Differential responses of rostral subnucleus caudalis and upper cervical dorsal horn neurons to mechanical and chemical stimulation of the parotid gland in rats.
Blockage of the salivary duct can produce pain and inflammation from the build up of saliva in the parotid gland. The processing of parotid inflammation-induced pain, however, is poorly understood. The purpose of this study was to clarify the functional involvement of the trigeminal subnucleus interpolaris/caudalis transition region (Vi/Vc) and upper cervical spinal cord (C1/C2) in processing nociceptive input relevant to parotitis. The effect of capsaicin-induced parotitis was examined on a total of 37 nociceptive neurons isolated from the Vi/Vc (n = 23) and C1/C2 (n = 14) regions. Eight of 23 Vi/Vc neurons responded to mechanical distention of the parotid gland, whereas no C1/C2 neurons responded to the parotid distention. Receptive field characteristics in all neurons were examined following capsaicin injections into the parotid gland. Mechanical and cold responses increased significantly in C1/C2 but not Vi/Vc neurons following capsaicin. Receptive field sizes also increased in C1/C2 but not Vi/Vc neurons. At the Vi/Vc transition region, pinch-evoked activity increased in neurons receiving convergent inputs from the parotid gland and facial skin when compared to non-convergent neurons. The present data indicate that the hyperalgesia and referred pain associated with parotitis may result from sensitization of C1/C2, but not Vi/Vc nociceptive neurons.
Ogawa
Akiko
A
Department of Oral Diagnosis, School of Dentistry, Nihon University, Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan; Department of Oral Diagnosis, School of Dentistry, Nihon University, Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan. Electronic address: ogawa-a@dent.nihon-u.ac.jp.
Meng
Ian D
ID
Division of Clinical Research, Dental Research Center, Nihon University School of Dentistry, Tokyo 101-8310, Japan; Department of Physiology, College of Osteopathic Medicine, University of New England, 11 Hills Beach Rd., Biddeford, ME 04005, USA.
Ren
Ke
K
Department of Physiology, College of Osteopathic Medicine, University of New England, 11 Hills Beach Rd., Biddeford, ME 04005, USA; Department of Biomedical Sciences, University of Maryland Dental School, Baltimore, Maryland 21201, USA.
Imamura
Yoshiki
Y
Department of Oral Diagnosis, School of Dentistry, Nihon University, Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan; Division of Clinical Research, Dental Research Center, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
Iwata
Koichi
K
Department of Physiology, School of Dentistry, Nihon University, Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan; Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002211:Capsaicin / Q000494:pharmacology; D002574:Cervical Vertebrae; D003080:Cold Temperature / Q000009:adverse effects; D006930:Hyperalgesia / Q000139:chemically induced / Q000503:physiopathology; D018836:Inflammation Mediators / Q000494:pharmacology; D008297:Male; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology*; D010146:Pain / Q000139:chemically induced / Q000503:physiopathology*; D010147:Pain Measurement / Q000379:methods; D017288:Pain Threshold / Q000187:drug effects / Q000502:physiology; D010306:Parotid Gland / Q000294:innervation* / Q000503:physiopathology; D010309:Parotitis / Q000139:chemically induced / Q000503:physiopathology; D010812:Physical Stimulation; D020671:Posterior Horn Cells / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012867:Skin / Q000294:innervation / Q000503:physiopathology; D014275:Trigeminal Caudal Nucleus / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*
D018836:Inflammation Mediators; D002211:Capsaicin