Abstract
Previous reports indicated that the hyperexcitability of primary afferent neurons under several different types of trigeminal nerve injury / inflammation models has been contributed to the pathological pain and mechanical allodynia. Although the multiple types of voltage-gated ionic channels are associated with the hyperexcitability of the neuron, voltage-gated K+ channels (Kv) are one of the important physiological regulators of membrane potentials in excitable tissues, including nociceptive sensory neuron. Since the opening of K+ channels leads to hyperpolarization of the cell membrane, which results in a decrease of the cell excitability, it has been suggest that several different types of Kv channels has been proposed as potential target candidates for the therapeutic approaches to pain. In this review, we focus on the common changes in the Kv channels in the several types of trigeminal neuropathic / inflammatory pain animal models, particulary the relationship between the change in Kv channels and the excitability of trigeminal ganglion (TRG) neurons. Therefore, we discuss the possibility that the Kv channel openers may be therapeutic agents for prevention of trigeminal neuropathic / inflammation pain, such as mechanical allodynia.
