Restraint-induced behavioral deficits are attenuated or impaired by pre- or post-injection of apomorphine: A context-based study

Apomorphine, a psycho stimulant, has neuroprotective effects due to its ability to decrease oxidative stress. Stress-induced dopaminergic dysfunction might lead to posttraumatic stress disorder, depression and related disorders. This dopaminergic dysfunction is more pre-dominant in basal ganglia and prefrontal cortex. Targeting of this dysfunction by psychostimulants, involves elevating dopamine in these brain regions and reduction of stress. On the other hand, stress itself can aggravate addictive effects to psycho stimulants. Present study was therefore designed to monitor the role of apomorphine in the attenuation of stress-induced behavioral deficits. Rats were exposed to 2hr restraint stress either before or after the apomorphine administration, to monitor effects of apomorphine administration on stress-induced behavioral deficits. Stress-induced decreases in food intake, growth rate and elevated plus maze activity were exacerbated if apomorphine was experienced during restraint stress. Conversely, these behavioral deficits were attenuated if apomorphine was experienced after restraint stress. It shows that apomorphine, if experienced during restraint stress, produces greater behavioral deficits, while the same were attenuated in rats receiving apomorphine after the termination of restraint stress. Results suggest that apomorphine and possibly the other CNS stimulants may help to cope stress by attenuating stress-induced behavioral deficits, if experienced after stress.