Role of Chloroquine and Cocaine Injection on Synaptophysin Protein Level in PTSD Model of Male Wistar Rat

Drug abuse could induce molecular changes in synapses, leading to mood-related disorders. In addition, some patients suffering from mood disease use drug to get comfort. In some behavioral disorders, autophagy inhibitor drugs are used.

In the current study, the effect of chloroquine (CQ, an autophagy inhibitor drug) in a rat model of Post-Traumatic Stress Disorder (PTSD), together with the role of cocaine abuse was examined. Rats were injected with the CQ and/or cocaine alone or following single-prolonged-stress exposure and were confirmed as PTSD, using elevated-plus maze (EPM) test and then protein level of synaptophysin (a synaptic vesicle glycoprotein) was investigated by western blotting tecnique. It should be noted that cocaine was administered intracerebroventricularly (i.c.v, 20µg/rat) and CQ was administered intraperitoneally (50 mg/kg, IP).

Obtained data revealed that PTSD and chronic administration of cocaine (i.c.v) in PTSD animals could increase the level of Synaphtophysin. CQ injection in them decreased Synaptophysin. So cocaine increase Synaphtophysin while CQ decrease it in PTSD animals.

The current data suggests altering neural plasticity by Synaptophysin protein level changes in brain on PTSD rats.