Role of intracellular calcium in thermal allodynia and hyperalgesia in diabetic mice

被引:29
作者
Ohsawa, M [1 ]
Kamei, J [1 ]
机构
[1] Hoshi Univ, Fac Pharmaceut Sci, Dept Pathophysiol & Therapeut, Shinagawa Ku, Tokyo 1428501, Japan
关键词
diabetes; calcium; allodynia; hyperalgesia; ryanodine; thapsigargin; spinal cord;
D O I
10.1016/S0006-8993(99)01506-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We examined the involvement of cytosolic calcium on thermal hyperalgesia and allodynia seen in diabetic mice. Tail-flick latencies at source voltages of a 50-W projection bulb to 35 and 50 V in diabetic mice were significantly shorter than those in non-diabetic mice. Tail-flick latencies at 35 and 50 V in diabetic mice were increased by pretreatment with ryanodine, which blocks Ca2+ release from Ca2+/caffeine-sensitive microsomal pools. On the other hand, intrathecal (i.t.) pretreatment with thapsigargin, which inhibits Ca2+ uptake into the inositol-1,4,5-trisphosphate-sensitive microsomal Ca2+ pool, decreased tail-flick latencies at 35 and 50 V in non-diabetic mice. Thus, it seems likely that thermal allodynia and hyperalgesia in diabetic mice may be due, in part, to the enhancement of intracellular calcium level in the spinal cord. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:278 / 281
页数:4
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