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Enhanced excitability of rat trigeminal root ganglion neurons via decrease in A-type potassium currents following
M Takeda1, T Tanimoto, M Ikeda
1Department of Physiology, School of Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo 102-8159, Japan. m-takeda@tokyo.ndu.ac.jp
Neuroscience
|January 3, 2006
Summary
Temporomandibular joint inflammation increases trigeminal nerve excitability by reducing potassium currents, potentially causing pain in temporomandibular joint disorders.
Area of Science:
- Neuroscience
- Physiology
Background:
- Temporomandibular joint (TMJ) disorders often involve inflammation.
- Trigeminal nerve pathways are crucial for TMJ sensation and pain signaling.
Purpose of the Study:
- To investigate how TMJ inflammation affects the excitability of trigeminal root ganglion (TRG) neurons.
- To identify the ionic mechanisms underlying these changes in TRG neuron excitability.
Main Methods:
- Induced TMJ inflammation in rats using complete Freund's adjuvant.
- Utilized the perforated patch-clamp technique on Fluorogold-labeled TRG neurons.
- Measured neuronal excitability, including action potential firing and ion currents.
Main Results:
- TMJ inflammation lowered the mechanical stimulation escape threshold.
- Reduced voltage-dependent transient K(+) current density and shifted its inactivation curve in TRG neurons.
- Decreased threshold current and increased action potential firing in inflamed TRG neurons.
Conclusions:
- TMJ inflammation enhances TRG neuron excitability by suppressing transient K(+) currents.
- This mechanism may contribute to trigeminal inflammatory allodynia in TMJ disorders.
