Mechanisms involved in modulation of trigeminal primary afferent activity in rats with peripheral mononeuropathy.
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.
Kitagawa
Junichi
J
Department of Physiology, School of Dentistry, Nihon University, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan.
Takeda
Mamoru
M
Suzuki
Ikuko
I
Kadoi
Jun
J
Tsuboi
Yoshiyuki
Y
Honda
Kuniya
K
Matsumoto
Shigeji
S
Nakagawa
Hiroshi
H
Tanabe
Aya
A
Iwata
Koichi
K
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*
D015221:Potassium Channels