The protective effects of escitalopram on synaptic plasticity in the CA1 region of chronically stressed and non-stressed male rats.

INTRODUCTION

Stress impairs cognitive processes and escitalopram affects them in various ways. The present study has compared the protective effects of two escitalopram doses on neural excitability and synaptic plasticity in the CA1 region of chronically stressed and non-stressed male rats.

METHODS

Forty-nine rats were randomly allocated into seven groups: Control (Co), stress (St), sham (Sh), escitalopram 10 and 20 mg/kg (Esc10 and Esc20), and stress-escitalopram 10 and 20 mg/kg (St-Esc10 and St-Esc20). Induction of restraint stress (6 h/day) and escitalopram injections were performed for 14 days. The fEPSP slope and amplitude were measured according to input-output functions and after the LTP induction in the hippocampal CA1 region. Also, serum corticosterone levels were evaluated in all experimental groups.

RESULTS

The fEPSP slope and amplitude decreased significantly in the St group and increased significantly in the Esc10 group compared with the Co group. In non-stressed states, significant increases in slope and amplitude occurred in the Esc10 group compared with the Esc20 group. Notably, these values were also significantly enhanced by both escitalopram doses under stressed conditions. Moreover, serum corticosterone levels significantly elevated in the St group although its levels decreased in both St-Esc groups compared with the St.

CONCLUSION

Stress significantly attenuated neural excitability and long-term plasticity in the CA1 area. Only escitalopram 10 mg/kg improved synaptic excitability, as well as LTP induction and maintenance in non-stressed subjects even more than normal levels. However, under stress conditions, both escitalopram doses enhanced neural excitability and memory probably due to reduced serum corticosterone levels.