Kazuharu Nakagawa
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Kazuharu Nakagawa has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
- Junichi Kitagawa
Department of Oral Physiology, School of Dentistry, Matsumoto Dental University, Shiojiri, Nagano, Japan
1 shared publication - Koichi Iwata
Department of Physiology, Nihon University School of Dentistry, 1-8-13 Kandasurugadai, Chiyoda-ku, Tokyo 101-8310, Japan
1 shared publication - Mamoru Takeda
Department of Physiology, School of Life Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo 102-8159, Japan
1 shared publication - Shigeji Matsumoto
Department of Physiology, Nippon Dental University, School of Life Dentistry at Tokyo, 1-9-20 Fujimi, Chiyoda-ku, Tokyo 102-8159, Japan
1 shared publication - Yoshiyuki Tsuboi
Department of Physiology, School of Dentistry, Nihon University
1 shared publication
Latest Publications
- Open Access
- 1 January 2011
- Published by SAGE Publications in Molecular Pain
- Vol. 7 (1) , 5
Potassium Channels as a Potential Therapeutic Target for Trigeminal Neuropathic and Inflammatory Pain
Previous studies in several different trigeminal nerve injury/inflammation models indicated that the hyperexcitability of primary afferent neurons contributes to the pain pathway underlying mechanical allodynia. Although multiple types of voltage-gated ion channels are associated with neuronal hyperexcitability, voltage-gated K+ channels (Kv) are one of the important physiological regulators of membrane potentials in excitable tissues, including nociceptive sensory neurons. Since the opening of K+ channels leads to hyperpolarization of cell membrane and a consequent decrease in cell excitability, several Kv channels have been proposed as potential target candidates for pain therapy. In this review, we focus on common changes measured in the Kv channels of several different trigeminal neuropathic/inflammatory pain animal models, particularly the relationship between changes in Kv channels and the excitability of trigeminal ganglion (TRG) neurons. We also discuss the potential of Kv channel openers as therapeutic agents for trigeminal neuropathic/inflammatory pain, such as mechanical allodynia.
- 1 January 2011
- Published by SAGE Publications in Molecular Pain
- Vol. 7 (1) , 5
Open AccessPotassium Channels as a Potential Therapeutic Target for Trigeminal Neuropathic and Inflammatory Pain
Previous studies in several different trigeminal nerve injury/inflammation models indicated that the hyperexcitability of primary afferent neurons contributes to the pain pathway underlying mechanical allodynia. Although multiple types of voltage-gated ion channels are associated with neuronal hyperexcitability, voltage-gated K+ channels (Kv) are one of the important physiological regulators of membrane potentials in excitable tissues, including nociceptive sensory neurons. Since the opening of K+ channels leads to hyperpolarization of cell membrane and a consequent decrease in cell excitability, several Kv channels have been proposed as potential target candidates for pain therapy. In this review, we focus on common changes measured in the Kv channels of several different trigeminal neuropathic/inflammatory pain animal models, particularly the relationship between changes in Kv channels and the excitability of trigeminal ganglion (TRG) neurons. We also discuss the potential of Kv channel openers as therapeutic agents for trigeminal neuropathic/inflammatory pain, such as mechanical allodynia.