title: Mechanisms involved in modulation of trigeminal primary afferent activity in rats with peripheral mononeuropathy.
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-, Abeta- and Adelta-units were identified on the basis of their conduction velocity. Adelta-units were frequently encountered at a later period after ION-CCI. The highest Adelta-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 Adelta-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 Adelta-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.
authors.affiliation: Department of Physiology, School of Dentistry, Nihon University, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan.
authors.forename: Junichi
authors.initials: J
authors.lastname: Kitagawa
authors.forename: Mamoru
authors.initials: M
authors.lastname: Takeda
authors.forename: Ikuko
authors.initials: I
authors.lastname: Suzuki
authors.forename: Jun
authors.initials: J
authors.lastname: Kadoi
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Tsuboi
authors.forename: Kuniya
authors.initials: K
authors.lastname: Honda
authors.forename: Shigeji
authors.initials: S
authors.lastname: Matsumoto
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakagawa
authors.forename: Aya
authors.initials: A
authors.lastname: Tanabe
authors.forename: Koichi
authors.initials: K
authors.lastname: Iwata
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001522:Behavior, Animal; D002452:Cell Count; D003251:Constriction, Pathologic; D004195:Disease Models, Animal; D004307:Dose-Response Relationship, Radiation; D004558:Electric Stimulation / Q000379:methods; D007839:Functional Laterality / Q000502:physiology; D008297:Male; D009475:Neurons, Afferent / Q000473:pathology / Q000502:physiology*; D010147:Pain Measurement / Q000379:methods; D017288:Pain Threshold / Q000502:physiology; D018408:Patch-Clamp Techniques / Q000379:methods; D010523:Peripheral Nervous System Diseases / Q000473:pathology* / Q000503:physiopathology*; D010812:Physical Stimulation / Q000379:methods; D015221:Potassium Channels / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014276:Trigeminal Nerve / Q000473:pathology* / Q000503:physiopathology*
chemical_list: D015221:Potassium Channels