The insulin receptor is colocalized with the TRPV1 nociceptive ion channel and neuropeptides in pancreatic spinal and vagal primary sensory neurons
Objectives Recent observations demonstrated the expression of the insulin receptor (InsR)
and its functional interaction with the transient receptor potential vanilloid type 1 receptor
(TRPV1) in sensory ganglion neurons. Because sensory nerves are implicated in pancreatic
inflammatory processes, we studied the colocalization of the InsR with TRPV1 and
proinflammatory neuropeptides in spinal and vagal pancreatic afferent neurons. Methods
Immunohistochemistry and quantitative morphometry were used to analyze the expression …
and its functional interaction with the transient receptor potential vanilloid type 1 receptor
(TRPV1) in sensory ganglion neurons. Because sensory nerves are implicated in pancreatic
inflammatory processes, we studied the colocalization of the InsR with TRPV1 and
proinflammatory neuropeptides in spinal and vagal pancreatic afferent neurons. Methods
Immunohistochemistry and quantitative morphometry were used to analyze the expression …
Abstract
Objectives
Recent observations demonstrated the expression of the insulin receptor (InsR) and its functional interaction with the transient receptor potential vanilloid type 1 receptor (TRPV1) in sensory ganglion neurons. Because sensory nerves are implicated in pancreatic inflammatory processes, we studied the colocalization of the InsR with TRPV1 and proinflammatory neuropeptides in spinal and vagal pancreatic afferent neurons.
Methods
Immunohistochemistry and quantitative morphometry were used to analyze the expression of TRPV1, InsR, substance P (SP), and calcitonin gene-related peptide (CGRP) in retrogradely labeled pancreatic dorsal root ganglion (DRG) and nodose ganglion (NG) neurons.
Results
The proportions of retrogradely labeled pancreatic TRPV1-, InsR-, SP-, and CGRP-immunoreactive neurons amounted to 68%, 48%, 33%, and 54% in DRGs and 64%, 49%, 40%, and 25% in the NGs. Of the labeled DRG and NG neurons, 23% and 35% showed both TRPV1 and InsR immunoreactivity. Colocalization of the InsR with SP or CGRP was demonstrated in 14% and 28% of pancreatic DRG and 24% and 8% of pancreatic NG neurons.
Conclusions
The present findings provide morphological basis for possible functional interactions among the nociceptive ion channel TRPV1, the InsR, and the proinflammatory neuropeptides SP and CGRP expressed by pancreatic DRG and NG neurons.
Lippincott Williams & Wilkins