Major Depression Essay

Major depression is severe debilitating psychiatric disorder associated with impairment in cognitive functions. We previously showed that depression-induced cognitive deficits are manifested due alterations in the dendritic arborization, volumes, levels of neurotransmitters and abnormal synaptic plasticity which were restored by chronic treatment with escitalopram or reboxetine. Unfortunately, most of the medications that target monoaminergic system are ineffective; produces recurrence and lack of response. Current research engendered a great deal of interest in glutamatergic targets for the treatment of depression. We hypothesized that restoring normal glutamatergic homeostasis would restore depression-induced cognitive deficits. Here, we
They were subjected to NAC treatment from PND 76-89 followed by behavioural and morphological studies. We found that depression resulted in increased immobility time in the forced swim test (FST) and anhedonia in the sucrose preference test (SPT). Further, they also exhibited enhanced anxiety-like behaviour in elevated plus maze (EPM) and open field. Depressed rats showed impaired spatial learning in the rewarded alternation task. They also showed differential morphological changes in hippocampus and amygdala. We observed decline in CA1, hilar region and dentate gyrus (DG) volumes with basolateral amygdalar hypertrophy (BLA). Interestingly, chronic treatment with NAC restored the depression-induced behavioural and cognitive deficits. We also found that chronic NAC treatment reverses the depression-induced declined volumes of CA1, hilar region and DG. Further, NAC also reversed the depression-induced hypertrophy of BLA. These results indicate that depression can produce potentially maladaptive morphological and behavioural responses that can be restored by chronic treatment with acetylating agent such as NAC. The present study has implications for depressive and anxiety disorders which were often coexisted with cognitive