The Depletion Of The Rat Model Of Monoamine

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In the present study, the rat model of depression induced by reserpine was used to evaluate whether caffeine could treat depression or exaggerate it. The present data revealed that the daily reserpine treatment for 30 days induced a significant decrease in the cortical and hippocampal serotonin, norepinephrine and dopamine levels. In addition, a decrease in the motor activity was observed. This was indicated from the data of the open field test that exhibited a significant decrease in the number of line crossings, number of rearings and number of groomings and a significant increase in the time spent in the central square and freezing time. Immobility is a state/posture that reflects the condition of hopelessness and despair (Holmes, …show more content…

As a consequence to the oxidative catabolism of cytosolic dopamine, norepinephrine and serotonin by monoamine oxidase, the cellular oxidant, hydrogen peroxide is produced (Youdim et al., 2006). In addition, monoamines, particularly DA and NA can undergo spontaneous oxidation in the cytoplasm, and this may lead to the damage of cellular structures ( Wasik et al., 2009). The byproducts of these reactions include a number of potentially neurotoxic species, such as hydrogen peroxide and ammonia ( Barros-Mi˜nones et al., 2015). In particular, hydrogen peroxide can trigger the production of reactive oxygen species and induce mitochondrial damage and neuronal apoptosis (Bortolato et al., 2008). The present findings revealed that reserpine induced oxidative stress in the cortex and hippocampus. This was indicated from the significant increase in lipid peroxidation (MDA) and nitric oxide (NO) levels together with the significant decrease in reduced glutathione (GSH). Under such conditions of inhibition of VMAT-2 induced by reserpine and the effect of monamine oxidase, the oxidative catabolism may explain the present oxidative stress induced in the cortex and hippocampus of rat model of depression. Malondialdehyde is produced from decomposition of products of lipid peroxidation (Gaweł et al., 2004). Thus, the observed increased MDA levels may arise from the attack of the neuronal membrane phospholipids by free radicals produced from monoamine catabolism. In addition, the

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