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
Major depressive disorder [MDD] is the leading cause of memory impairment in general population. The serotonin hypothesis provides a target model for the treatment of depression and depression-associated memory loss. 5- HT-1B receptor is suggested as a potential candidate in the pathophysiology of depressive illness. Dysfunction of 5-HT- 1B receptors has been observed previously in depressive patients. Zolmitriptan, 5-HT-1B agonist is clinically recommended for the treatment of migraine. However, in present study this drug was tested as a potential treatment for depression and associated memory loss by altering the serotonergic function at receptor level. Rats [n=24] were equally divided into unstressed and stressed groups. Depression was induced by 19 days of restraint stress for 4 h which was followed by forced swim test and pattern separation test to assess depressive symptoms and memory impairment, respectively. The initial sign of depression-associated memory loss involves impaired pattern separation which is regarded as pseudodementia. In this study stressed rats showed depression- and pseudodementia-like symptoms. After the induction of depression, rats were treated with zolmitriptan at a dose of 0.3 mg/kg which resulted in a significant attenuation of depression and depression-associated memory impairment. Results are discussed with reference to the modulation of function of 5-HT-1B receptor following the administration of exogenous agonist
ABSTRACT
Excessive exposure of cadmium which is regarded as a neurotoxin can stimulate aging process by inducing abnormality in neuronal function. It has been reported that supplementation of almond and walnut attenuate age-related memory loss. Present study was designed to investigate the weekly administration of cadmium for one month on learning and memory function with relation to cholinergic activity. Cadmium was administered at the dose of 50 mg/kg/week. Whereas, almond and walnut was supplemented at the dose of 400 mg/kg/day along with cadmium administration to separate set of rats. At the end of experiment, memory function was assessed by Morris water maze, open field test and novel object recognition test. Results of the present study showed that cadmium administration significantly reduced memory retention. Reduced acetylcholine levels and elevated acetyl cholinesterase activity were also observed in frontal cortex and hippocampus of cadmium treated rats. Malondialdehyde levels were also significantly increased following the administration of cadmium. Daily supplementation of almond and walnut for 28 days significantly attenuated cadmium-induced memory impairment in rats. Results of the present study are discussed in term of cholinergic activity in cadmium-induced memory loss and its attenuation by nuts supplementation in rats
ABSTRACT
Alzheimer's disease [AD] is an age-related neurodegenerative disorder associated with neurochemical and neurobehavioural alterations. Aluminium [Al] is considered as a contributing factor in the etiology of several neurodegenerative disorders like AD. D-galactose [D-gal] is a physiological nutrient but over supply induces some neurochemical and biochemical changes that exacerbate natural aging process. In this study, we aimed to develop AD animal model by co-administration of Al and D-gal in rats. Male albino Wistar rats were intraperitoneally injected with AlCl[3] and D-gal at a dose of 150mg/kg and 300mg/kg respectively for one week. After one week rats were subjected to behavioural analysis. After behavioural analysis rats were decapitated to remove their brain. Biochemical and neurochemical analysis were conducted in whole brain. AlCl[3]+D-gal significantly induced depressive and anxious behaviour in rats. Rats cognitive abilities were also significantly impaired following AlCl[3] and D-gal co-administration. AlCl[3]+D-gal significantly altered antioxidant enzyme activities and biogenic amine levels in whole brain. A marked increase in brain lipid peroxidation and acetylcholinesterase activity was found in test rats. These findings suggest that co-administration of AlCl[3] and D-gal for one week could induce AD like symptoms and may be used to develop AD animal model
ABSTRACT
Rotenone [organic pesticide and inhibitor of mitochondrial complex I] is used to generate an experimental model of Parkinson's disease [PD]. In the present study, we investigated rotenone-induced locomotor deficits, gait dynamics and muscular weakness in rats. The study also determined dopamine [DA] and dihydroxyphenylacetic acid [DOPAC] levels following rotenone administration. In the study, adult male rats were administered subcutaneously [s.c.] with rotenone [1.5 mg/kg/day] for 8 days. Motor activities were monitored by the Kondziela's inverted screen test, beam walking test and footprint test. Animals were decapitated after behavioral analysis and brains were dissected out for neurochemical estimation. Results showed that the levels of DA and DOPAC were significantly decreased, which further supported by significant impaired motor coordination in rotenone treated rats. In conclusion, the behavioral and neurochemical findings of our study further strengthen the previous report and emphasizes on short term administration of rotenone producing PD-like symptoms in rats
ABSTRACT
Energy drinks enhance physical endurance and cognitive ability. The ingredients present in these drinks are considered as ergogenic and have memory boosting effects. In the present study effects of taurine administration for one week was monitored on physical exercise and memory performance in rats. Animals were divided into two groups namely control and test. Taurine was injected intraperitoneally to the test group at the dose of 100mg/kg. After one week of treatment rats were subjected to physical exercise and memory task. Results of this study revealed that rats injected with taurine for one week exhibited improved muscular strength as well as enhanced memory performance in Morris water maze and elevated plus maze. Biomarker of lipid peroxidation was significantly reduced in brain and plasma of test animals. Taurine administration also resulted in higher levels of corticosterone in this study. The results highlight the significance of taurine ingestion in energy demanding and challenging situations in athletes and young subjects
ABSTRACT
Schizophrenia [SZ] is categorized as neuropsychiatric disorder with reduced lifespan and significant impairments in social and vocational functioning. One of the best proposed pharmacological animal models is dizocilpine, as it can mimic the full spectrum of schizophrenic disorder including positive and negative symptoms along with cognitive deficits. Dizocilpine is N-methyl-D-aspartate [NMDA] receptor antagonist known to induce hyperlocomotion and stereotyped behavior in rodents. Present study was designed to develop an animal model of SZ via intraperitoneal administration of dizocilpine in rats [100-150g] at a dose of 0.3 mg/kg for eight days. For the evaluation of positive symptoms, hyperlocomotor behavior was monitored. Negative symptoms were assessed by sucrose preference test [SPT] and social interaction test [SIT]. Moreover, Cognitive deficits were evaluated by novel object recognition test [NORT]. After behavioral assessments animals were decapitated for further evaluation of biochemical and neurochemical estimations. Present findings revealed that dizocilpine injected rats exhibited significant hyperlocomotor behavior, depressive symptoms and cognitive deficits. Results are further strengthened with a marked increase in lipid per oxidation [LPO] in brain and a decline in reduced glutathione [GSH] levels. Biogenic amine levels [Dopamine, DA; 5-hydroxytryptamine, 5-HT] were also significantly increased and decreased respectively. Thus, present findings suggest that dizocilpine can be used as one of the best drug to develop psychosis-like symptoms in rats and to develop an animal model following a short-term study