Neuropeptides and ATP signaling in the trigeminal ganglion

Goto, Tetsuya; Iwai, Haruki; Kuramoto, Eiichi; Yamanaka, Akira

doi:10.1016/j.jdsr.2017.01.003

Cited by 55 publications

(57 citation statements)

References 84 publications

(86 reference statements)

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“…The activity of spinal trigeminal neurons with afferent input from inflamed temporomandibular joint and facial skin was decreased by injection of an NK1 receptor antagonist into the trigeminal ganglion (Takeda et al 2012). However, it is not likely that NK1 receptors in the trigeminal ganglion are crucially involved in the generation of migraine pain, since NK1 receptor antagonists are ineffective in migraine therapy or prevention of migraine (Goldstein et al 1997(Goldstein et al , 2001. PACAP binds to the three receptor subtypes of the VIP/PACAP receptor family, VPAC1, VPAC2 and PAC1, immunoreactivity of which was found in small diameter neurons in rat and human trigeminal ganglion (Chaudhary and Baumann 2002;Knutsson and Edvinsson 2002).…”

Section: Neuropeptide Receptors In the Trigeminal Ganglionmentioning

confidence: 99%

“…Many of the gene products like CGRP, CGRP receptor proteins and BDNF can crucially influence neuronal transduction and synaptic transmission, because they are delivered by axonal transport through the neuronal processes to the peripheral and/or central terminals of trigeminal afferents Other signaling mechanisms between primary afferent neurons, SGCs and immune cells do not directly involve neuropeptides and NO. Intraganglionic signaling by ATP has been reviewed elsewhere (Goto et al 2017). Neurons may signal via ATP to other neurons and to SGCs, and these may signal to microglia/macrophage-like cells (MLCs).…”

Section: Intercellular Cross-talk Within the Trigeminal Ganglionmentioning

confidence: 99%

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Cross-talk signaling in the trigeminal ganglion: role of neuropeptides and other mediators

2020

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The trigeminal ganglion with its three trigeminal nerve tracts consists mainly of clusters of sensory neurons with their peripheral and central processes. Most neurons are surrounded by satellite glial cells and the axons are wrapped by myelinating and non-myelinating Schwann cells. Trigeminal neurons express various neuropeptides, most notably, calcitonin generelated peptide (CGRP), substance P, and pituitary adenylate cyclase-activating polypeptide (PACAP). Two types of CGRP receptors are expressed in neurons and satellite glia. A variety of other signal molecules like ATP, nitric oxide, cytokines, and neurotrophic factors are released from trigeminal ganglion neurons and signal to neighboring neurons or satellite glial cells, which can signal back to neurons with same or other mediators. This potential cross-talk of signals involves intracellular mechanisms, including gene expression, that can modulate mediators of sensory information, such as neuropeptides, receptors, and neurotrophic factors. From the ganglia cell bodies, which are outside the blood-brain barrier, the mediators are further distributed to peripheral sites and/or to the spinal trigeminal nucleus in the brainstem, where they can affect neural transmission. A major question is how the sensory neurons in the trigeminal ganglion differ from those in the dorsal root ganglion. Despite their functional overlap, there are distinct differences in their ontogeny, gene expression, signaling pathways, and responses to anti-migraine drugs. Consequently, drugs that modulate cross-talk in the trigeminal ganglion can modulate both peripheral and central sensitization, which may potentially be distinct from sensitization mediated in the dorsal root ganglion.

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Section: Neuropeptide Receptors In the Trigeminal Ganglionmentioning

confidence: 99%

Section: Intercellular Cross-talk Within the Trigeminal Ganglionmentioning

confidence: 99%

Cross-talk signaling in the trigeminal ganglion: role of neuropeptides and other mediators

2020

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“…The neurotransmitters glutamate and ATP have also been implicated in the communication within the trigeminal ganglion. Experimental studies have demonstrated the expression of excitatory glutamate receptors and ATP receptors in sensory neurons [140,141].…”

Section: Intraganglionic Mechanisms Involved In Nociceptor Sensitizationmentioning

confidence: 99%

TRP Channels in the Focus of Trigeminal Nociceptor Sensitization Contributing to Primary Headaches

