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[MrgC receptor activation reverses chronic morphine-evoked alterations of glutamate transporters and nNOS in rats.] [Article in Chinese]

HUANG Hao, LI Qi, HONG Yan-Guo, WANG Dong-Mei^*

Provincial Key Laboratory of Developmental and Neurological Biology, College of Life Sciences, Fujian Normal University, Fuzhou 350108, China

Abstract

This study was aimed to investigate the mechanisms underlying the modulation effect of Mas-related gene (Mrg) C receptors (MrgC) on morphine tolerance. Saline, morphine (20 μg), morphine plus bovine adrenal medulla 8-22 (BAM8-22, 1 nmol) or (Tyr⁶)-2-MSH-6-12 (MSH, 5 nmol) were administered intrathecally in rats for 6 days. Pain-related molecules in the spinal cord and dorsal root ganglion (DRG) were examined using Western blot, immunocytochemistry and RT-PCR techniques. The results showed that intrathecal administration of the selective MrgC receptor agonists (BAM8-22 or MSH) remarkably attenuated or abolished chronic morphine-evoked reduction in glutamate transporters (GLAST, GLT-1 and EAAC1) in the spinal cord and increase in neuronal nitric oxide synthase (nNOS) in the spinal cord as well as DRG. In addition, MrgC receptor-like immunoreactivity (IR) was detected in superficial laminae of the spinal cord. Chronic morphine induced significant increases in MrgC receptor-IR in the spinal cord and MrgC receptor mRNA levels in DRG. These results suggest that the modulation of pro-nociceptive mediators in the spinal cord and DRG underlies the inhibition of morphine tolerance by MrgC receptor activation.

Key words: Mas-related gene (Mrg) C receptors; morphine tolerance; glutamate transporter; neuronal nitric oxide synthase

Received: 2013-12-04　　Accepted: 2014-02-01

Corresponding author: 王冬梅　　E-mail: dmwang@fjnu.edu.cn

Citing This Article：

HUANG Hao, LI Qi, HONG Yan-Guo, WANG Dong-Mei. [MrgC receptor activation reverses chronic morphine-evoked alterations of glutamate transporters and nNOS in rats.] [Article in Chinese]. Acta Physiol Sin 2014; 66 (4): 449-456 (in Chinese with English abstract).