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Abstract
Enhancing cyclic nucleotides signaling by inhibition of phosphodiesterases (PDEs)
is known to be beneficial in disorders associated with cognitive decline. The present
study was designed to investigate the effect of vinpocetine (PDE1 inhibitor) on intracerebroventricular
(i.c.v.) streptozotocin induced experimental sporadic dementia of Alzheimer's type.
Infusion of streptozotocin impaired learning and memory, increased oxidative-nitritive
stress and induced cholinergic hypofunction in rats. Chronic treatment with vinpocetine
(5, 10 and 20 mg/kg i.p.) for 21 days following first i.c.v. streptozotocin infusion
significantly improved learning and memory in Morris water maze and passive avoidance
paradigms. Further, vinpocetine significantly reduced the oxidative-nitritive stress,
as evidenced by decrease in malondialdehyde (MDA) and nitrite levels, and restored
the reduced glutathione (GSH) levels. Significant increase in acetylcholinesterase
activity and lactate dehydrogenase levels was observed in the present model indicating
cholinergic hypofunction and increase in neuronal cell damage. Chronic treatment with
vinpocetine also reduced significantly the increase in acetylcholinesterase activity
and lactate dehydrogenase levels indicating restorative capacity of vinpocetine with
respect to cholinergic functions and preventing the neuronal damage. The observed
beneficial effects of vinpocetine on spatial memory may be due to its ability to favorably
modulate cholinergic functions, prevent neuronal cell damage and possibly through
its antioxidant mechanism also.