Tissue glucose level modulates the mechanical responses of cutaneous nociceptors in streptozotocin-diabetic rats but not normal rats in vitro.
The maintenance of normoglycemia has been reported to reduce painful sensations in diabetic subjects. This suggests that lowering the tissue glucose concentration might inhibit the increased cutaneous nociceptor activities seen in a diabetic conditin. To test this hypothesis, we studied the effect of changing the glucose concentration in the superfusate of in vitro preparations (high, HG: 20 mM or normal glucose, NG: 6.7 mM) on the mechanical response of C-fiber polymodal receptors (C-polymodal receptors). Single fiber activities of C-polymodal receptors were recorded from skin-nerve in vitro preparations of streptozotocin-induced diabetic and age-matched control rats. Pressure stimulation was applied to the receptive field by a servo-controlled mechanical stimulator. C-polymodal receptors from diabetic preparations superfused with HG-solution showed increased spontaneous activity, lowered response threshold, increased response magnitude and a less adaptive response pattern to mechanical stimulation compared with those from control preparations superfused with NG-solution. C-polymodal receptors from diabetic preparations superfused with NG-solution showed no such changes. The responsiveness of C-polymodal receptors from control preparations was not different in NG- or HG-conditions. These data demonstrated that normalization of the glucose concentration normalized the responsiveness of C-polymodal receptors in diabetic animals. This response may be associated with the fact that normoglycemia reduces painful sensations in diabetic subjects.
Suzuki
Yoshiaki
Y
Department of Anesthesiology, Banbuntane Houtokukai Hospital, Fujita-Health University, Nagoya, 454-8509 Japan Department of Neural Regulation, Research institute of Environmental Medicine, Nagoya University, Furo-cho Chikusa-ku, Nagoya, Japan, 464-8601.
Sato
Jun
J
Kawanishi
Minoru
M
Mizumura
Kazue
K
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D036421:Nerve Fibers, Unmyelinated / Q000187:drug effects / Q000502:physiology; D009619:Nociceptors / Q000502:physiology*; D010812:Physical Stimulation / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D012867:Skin / Q000294:innervation*; D014018:Tissue Distribution / Q000187:drug effects / Q000502:physiology
D005947:Glucose