Pain mechanismEnhanced excitability of rat trigeminal root ganglion neurons via decrease in A-type potassium currents following temporomandibular joint inflammation
Section snippets
Experimental procedures
The experiments were approved by the animal use and care committee of Nippon Dental University and were consistent with the ethical guidelines of the International Association for the Study of Pain (Zimmermann, 1983). Double-blind experiments were carried out and all possible efforts were made to minimize the number of animals used and their suffering.
Induction of TMJ inflammation and allodynia
After CFA injection, the animals were tested for abnormal pain sensation by probing the injected site and/or the orofacial skin with von Frey filaments. In the TMJ-inflamed rats, the threshold for escape from mechanical stimulation applied to the whisker pad area was significantly reduced from 51.3±6.3 mN to 19.1±2.1 mN at 48 h after CFA injection (n=18, P<0.05). No significant changes in the contralateral threshold in the whisker pad area were observed in either group (control vs. inflamed;
Discussion
The results presented herein provide evidence that TMJ inflammation potentiates the excitability of small-diameter TRG neurons innervating TMJ, by suppressing A-currents via a leftward, hyperpolarizing, shift in the inactivation curve without any changes in the activation curve. The IA suppression of the TRG neuron innervating TMJ may contribute to trigeminal inflammatory allodynia in the TMJ disorder.
Acknowledgments
This study was supported by a grant from the Ministry of Education, Science and Culture of Japan (No.15591980).
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2018, Neuroscience ResearchCitation Excerpt :Kv channels are involved in several important functions in the nervous system including setting the resting membrane potential, setting action potential shape, neuronal repolarization, and neurotransmitter release (Ficker and Heinemann, 2001; Pearce and Duchen, 1994; Hille, 2001; Lawson, 2006) via slow-inactivating sustained (K-current; IK) and fast-inactivating transient (A-current; IA) channels. Takeda et al. (2006) previously observed that a reduction in IA density, but not in dominant sustained current (Ik), contributes to the increased excitability of small-diameter TG neuron in intact rats. In fact, applying an A-type potassium channel blocker to TG neurons in vivo also enhances Aδ/C-TG neuronal activities innervating the temporomandibular joint (TMJ) region in intact rats (Hara et al., 2012).