Physical exercise prevents memory impairment through modulation of CD39 and CD73 activities and A2A receptor expression

Focal sensory system work has been rising as a way to deal with comprehend hypertensionmediated memory brokenness, and ceaseless exercise can tweak the purinergic framework. Thus, we examined the impact of interminable swimming preparing on the purinergic framework in cortex and hippocampus of L-NAME-initiated hypertensive rodents. Method:Male Wistar rodents were separated into four gatherings: Control, Exercise, L-NAME and Exercise L-NAME. Inhibitory shirking test was utilized to survey memory status. NTPDase, CD73 and adenosine deaminase exercises and articulation, and P2 receptors articulation were investigated. Information were investigated utilizing two-way ANOVA and Kruskal–Wallis tests, considering P under 0.05. Results: Physical exercise decreased the pulse and forestalled memory impedance actuated by L-NAME model of hypertension. L-NAME treatment advanced an expansion in NTPDase1, NTPDase3 and CD73 articulation and action in the cortex. A2A articulation is expanded in hippocampus and cortex in the hypertension gathering and exercise forestalled this overexpression. End: These progressions propose that hypertension builds adenosine age, which acts through A2A receptors, and exercise forestalls these impacts. These information may show a potential instrument by which exercise may forestall memory impedance actuated by L-NAME.


Andréia Machado

Abstract | PDF

Share this  Facebook  Twitter  LinkedIn  Google+