scholarly journals Neurokinins and their receptors in the rat trigeminal system: Differential localization and release with implications for migraine pain

2021 ◽  
Vol 17 ◽  
pp. 174480692110594
Author(s):  
Jacob CA Edvinsson ◽  
Philip V Reducha ◽  
Majid Sheykhzade ◽  
Karin Warfvinge ◽  
Kristian A Haanes ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
Enzyme Linked Immunosorbent Assay ◽  
Trigeminal System ◽  
Neurokinin A ◽  
Trigeminovascular System ◽  
Drug Candidates ◽  
Cell Counts ◽  
Neurokinin Receptor ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons

Substance P (SP) and calcitonin gene-related peptide (CGRP) have both been considered potential drug candidates in migraine therapy. In recent years, CGRP receptor inhibition has been established as an effective treatment, in particular as a prophylactic for chronic migraine. Curiously, inhibition of neurokinin receptor 1 (NK1R) failed to alleviate acute migraine attacks in clinical trials, and the neurokinins were consequently abandoned as potential antimigraine candidates. The reason behind this has remained enigmatic. Utilizing immunohistochemistry and semi-quantitative cell counts the expression of neurokinins and their associated receptors was examined in the rat trigeminal ganglion. Immunohistochemistry results revealed SP co-localization in CGRP positive neurons and C-fibres, where it mainly concentrated at boutons. Neurokinin A (NKA) was observed in a population of C-fibres and small neurons where it could co-localize with SP. In contrast, neurokinin B (NKB) did not co-localize with SP and was observed in large/medium sized neurons and Aδ-fibres. All neurokinin receptors (NK1-3R) were found to be expressed in a majority of trigeminal ganglion neurons and A-fibres. The functional release of SP and CGRP in the trigeminovascular system was stimulated with either 60 mM K+ or 100 nM capsaicin and measured with an enzyme-linked immunosorbent assay (ELISA). ELISA results established that SP can be released locally from trigeminovascular system. The released SP was comparatively minor compared to the CGRP release from stimulated dura mater, trigeminal ganglion neurons and fibres. We hypothesize that SP and CGRP signalling pathways may work in tandem to exacerbate painful stimuli in the TGV system.

Effects of WIN 55, 212-2 onI K current in cultured trigeminal ganglion neurons of rat

2005 ◽  
Vol 25 (2) ◽  
pp. 124-126
Author(s):  
Ming Zhangyin ◽  
Tan Yan ◽  
Fu Hui ◽  
Cao Xuehong ◽  
Pan Jianping ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
K Current ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons ◽  
Win 55

Capsaicin and nicotine both activate a subset of rat trigeminal ganglion neurons

1996 ◽  
Vol 270 (6) ◽  
pp. C1807-C1814 ◽  
Author(s):  
L. Liu ◽  
S. A. Simon
Keyword(s):  
Trigeminal Ganglion ◽  
Acetylcholine Receptors ◽  
Ganglion Cells ◽  
Whole Cell Patch Clamp ◽  
Current Voltage ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons ◽  
Relationship Of ◽  
Current Voltage Relationship ◽  
Voltage Relationship

Nicotine and capsaicin produce many similar physiological responses that include pain, irritation, and vasodilation. To determine whether neuronal nicotine acetylcholine receptors (nAChR) are present on capsaicin-sensitive neurons, whole cell patch-clamp recordings were performed on rat trigeminal ganglion cells. It was found that approximately 20% of the total number of neurons tested was activated by both 100 microM nicotine and 1 nM capsaicin. Other subsets of neurons were activated by only one of these compounds, whereas a fourth subset was not activated by either compound. At -60 mV, the magnitude of the capsaicin-activated currents was about three times larger than the magnitude of the nicotine-activated currents. The current-voltage relationship of the nAChR exhibited marked rectification, such that for voltages > or = 0 mV the current was essentially zero. In contrast, the current-voltage relationship of the capsaicin-activated current was ohmic from +/- 60 mV. These data indicate the existence of subsets of capsaicin-sensitive afferent neurons.

Pathophysiology of trigeminal neuralgia: new evidence from a trigeminal ganglion intraoperative microneurographic recording

2004 ◽  
Vol 101 (5) ◽  
pp. 872-873 ◽  
Author(s):  
Kim J. Burchiel ◽  
Thomas K. Baumann
Keyword(s):  
Trigeminal Neuralgia ◽  
Trigeminal Ganglion ◽  
Physiological Mechanism ◽  
Vascular Compression ◽  
Entry Zone ◽  
Content Type ◽  
Root Entry Zone ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons ◽  
New Evidence

✓ The origin of trigeminal neuralgia (TN) appears to be vascular compression of the trigeminal nerve at the root entry zone; however, the physiological mechanism of this disorder remains uncertain. The authors obtained intraoperative microneurographic recordings from trigeminal ganglion neurons in a patient with TN immediately before percutaneous radiofrequency-induced gangliolysis. Their findings are consistent with the idea that the pain of TN is generated, at least in part, by an abnormal discharge within the peripheral nervous system.

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