Regulation of Neuropeptide Y, Vasoactive Intestinal Polypeptide, and Their Receptors in Trigeminal Ganglion Neurons and Glia in Response to Adjuvant-Induced Inflammation
type: CreativeWork
description: Activation of trigeminal nerves is involved in temporomandibular joint (TMJ) inflammation and pain transmission. Neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), and their receptors have been implicated in the underlying pathology of temporomandibular joint disorders. The goal of this study was to investigate activation of NPY, VIP, and their receptors in a model of TMJ inflammation using immunohistochemistry. TMJ inflammation was created by bilateral injections of complete Freund's adjuvant (CFA) into the joint of rats, mimicking mechanical allodynia seen in TMJ disorder. Trigeminal ganglia were dissected after 1, 3, and 5 days after CFA-treatment. NPY expression was observed in Day 1 and Day 5 tissues, with localization to glial cells, and to both neurons and glial cells, respectively. NPY receptor, NPY Y₂ was upregulated in Day 1 tissues, localized to neurons and glia. VIP expression was observed in Day 1 and Day 5 tissues, with localization to glial cells, and to both neurons and glial cell, respectively. VIP receptor, VIP R1 was upregulated in Day 3 tissues. Results from my study provide evidence to support a role of NPY, VIP, and their receptors in mediating neuronal and glial cell activation in trigeminal ganglion that is likely to contribute to TMJ pathology and contribute to peripheral sensitization within the ganglion.
abstract: Activation of trigeminal nerves is involved in temporomandibular joint (TMJ) inflammation and pain transmission. Neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), and their receptors have been implicated in the underlying pathology of temporomandibular joint disorders. The goal of this study was to investigate activation of NPY, VIP, and their receptors in a model of TMJ inflammation using immunohistochemistry. TMJ inflammation was created by bilateral injections of complete Freund's adjuvant (CFA) into the joint of rats, mimicking mechanical allodynia seen in TMJ disorder. Trigeminal ganglia were dissected after 1, 3, and 5 days after CFA-treatment. NPY expression was observed in Day 1 and Day 5 tissues, with localization to glial cells, and to both neurons and glial cells, respectively. NPY receptor, NPY Y₂ was upregulated in Day 1 tissues, localized to neurons and glia. VIP expression was observed in Day 1 and Day 5 tissues, with localization to glial cells, and to both neurons and glial cell, respectively. VIP receptor, VIP R1 was upregulated in Day 3 tissues. Results from my study provide evidence to support a role of NPY, VIP, and their receptors in mediating neuronal and glial cell activation in trigeminal ganglion that is likely to contribute to TMJ pathology and contribute to peripheral sensitization within the ganglion.
author: DeLoach, Debra D.
keywords: trigeminal nerve, NPY, VIP, temporomandibular joint, inflammation, Biology
date published: 2008-01-01T08:00:00Z
date modified: 2026-07-24T03:16:17Z
provider: Missouri State University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Missouri State University