Infrared-sensitive pit organ and trigeminal ganglion in the crotaline snakes

Some types of cancer are commonly associated with intense pain even at the early stages of the disease. The mandible is particularly vulnerable to metastasis from breast cancer, and this process has been studied using a bioluminescent human breast cancer cell line (MDA-MB-231LUC+). Using this cell line and anatomic and neurophysiologic methods in the trigeminal ganglion (TG), we examined the impact of cancer seeding in the mandible on behavioral evidence of hypersensitivity and on trigeminal sensory neurons. Growth of cancer cells seeded to the mandible after arterial injection of the breast cancer cell line in Foxn1 animals (allogeneic model) induced behavioral hypersensitivity to mechanical stimulation of the whisker pad and desensitization of tactile and sensitization of nociceptive mechanically sensitive afferents. These changes were not restricted to the site of metastasis but extended to sensory afferents in all three divisions of the TG, accompanied by widespread overexpression of substance P and CGRP in neurons through the ganglion. Subcutaneous injection of supernatant from the MDA-MB-231LUC+ cell culture in normal animals mimicked some of the changes in mechanically responsive afferents observed with mandibular metastasis. We conclude that released products from these cancer cells in the mandible are critical for the development of cancer-induced pain and that the overall response of the system greatly surpasses these local effects, consistent with the widespread distribution of pain in patients. The mechanisms of neuronal plasticity likely occur in the TG itself and are not restricted to afferents exposed to the metastatic cancer microenvironment.

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Nav1.7 via Promotion of ERK in the Trigeminal Ganglion Plays an Important Role in the Induction of Pulpitis Inflammatory Pain

BioMed Research International ◽

10.1155/2019/6973932 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11 ◽

Cited By ~ 2

Author(s):

Shukai Sun ◽

Jiangxing Sun ◽

Wenkai Jiang ◽

Wei Wang ◽

Longxing Ni

Keyword(s):

Trigeminal Ganglion ◽

Inflammatory Pain ◽

Pain Threshold ◽

Expression Levels ◽

Extracellular Signal Regulated Kinase ◽

Extracellular Signal ◽

Pulp Exposure ◽

Mechanical Pain Threshold ◽

Hematoxylin Eosin ◽

Inhibitor Dose

The trigeminal ganglion (TG) refers to sensory neurons bodies that innervate the spinal cord and peripheral axons that innervate teeth. The tetrodotoxin-sensitive sodium (NA) channels (Nav1.7) play important roles in the pathophysiology of pain. In this study, we investigated the TG expression of Nav1.7 and extracellular signal-regulated kinase (ERK) in a rat model of pulpitis to explore the correlation between these channels and inflammatory pain. Pulpitis was confirmed by hematoxylin-eosin staining. In this study, we demonstrated that the reflex of rats to mechanical stimulation increases after pulp exposure and that the exposed rat molar pulp can upregulate the expression of Nav1.7 and ERK in the rat TG. Three days after rat pulp exposure, the expression levels of the two ion channels in the TG increased. TG target injection of PF04856264, a Nav1.7 inhibitor, dose-dependently increased the mechanical pain threshold and was able to inhibit ERK expression. TG target injection of PD98059, an ERK inhibitor, dose-dependently increased the mechanical pain threshold. These factors simultaneously resulted in the highest production. In this study, with the established link to inflammatory pain, we found that Nav1.7 and ERK both play important roles in the induction of inflammatory pain caused by pulpitis. We also found a correlation between the expression levels of Nav1.7 and ERK and the degree of inflammatory pain. Furthermore, ERK signaling pathways were promoted by the Nav1.7 in TG after pulpitis.

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Revisiting the Labial Pit Organ Pathway in the Noctuid Moth, Helicoverpa armigera

Frontiers in Physiology ◽

10.3389/fphys.2020.00202 ◽

2020 ◽

Vol 11 ◽

Cited By ~ 1

Author(s):

Pramod KC ◽

Xi Chu ◽

Pål Kvello ◽

Xin-Cheng Zhao ◽

Gui-Rong Wang ◽

...

Keyword(s):

Helicoverpa Armigera ◽

Noctuid Moth ◽

Pit Organ ◽

Helicoverpa Armígera

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Tunicamycin-Induced Cell Death in the Trigeminal Ganglion is Suppressed by Nerve Growth Factor in the Mouse Embryo

Cellular and Molecular Neurobiology ◽

10.1007/s10571-009-9471-6 ◽

2009 ◽

Vol 30 (3) ◽

pp. 461-467

Author(s):

Hiroyuki Ichikawa ◽

Bing-Ran Zhao ◽

Mitsuhiro Kano ◽

Yoshinaka Shimizu ◽

Toshihiko Suzuki ◽

...

Keyword(s):

Cell Death ◽

Nerve Growth Factor ◽

Growth Factor ◽

Trigeminal Ganglion ◽

Mouse Embryo ◽

Nerve Growth

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Calcitonin gene-related peptide receptors in rat trigeminal ganglion do not control spinal trigeminal activity

Journal of Neurophysiology ◽

10.1152/jn.00167.2011 ◽

2012 ◽

Vol 108 (2) ◽

pp. 431-440 ◽

Cited By ~ 20

Author(s):

Oana Covasala ◽

Sören L. Stirn ◽

Stephanie Albrecht ◽

Roberto De Col ◽

Karl Messlinger

Keyword(s):

Trigeminal Ganglion ◽

Dura Mater ◽

Calcitonin Gene Related Peptide ◽

Afferent Input ◽

Nitric Oxide Donor ◽

Cgrp Receptor ◽

Related Peptide ◽

Trigeminal Neurons ◽

Calcitonin Gene ◽

Evoked Activity

Calcitonin gene-related peptide (CGRP) is regarded as a key mediator in the generation of primary headaches. CGRP receptor antagonists reduce migraine pain in clinical trials and spinal trigeminal activity in animal experiments. The site of CGRP receptor inhibition causing these effects is debated. Activation and inhibition of CGRP receptors in the trigeminal ganglion may influence the activity of trigeminal afferents and hence of spinal trigeminal neurons. In anesthetized rats extracellular activity was recorded from neurons with meningeal afferent input in the spinal trigeminal nucleus caudalis. Mechanical stimuli were applied at regular intervals to receptive fields located in the exposed cranial dura mater. α-CGRP (10−5 M), the CGRP receptor antagonist olcegepant (10−3 M), or vehicle was injected through the infraorbital canal into the trigeminal ganglion. The injection of volumes caused transient discharges, but vehicle, CGRP, or olcegepant injection was not followed by significant changes in ongoing or mechanically evoked activity. In animals pretreated intravenously with the nitric oxide donor glyceryl trinitrate (GTN, 250 μg/kg) the mechanically evoked activity decreased after injection of CGRP and increased after injection of olcegepant. In conclusion, the activity of spinal trigeminal neurons with meningeal afferent input is normally not controlled by CGRP receptor activation or inhibition in the trigeminal ganglion. CGRP receptors in the trigeminal ganglion may influence neuronal activity evoked by mechanical stimulation of meningeal afferents only after pretreatment with GTN. Since it has previously been shown that olcegepant applied to the cranial dura mater is ineffective, trigeminal activity driven by meningeal afferent input is more likely to be controlled by CGRP receptors located centrally to the trigeminal ganglion.

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