Background: Considering the increased activity of hypothalamic orexinergic neurons due to morphine administration, and its extensive projections to the hippocampus, it is probable that morphine effect on CA1 neuronal function is mediated by orexinergic system. So the effect of hippocampal orexin-1 receptors (OX1R) blockade on CA1 baseline synaptic response and short term synaptic plasticity was investigated.

Materials and Methods: In this experimental study, animals received morphine 10 mg/kg/12h/(SC) for 10 days. SB-334867-A, OX1R antagonist (0.5&mug/0.5 &mul), was microinjected intrahippcampally for OX1R inhibition before each morphine injection. Baseline synaptic response and short term synaptic plasticity were evaluated by field potential recording. fEPSP was recorded from CA1 following Schaffer collaterals stimulation. After Input/Output construction, short term synaptic plasticity was induced by paired pulse stimulations.

Results: Chronic use of morphine did not affect the baseline synaptic response (p>0.05). SB- 334867-A microinjection in CA1 did not have any effect on baseline synaptic response in morphine dependent rats. Morphine increased paired pulse index (PPI) at 80 ms inter pulse interval (IPI, p<0.05). SB-334867-A pretreatment did not affect this morphine induced PPI change.

Conclusion: The results suggest that orexin-1 receptors (OX1R) do not mediate the effect of morphine on baseline synaptic response and short term synaptic plasticity in CA1 area of the hippocampus.

Background: Considering the increased activity of hippocampal glial cells due to chronic morphine administration and the involvement of hippocampus in restoration of the addictive drug-associated experience, the role of these cells on morphine induced conditioned place preference (CPP) was investigated.

Materials and Methods: In this experimental study, four groups of animals were evaluated. After habituation to CPP apparatus on the first day, conditioning was done by injection of morphine (5 mg/kg) or its vehicle (saline) during three consecutive days. On the fifth day, the time spent in each compartment of CPP cage and locomotor activity was recorded for 20 min. To investigate the role of hippocampal glial cells in CPP, these cels were inbibited by bilaterally injecting fluorocitrate (1nmol/1ml), before each morphine injection. CPP testing in this group and animals received fluorocitrate vehicle (Phosphate buffer saline) was done before morphine injection.

Results: Fluorocitrate pretreatment reduced morphine induced conditioned place preference acquisition, so that a significant decrease was observed in conditioning score (unpaired t-test, p<0.01) in this group (n=8) compared to animals received morphine (n=9). Neither morphine nor fluorocitrate pretreatment did not affect locomotor activity (ANOVA, p>0.05).

Conclusion: The results suggest that glial cells in the hippocampus are involved in morphine induced conditioned place preference.