Abstract
BACKGROUND: Escitalopram, a pharmacological compound, and crocin, the active compound of saffron, influence brain functions and serotonin levels. This study examined the efficacy of escitalopram with and without crocin in restoring the input-output (I/O) functions and long-term potentiation (LTP) within the hippocampal cornu ammonis 1 (CA1) region of stressed rats. MATERIALS AND METHODS: Rats were divided into six groups: control (Co), sham (Sh), stress-recovery (St-Rec), stress-escitalopram (St-Esc), stress-crocin (St-Cr), and stress-escitalopram-crocin (St-Esc-Cr) groups. They underwent 14 days of restraint stress (6 h/day). After being subjected to stress, they received 14 days of escitalopram (20 mg/kg) and crocin (30 mg/kg), as well as co-administration of these two compounds during the next 14 days. The field excitatory postsynaptic potential (fEPSP) slope and amplitude were measured using I/O functions and LTP induction in the CA1 region. Corticosterone (CORT) levels were also evaluated. RESULTS: The fEPSPs slope and amplitude in the I/O functions and LTP induction significantly decreased in stressed rats without therapeutic intervention. These variables in the I/O functions declined in rats with escitalopram administration alone. All electrophysiological parameters showed an increase in rats treated with crocin alone compared to stressed subjects without any treatment. Serum CORT levels decreased only with crocin treatment for stressed rats. CONCLUSION: Neural excitability and memory within the CA1 region were severely disrupted among stressed rats without any treatment. Furthermore, administering crocin alone improved neural excitability and memory post-chronic stress. Treatment with escitalopram alone also impaired neural excitability within the CA1 region. The use of escitalopram with and without crocin did not enhance memory under chronic stress.