ABSTRACT
Curcumin possesses wide spectrum of biological actions, on that account the current study was aimed to investigate the beneficial effectiveness of curcumin on memory and oxidative stress if any, over synthetic drug donepezil approved for the treatment of memory disorders. Eighteen Albino wistar [male] rats were divided into 3 groups namely vehicle control which received neutral oil orally and 0.9% saline intraperitoneally, curcumin which received curcumin orally dissolved in neutral oil at the dose of 100mg/ml/kg for seven days, donepezil which received donepezil intraperitoneally at the dose of 1mg/ml/kg for seven days. To assess memory and cognition Elevated Plus Maze and Morris Water Maze tests were performed. Rats were sacrificed after behavioral analysis and their brains were removed for biochemical assays including lipid peroxidation and antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase. Acetylcholine esterase activity and acetylcholine levels were also determined. Our results showed that both curcumin and donepezil improved memory and inhibited acetylcholinesterase, however curcumin inhibited AchE with more potency than donepezil when compared to vehicle control rats. Moreover curcumin exhibited greater antioxidant potential to decrease the load of oxidative stress in brain cells than donepezil as compared to vehicle control rats. In conclusion present study proposed that increased antioxidant potential of curcumin may be responsible for its increased acetylcholine levels and associated enhanced memory performance
ABSTRACT
Post-traumatic stress disorder [PTSD] is a condition which is triggered shortly after experiencing traumatic events. PTSD is complicated by the fact that people with PTSD often develop additional disorders such as phobias, addiction, depression, panic disorder and obsessive-compulsive disorder. Beta-adrenergic and cholinergic system both are involved in memory formation as well as in emotional response associated with memory. It is reported that the administration of beta-adrenergic and cholinergic antagonist results in the impairment in memory formation. Here, we examined the potential of beta-adrenergic antagonist propranolol and muscarinic cholinergic antagonist atropine for impairing the recently formed fear memory associated with PTSD. Reconsolidation is the memory process during which labile memory converts into permanent memory. In this study it is hypothesized that if recently formed fear memory is disturbed during reconsolidation phase by pharmacological intervention then it could be possible to impair wellconsolidated fear memory. Atropine and propranolol were injected in separate set of rats [n=6] just after the reactivation of fear memory. Short term memory and long term memory were monitored after 2 h and 24 h of reactivation respectively. Results of current study demonstrated that only atropine showed significant impairment of reconsolidation of newly formed fear memory whereas propranolol did not show fear memory disrupting effects. The results emphasize the significance of pharmacological intervention to impair reconsolidation of newly formed fear memory
ABSTRACT
This study was designed to investigate the role of enriched environment in preventing and/or reducing the neurobehavioral deficits produced after nicotine administration in albino Wistar rats. Equal numbers of rat in two groups were either placed in social environment [control group] or social along with physically enriched environment for four weeks before the administration of nicotine. Exposure to different environmental conditions was followed by the intraperitoneal injection of nicotine at the dose of 0.6 mg/kg for seven consecutive days during which addictive behavior was monitored using conditioned placed preference paradigm. Behavioral responses to locomotor activity, anxiety and retention of short term memory were investigated in control and nicotine injected groups exposed to different environments. Results of this study showed that the rats pre-exposed to physical along with social enrichment exhibited a decrease in drug seeking behavior, hyper locomotion, anxiogenic effects along with improvement of working memory as compared to control and nicotine injected groups that were kept in social environment alone. This behavioral study suggests that the exposure to physical enrichment along with socialization in young age can later reduce the chances of compulsive dependence on nicotine and related neurobehavioral deficits
ABSTRACT
Simvastatin, an important member of statin family is widely prescribed as cholesterol-lowering agent. Like other statins it acts by inhibiting the rate limiting enzyme 3-hydroxy-3-methylglutaryl-CoA [HMG-CoA] reductase, responsible for the endogenous production of cholesterol which forms an essential part of neuronal cell membranes. Lowering of cholesterol has been reported to alter the brain chemistry and hence neurotransmission. To understand the association between low cholesterol and brain serotonin [5-HT] we monitored the effect of oral administration of simvastatin for 4 weeks on brain serotonin levels. Drug treated rats exhibited significantly low plasma cholesterol levels. Brain serotonin and 5- HIAA[5-hydroxyindole acetic acid] levels were also decreased in drug treated rats. Plasma tryptophan [TRP] was significantly increased but brain tryptophan levels were significantly decreased in drug treated rats. Weekly food intake during the entire experimental period was comparable in control and drug treated rats. Results of the present study suggest that simvastatin induced lowering of cholesterol may be responsible for the decrease in brain 5-HT neurotransmission and hence may be a cause of depression observed in subjects taking simvastatin to lower cholesterol levels