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Mechanisms involved in modulation of trigeminal primary afferent activity in rats with peripheral mononeuropathy

Authors

  • Junichi Kitagawa,

    1. Department of Physiology, School of Dentistry, Nihon University, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
    2. Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
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  • Mamoru Takeda,

    1. Department of Physiology, School of Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo, 102-8159, Japan
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  • Ikuko Suzuki,

    1. Department of Physiology, School of Dentistry, Nihon University, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
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  • Jun Kadoi,

    1. Department of Physiology, School of Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo, 102-8159, Japan
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  • Yoshiyuki Tsuboi,

    1. Department of Physiology, School of Dentistry, Nihon University, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
    2. Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
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  • Kuniya Honda,

    1. Department of Oral and Maxillofacial Surgery, School of Dentistry, Nihon University, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
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  • Shigeji Matsumoto,

    1. Department of Physiology, School of Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo, 102-8159, Japan
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  • Hiroshi Nakagawa,

    1. Department of Physiology, School of Dentistry, Nihon University, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
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  • Aya Tanabe,

    1. Department of Physiology, School of Dentistry, Nihon University, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
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  • Koichi Iwata

    1. Department of Physiology, School of Dentistry, Nihon University, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
    2. Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan
    3. Division of Applied System Neuroscience Advanced Medical Research Center, Nihon University Graduate School of Medical Science, 30-1 Ohyaguchi-Kamimachi Itabashi, Tokyo 173-8610 Japan
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Dr K. Iwata, 1Department of Physiology, as above.
E-mail: iwata-k@dent.nihon-u.ac.jp

Abstract

In order to clarify the mechanisms underlying the changes in primary afferent neurons in trigeminal neuropathic pain, a chronic constriction nerve injury model of the infraorbital nerve (ION-CCI) was developed in rats. Mechanical allodynia was observed at 3 days after ION-CCI and lasted more than 14 days. Single-unit activities were recorded from the ION of anesthetized rats. C-, Aβ- and Aδ-units were identified on the basis of their conduction velocity. Aδ-units were frequently encountered at a later period after ION-CCI. The highest Aδ-spontaneous activity was recorded at 3 days after ION-CCI and progressively decreased after that, but spontaneous activity was still higher at 14 days after ION-CCI than that of naïve rats. Mechanical-evoked responses of Aδ-units were also highest at 3 days after ION-CCI and then gradually decreased. In consideration of these data, patch-clamp recordings were performed on medium to large size neurons of the dissociated trigeminal ganglion (TRG). Patch-clamp recordings revealed that the IK (sustained) and IA (transient) in rats with ION-CCI were significantly smaller than those of naïve rats, and correlated with an increase in duration of repolarization phase and a decrease in duration of depolarization phase, respectively. The hyperpolarization-activated current (Ih) was significantly larger in TRG neurons of rats with ION-CCI as compared with those of naïve rats. The present results suggest that Ih, IK and IA in Aδ-afferent neurons in TRG are significantly involved in the changes in afferent spontaneous activity and mechanically evoked activity that accompany mechanical allodynia produced by trigeminal nerve injury.

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