Cadmium Chloride Induced Cognitive Decline in Female Wistar Rats Exposed to Chronic Restraint Stress

Abstract

Cadmium (Cd) is known to have some adverse effects on different biochemical and physiological functions causing neurotoxicity leading to neurodegeneration and increasing the risk factor for neurodegenerative disorders. Restraint stress is also associated with changes in behavioral, neuroendocrine function, and brain morphology. The study aimed to evaluate the effects of cadmium chloride administration and restraint stress exposure on cognitive function of female Wistar rats. 24 female Wistar rats (180-220g) were randomly divided into 4 groups (n=6 each): Control (CTL), Restraint stress alone (RSS), Cadmium alone (CCC), Cadmium + Restraint stress (RSC). The experimental groups were subjected to cadmium chloride 100mg/kg orally and restraint stress for 30 minutes using wire mesh. Prior to the animal sacrifice, behavioral tests were carried out to assess the effects of cadmium chloride and restraint stress on cognitive performance of rats. 24 hours post last cadmium administration and restraint stress exposure, all animals were anesthetized and sacrificed. The brain was excised, weighed and homogenized for biochemical analysis (Serotonin and acetylcholinesterase activity). Results showed that there was significant (p<0.05) decrease in serotonin level in Cadmium alone group when compared to the control group. The restraint stress + cadmium group showed a significant (p<0.05) increase in acetylcholine esterase level when compared control, cadmium alone and restraint stress alone groups. The findings also revealed that Cadmium exposure led to a significant (p<0.05) decrease on number of entries in open arms of elevated plus maze. Furthermore, spontaneous alteration (Y maze) was significantly (p<0.05) decrease in restraint stress alone, cadmium alone and restraint stress + cadmium groups when compared to the control group. In conclusion, cadmium exposure and restraint stress altered neurotransmission, increased anxiety-like behavior, decreased cognitive abilities, increased alteration in hippocampal architecture and neuronal depletion as revealed in the histological evaluation resulting in cognitive deficits.