Dux

Rosta

Meßlinger

2020

IJMS

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Pain in trigeminal areas is driven by nociceptive trigeminal afferents. Transduction molecules, among them the nonspecific cation channels transient receptor potential vanilloid 1 (TRPV1) and ankyrin 1 (TRPA1), which are activated by endogenous and exogenous ligands, are expressed by a significant population of trigeminal nociceptors innervating meningeal tissues. Many of these nociceptors also contain vasoactive neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P. Release of neuropeptides and other functional properties are frequently examined using the cell bodies of trigeminal neurons as models of their sensory endings. Pathophysiological conditions cause phosphorylation, increased expression and trafficking of transient receptor potential (TRP) channels, neuropeptides and other mediators, which accelerate activation of nociceptive pathways. Since nociceptor activation may be a significant pathophysiological mechanism involved in both peripheral and central sensitization of the trigeminal nociceptive pathway, its contribution to the pathophysiology of primary headaches is more than likely. Metabolic disorders and medication-induced painful states are frequently associated with TRP receptor activation and may increase the risk for primary headaches.

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“…For a long time after the IANX, various molecules are generated in uninjured, as well as injured, trigeminal ganglion (TG) neurons, which are sensitized [5]. Neuropeptides, ATP, and chemokines are produced in TG neurons, and these molecules are released from TG neurons with injured axons [6]. Takeda et al reported that after temporomandibular joint inflammation, substance P (SP) production is enhanced in small-diameter TG neurons, which release SP via a paracrine mechanism [7].…”

Section: Introductionmentioning

confidence: 99%

“…Many of the GFAP-IR cells in the TG also express the P2Y 12 receptor, suggesting that ATP is released from TG neurons and binds to the P2Y 12 receptor to activate satellite glial cells. SP, calcitonin gene-related peptide (CGRP), and tumor necrosis factor α are also released from TG neurons and involved in the activation of satellite glial cells [6]. Furthermore, connexin 43 expression is significantly enhanced in satellite glial cells suggesting that propagation of satellite glial cell activation occurs via connexin 43 [12].…”

Section: Introductionmentioning

confidence: 99%

Involvement of Satellite Cell Activation via Nitric Oxide Signaling in Ectopic Orofacial Hypersensitivity

Lee

Ohara

Shinoda

et al. 2020

IJMS

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The mechanical head-withdrawal threshold (MHWT) was significantly reduced following inferior alveolar nerve transection (IANX) in rats. Nitrate and nitrite synthesis was dramatically increased in the trigeminal ganglion (TG) at 6 h after the IANX. The relative number of neuronal nitric oxide synthase (nNOS)-immunoreactive (IR) cells was significantly higher in IANX rats compared to sham-operated and N-propyl-L-arginine (NPLA)-treated IANX rats. On day 3 after NPLA administration, the MHWT recovered considerably in IANX rats. Following L-arginine injection into the TG, the MHWT was significantly reduced within 15 min, and the mean number of TG cells encircled by glial fibrillary acidic protein (GFAP)-IR cells was substantially higher. The relative number of nNOS-IR cells encircled by GFAP-IR cells was significantly increased in IANX rats. In contrast, after NPLA injection into the TG, the relative number of GFAP-IR cells was considerably reduced in IANX rats. Fluorocitrate administration into the TG significantly reduced the number of GFAP-IR cells and prevented the MHWT reduction in IANX rats. The present findings suggest that following IANX, satellite glial cells are activated via nitric oxide (NO) signaling from TG neurons. The spreading satellite glial cell activation within the TG results in mechanical hypersensitivity of face regions not directly associated with the trigeminal nerve injury.

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Neuropeptides and ATP signaling in the trigeminal ganglion

Cited by 55 publications

References 84 publications

Cross-talk signaling in the trigeminal ganglion: role of neuropeptides and other mediators

Cross-talk signaling in the trigeminal ganglion: role of neuropeptides and other mediators

TRP Channels in the Focus of Trigeminal Nociceptor Sensitization Contributing to Primary Headaches

Involvement of Satellite Cell Activation via Nitric Oxide Signaling in Ectopic Orofacial Hypersensitivity

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