB, decreased GSK-3β, and balanced oxidative stress markers.

Conclusions:

• Telmisartan effectively protected against cognitive and biochemical damage induced by chronic REM sleep deprivation.
• The protective effects are likely mediated by modulating the GSK-3β/CREB/BDNF signaling pathway and reducing oxidative stress.