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Neurochem Res (2010) 35:279287 DOI 10.1007/s11064-009-0051-4
ORIGINAL PAPER
Scopolamine Induced Amnesia is Reversed by Bacopa monniera
Through Participation of Kinase-CREB Pathway
Manish Kumar Saraf Akshay Anand Sudesh Prabhakar
Accepted: 13 August 2009 / Published online: 16 September 2009 Springer Science+Business Media, LLC 2009
Abstract Scopolamine, an anticholinergic drug, is reported to produce amnesia by interference of long term potentiation and has been used for discerning the efcacy of various antiamnesic drugs. The intoxication with anti-cholinergics and benzodiazepines tend to produce neuro-degeneration which cause memory decits. Our earlier reports have shown the antiamnesic drug, B. monniera to be capable of alleviating diazepam induced memory decits. We have now tested how scopolamine affects downstream signaling molecules of long term potentiation and ifB. monniera can also modulate the scopolamine induced amnesia. We used Morris water maze scale to test the amnesic effect of scopolamine and its reversal byB. monniera. Rota-rod test was used to screen muscle coordination activity of mice before water maze investigations were carried out. The results showed that scopolamine downregulated protein kinase C and iNOS without affecting cAMP, protein kinase A, calmodulin, MAP kinase, nitrite, CREB and pCREB. B. monniera reversed the scopolamine induced amnesia by signicantly improving calmodulin and by partially attenuating protein kinase C and pCREB. These observations suggest involvement of calmodulin in evoking antiamnesic effects of B. monniera.
Keywords Amnesia Bacopa monniera Calmodulin
CREB Scopolamine Water maze
Introduction
Dementia is one of the causes of memory loss [17], which affects 7% population older than 65 years and upto 3050% population by the age of 85 years. This is growing with increase in life span [17, 25, 29]. Cholinergic antagonism is reported to produce cognition decit which imitates Alzheimers disease [14] similar to hippocampal lesion induced cognitive decits [1, 46]. The degeneration of glutamatergic neurons, in addition to cholinergic neurons [3], is reported in hippocampus and cortex of AD (Alzheimer disease) patients [4, 16]. Long term potentiation (LTP) which is a well accepted mechanism of learning and memory is activated due to high frequency presynaptic stimulation [7, 8]. It subsequently activates postsynaptic downstream signalling which comprises of retrograde messengers, kinases, calmodulin, cAMP response element binding protein etc. [22, 23]. Scopolamine, an acetylcho-line receptor antagonist, has been reported to impair LTP [30, 34], and...