On the possible role of ERK, p38 and CaMKII in the regulation of CGRP expression in morphine-tolerant rats.

ABSTRACT:

Background

The neuropeptide, calcitonin gene-related peptide (CGRP) has been proposed to be a regulator of the development of morphine analgesic tolerance and thereby could be a target to reduce the induction of this phenomenon under clinical conditions. However, the mechanisms of CGRP regulation are unclear. We investigated here the possible role of the extracellular signal-regulated protein kinase (ERK), p38 and calcium/calmodulin-dependent protein kinase II (CaMKII) in CGRP regulation following chronic morphine treatment.

Results

A 7-day treatment with morphine (15 μg/day) led to an increase in CGRP contents in the spinal cord dorsal horn (SCDH) and dorsal root ganglion (DRG) and this effect was prevented by the inhibition of the ERK, p38 or CaMKII pathway. The phosphoryl

SUBMITTER: Wang Z 

PROVIDER: S-EPMC3190348 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature