Comparing of the Effects of Hypericin and Synthetic Antidepressants on the Expression of Morphine-Induced Conditioned Place Preference

Authors

  • Abolghasem Jouyban Department of Pharmaceutical and Food Control, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.
  • Assad Assadi Science and Research Branch, Islamic Azad University (IAU), Tehran, Iran.
  • Mohammad Reza Zarrindast Department of Pharmacology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
  • Morteza Samini Department of Pharmacology, Faculty of Specialized Veterinary Science, Science and Research Branch, Islamic Azad University (IAU), Tehran, Iran.
Abstract:

The effect of hypericin on the expression of morphine-induced conditioned place preference (CPP) was investigated and compared with the effect of the synthetic antidepressants. The CPP paradigms took place over six days using an unbiased procedure. The results demonstrate that intra-peritoneal (IP) injection of morphine sulfate (2.5, 5 and 10 mg/Kg) significantly induce the CPP in rat. Intra-peritoneal and intracerebroventricular (ICV) injection of hypericin and/or synthetic antidepressants augmented morphine-induced CPP. It has been suggested that the adrenergic, serotonergic and dopaminergic neurotransmissions play an important role in mediating the antidepressant effect of hypericin and this effect may be due to its inhibitory effect on the reuptake of neurotransmitters. Morphine produces a reinforcement (reward) effect by activating. The μ-receptors that facilitate dopaminergic transmission. Serotonin is also a potent stimulator of dopamine release in such a way that an increase in brain serotonin could possibly stimulate the dopaminergic system. In conclusion, it may suggest that the augmentation of morphine-induced CPP by hypericin and synthetic antidepressants may be related to the increasing dopamine and serotonin concentrations in synaptic clefts.

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Journal title

volume Volume 10  issue Number 3

pages  619- 626

publication date 2011-09-17

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