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

scholarly journals Insulin-Like Growth Factor-1 Receptor-Mediated Inhibition of A-type K+ Current Induces Sensory Neuronal Hyperexcitability Through the Phosphatidylinositol 3-Kinase and Extracellular Signal-Regulated Kinase 1/2 Pathways, Independently of Akt

Endocrinology ◽  
2014 ◽  
Vol 155 (1) ◽  
pp. 168-179 ◽  
Author(s):  
Hua Wang ◽  
Jianzhong Qin ◽  
Shan Gong ◽  
Bo Feng ◽  
Yuan Zhang ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
Kinase Inhibitor ◽  
Delayed Rectifier ◽  
Phosphatidylinositol 3 Kinase ◽  
Neuronal Hyperexcitability ◽  
Type K ◽  
K Current ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons ◽  
Phosphatidylinositol 3

Although IGF-1 has been implicated in mediating hypersensitivity to pain, the underlying mechanisms remain unclear. We identified a novel functional of the IGF-1 receptor (IGF-1R) in regulating A-type K+ currents (IA) as well as membrane excitability in small trigeminal ganglion neurons. Our results showed that IGF-1 reversibly decreased IA, whereas the sustained delayed rectifier K+ current was unaffected. This IGF-1–induced IA decrease was associated with a hyperpolarizing shift in the voltage dependence of inactivation and was blocked by the IGF-1R antagonist PQ-401; an insulin receptor tyrosine kinase inhibitor had no such effect. An small interfering RNA targeting the IGF-1R, or pretreatment of neurons with specific phosphatidylinositol 3-kinase (PI3K) inhibitors abolished the IGF-1–induced IA decrease. Surprisingly, IGF-1–induced effects on IA were not regulated by Akt, a common downstream target of PI3K. The MAPK/ERK kinase inhibitor U0126, but not its inactive analog U0124, as well as the c-Raf-specific inhibitor GW5074, blocked the IGF-1–induced IA response. Analysis of phospho-ERK (p-ERK) showed that IGF-1 significantly activated ERK1/2 whereas p-JNK and p-p38 were unaffected. Moreover, the IGF-1–induced p-ERK1/2 increase was attenuated by PI3K and c-Raf inhibition, but not by Akt blockade. Functionally, we observed a significantly increased action potential firing rate induced by IGF-1; pretreatment with 4-aminopyridine abolished this effect. Taken together, our results indicate that IGF-1 attenuates IA through sequential activation of the PI3K- and c-Raf-dependent ERK1/2 signaling cascade. This occurred via the activation of IGF-1R and might contribute to neuronal hyperexcitability in small trigeminal ganglion neurons.

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.

scholarly journals Toll-like receptor 4 signaling in trigeminal ganglion neurons contributes tongue-referred pain associated with tooth pulp inflammation

2013 ◽  
Vol 10 (1) ◽  
pp. 139 ◽  
Author(s):  
Kinuyo Ohara ◽  
Kohei Shimizu ◽  
Shingo Matsuura ◽  
Bunnai Ogiso ◽  
Daisuke Omagari ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
Referred Pain ◽  
Tooth Pulp ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Pulp Inflammation ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion 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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