The localization of calcitonin gene-related peptide in the human trigeminal ganglion and masseter muscle.

The localization of calcitonin gene-related peptide (CGRP) is similar to that of a neurotransmitter which indicates masticatory muscle pain in the area of the masseter fascia. CGRP is released from the trigeminal ganglion (TG). The aim of this study was to analyze the distribution of CGRP in the fascia of the masseter muscle (FMM) and TG in a morphometric manner, with respect to the location and density of CGRP-immunopositive reaction fiber (CGRP-IRF). A higher number of the CGRP-IRF were mainly found located around elongated blood vessels and small nerves on the origin side of the middle zone FMM in the O group (presented with occlusion). In the sectional histochemical analysis of the O group, the CGRP-IRF were clearly detected in oval vessels, large elongated vessels and large nerves in contrast with that of the Non-O group (presented with no occlusion) samples. The number of CGRP-immunopositive ganglion cells (CGRP-IPGCs) in the O group mandibular nerve division was higher than that of other divisions. A reduction of the CGRP-IRF numbers were found in the no-loading groups. The characterization of these locations of CGRP-IPGCs can also provide useful data for the understanding of myofascial pain syndrome of the masseter muscle (MM).

Expression of CGRP in embryonic mouse masseter muscle.

Neuropeptide calcitonin gene-related peptide (CGRP) is a mediator of inflammation and head pain that influences the functional vascular blood supply. The CGRP also regulate myoblast and acetylcholine receptors on neuromuscular junctions in development. However, little is known about its appearance and location during mouse masseter muscle (MM) development. We detected the mRNA abundance of CGRP, vascular genesis markers (Vascular endothelial growth factor A (VEGF-A), PECAM (CD31), lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1)) and embryonic and adult myosin heavy chain (MyHCs) (embryonic, IIa, IIb, and IIx) using real-time RT-PCR during development from the embryonic stage to after birth (E12.5, E14.5, E17.5, E18.5, P0, P1 and P5). We also endeavored to analyze the expression and localization of CGRP in situ hybridization in the developing mouse MM during development from the embryonic stage to after birth (E12.5, E14.5, E17.5, and P1). The antisense probe for CGRP was detected by in situ hybridization at E12.5, E14.5 E17.5 and then no longer detected after birth. The CGRP, CD31, embryonic MyHC abundance levels are highest at E17.5 (p<0.001) and they show a pattern similar to that of the other markers from E12.5 to P5. PCA analysis indicates a specific relation between CGRP and embryonic MyHC, CD31, and LYVE-1 in MM development. Cluster analyses identified the following distinct clusters for mRNA abundance in the MM: cluster 1, P5; cluster 2, E12.5, E14.5, E17.5, E18.5, P0, and P1. The positive correlation between CGRP and embryonic MyHC (Pearson's r>0.65; p<0.01) was analyzed. These data suggested that CGRP may have an influence on embryonic MyHC during mouse MM development. CGRP also affects the angiogenesis markers at embryonic stages.