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