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It is known that calcitonin gene-related peptide (CGRP) plays a key role in pain modulation in the brain. There are high expressions of CGRP and CGRP receptor in anterior cingulate cortex (ACC), an important brain structure in pain modulation. The present study explored the role and mechanisms of CGRP and CGRP receptor in nociceptive modulation in ACC in naïve rats and inflammatory rats. Administration of different does of CGRP in ACC induced significant antinociception in a dose-dependent manner in both naïve rats and rats with inflammatory pain. The CGRP-induced antinociception was attenuated by injection of the CGRP receptor antagonist CGRP8-37 in ACC. Interestingly, both CGRP-induced antinociception and CGRP receptor expression decreased in ACC in rats with inflammatory pain compared with naïve rats. Knockdown of CGRP receptor in ACC by siRNA targeting to CGRP receptor attenuated both the CGRP receptor expression and the CGRP-induced antinociception significantly in rats. These findings demonstrate that CGRP and CGRP receptor participate in nociceptive modulation in ACC in rats, inhibiting CGRP receptor expression induces decrease in CGRP-induced antinociception in ACC.

Heat stroke often leads to multiple organ dysfunction syndrome (MODS) with a neurological morbidity of 30%. Current studies suggested that pathophysiological responses to heat stroke may be due to a systemic inflammatory response syndrome and a series of peptidergic nerve reactions. The mechanisms underlying the high neurological morbidity in heat stroke have remained largely elusive. In recent years, calcitonin gene-related peptide (CGRP) has been considered to have a positive role in central nervous system injury. The present study investigated the influence of CGRP on brain injury induced by heat stroke. A rat model of heat stroke was established in a pre-warmed artificial climate chamber with a temperature of 35.5±0.5°C and a relative humidity of 60±5%. The rectal core temperature (Tc) was monitored. Heat stress was halted at a Tc of no more than 41°C A bolus injection of CGRP was administered to each rat in the HS+CGRP group and a bolus injection of CGRP8-37 was administered to each rat in the HS+CGRP8-37 group after heat stress. After 2 h, electroencephalograms were recorded and the pathological morphology of brain tissue as well as brain cell apoptosis and caspase-3 protein levels in the brain were measured. The EEG of rats in the HS+CGRP group was characterized by a short- to long-term α-wave and low-voltage β-waves as well as a large amount of intermittent δ- and θ-waves. Compared with the HS group, the θ-wave decreased and the α-wave increased significantly (P

The physiological significance of calcitonin gene-related peptide (CGRP) during biomineralization was investigated by assessing the effect of human CGRP on the carbonic anhydrase activity in gill membranes of the pearl oyster, Pinctada margaritifera. Salmon CT and human CGRP were able to induce a 150% increase of the basal activity. No additive effect was observed suggesting that both activities are mediated by the same receptor. The CGRP-stimulated effect was specific as demonstrated by the inhibition produced by the CGRP antagonist, hCGRP8-37. So, CGRP by its specific action on gill carbonic anhydrase controls the calcification process, an ancient role both in invertebrates and non-mammalian vertebrates.