Increase in trigeminal ganglion neurons that respond to both CGRP and PACAP in mouse models of chronic migraine and post-traumatic headache

Pain ◽  
2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Zhaohua Guo ◽  
Katherine Czerpaniak ◽  
Jintao Zhang ◽  
Yu-Qing Cao
Keyword(s):  
Chronic Migraine ◽  
Mouse Models ◽  
Trigeminal Ganglion ◽  
Post Traumatic ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons

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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