Effect of Escitalopram on GABA level and anti-oxidant markers in prefrontal cortex and nucleus accumbens of chronic mild stress-exposed albino rats

Abstract

Oxidative stress is a critical route of damage in various psychological stress-induced disorders, such as depression. Antidepressants are widely prescribed to treat these conditions; however, few animal studies have investigated the effect of these drugs on endogenous antioxidant status in the brain. The present study employed a 3 weeks chronic regimen of random exposure to chronic mild stress (CMS) to induce oxidative stress in brain, and behavioural aberrations (anhedonia), in rats. The sucrose preference test was used to identify depression-like phenotypes, and reversal in these indices indicated the effectiveness of treatment with escitalopram 2.5mg/kg daily orally following CMS. The level of superoxide dismutase enzyme(SOD) as an antioxidant markers in erythrocyte lysates was reduced in CMS control group while it was elevated in CMS group treated with escitalopram. Also escitalopram significantly reduce the thiobarbituric acid reactive substance(TBARS) levels in selected brain areas homogenates to a level comparable to control group. Catalase activity and GABA levels in these brain areas were also increase in escitlopram treated group. In conclusion, escitalopram is suggested to have antioxidant effect associated with an increase in GABA level in frontal cortices and nucleus accumbens homogenates from rats exposed to CMS.

Figure 1

reversal of anhedonia after daily oral administration of escitalopram for 3 weeks in mice.

Figure 2

(A}. Effect of escitalopram administration (3 weeks) of on the GABA level in the prefrontal cortex of rats exposed to CMS protocol. B. Effect of escitalopram administration (3 weeks) on the GABA level in the nucleus accumbens [NAc] of rats exposed to CMS protocol.