Document Type : Original Article

Authors

1 Ph.D student, Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran

2 Associate Professor, Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran

3 Professor, Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran

Abstract

Introduction: The neuropeptide orexin is synthetized in the lateral hypothalamus (LH) and is involved in naloxone-precipitated morphine withdrawal syndrome via orexin type 1 receptors (OX1R). Locus coeruleus (LC) is a sensitive site for the expression of somatic aspects of morphine withdrawal. The orexinergic and GABA-A-ergic systems are involved in morphine withdrawal syndrome. In this study, the effect of OX1R at the LC neurones on GABA-A-ergic inhibitory system activity in morphine withdrawal syndrome was investigated.
Materials and Methods: Male Wistar rats (14-21 days) were made dependent on morphine (20 mg/kg, i.p., for 7 days). Then the effect of orexin-A on spontaneous and evoked inhibitory post synaptic currents in LC neurons using whole-cell patch clamp recordings was assessed.
Results: The findings of this study indicated that orexin-A through OX1R in the presence of naloxone may induce an inhibitory effect on GABAergic system in the LC neurons. It seems that the orexin-A administration decreased the eIPSCs amplitude in LC neurons. OrexinA decreased spontaneous sIPSCs frequency of LC neurons, but did not change the sIPSCs amplitude in the presence of naloxone.
Conclusion: These findings implicated evidence that orexin-A via OX1R may participate in expression of naloxone-precipitated morphine withdrawal syndrome through decreasing of GABAA receptor activity. 

Keywords

Main Subjects

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