Extensive evidence indicates that stress and glucocorticoids modulate memory retrieval in both animals and humans, but the underlying mechanisms are not known. It appears that glucocorticoid effects on memory retrieval occur too rapidly to be mediated via the classic genomic action via intracellular receptors. Thus, it is likely that the observed rapid effects of corticosterone on memory retrieval may involve an interaction with several neurotransmitters in the brain including opiate system, dopaminergic system, and noradrenergic transmission in the hippocampus and amygdala through membrane glucocorticoids receptors that are independent from the classical glucocorticoid receptors. In this work, we have pointed on interaction between glucocorticoids and opiate system on memory retrieval processes in both spatial and contextual memories in rats. Our results show that peripheral and intra-hippocampal injections of corticosterone impair retrieval long term memory in different tasks. Peripheral and intra-hippocampal injections of opioid antagonist (Naloxone or Naltrexone) blocked glucocorticoid-induced deficit in memory retrieval. Further, we have demonstrated that the hippocampal kappa opioid receptors don't interact with glucocorticoids in influencing long-term memory retrieval.