The effects of crocin on fear condition memory impairment caused by morphine in relation to gene expression of amygdala HSP70, HSP90 and NF-kB

Background: Some studies have shown that morphine causes memory impairment through different mechanisms. The roles of inflammation/NF-xB and BDNF/TrkB/CREB pathways are significant in the memory deficits caused by morphine. Aim: In this study, the effect of crocin on the impairment of fear memory caused by morphine was investigated, and the expression of HSP70, HSP90, and NF-kB genes that play an important role in memory in male Wistar rats was measured. Material and method: The fear conditioning test was used to check the fear memory of rats, and total Freezing time was considered as an index of memory. Rats (96 Wistar rats) were randomly divided into 12 groups. The rats were injected with saline (1 ml/kg) or different doses of morphine (0.5, 2.5, and 5 mg/kg) 5 min after injection of saline (1 ml/kg) or subthreshold doses of crocin (60 mg/kg). Real-time PCR method was used for HSP70, HSP90, and NF-kB gene expression in the Amygdala. Result: Administration of morphine 5 mg/kg decreased the total freezing and increased the latency freezing (P < 0.001). Also, the results showed that crocin 60 mg/kg reduced memory impairment induced by morphine. Realtime PCR analysis showed that morphine 5 mg/kg significantly increased the expression of the HSP70, HSP90, and NF-kB genes. However, the subthreshold dose of crocin (60 mg/kg) reduced the increase in gene expression. Conclusion: The study showed that morphine impacts memory and boosts gene expression of HSP70, HSP90, and NF-kB, while crocin could potentially reverse this effect by regulating these amygdala genes, suggesting avenues for future research.