权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Long lasting slow IPSP in substantia gelatinosa of the rat spinal cord

大鼠脊髓胶质质中持久缓慢的 IPSP

基本信息

批准号：
07680905
负责人：
YOSHIMURA Megumu
金额：
$ 1.41万
依托单位：
Saga Medical School (1996)Kurume University (1995)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07680905/
关键词：
PEPTIDE DORSAL HORN SLICE PAIN SOMATOSTATIN NOCICEPTION SLOW IPSP SUBSTANTIA GELATINOSA ソマトスタチン痛覚 GABA グリシン第一次求心線維

项目摘要

Intracellular recordings were made from neurons located in substantia gelatinosa (SG,lamina II of Rexed) in slices of the adult rat spinal cord which retained an attached dorsal root. Stimulation of primary afferent A delta fibers evoked glycinergic and/or GABAergic IPSPs with a duration less than 100 ms. After blocking these IPSPs by strychnine and bicuculline, an additional slow IPSP with an exceptionally long time course, lasting 30-180s following a single stimulus, appeared. Stimulation of A delta fibers alone, not including C fibers, could generate the slow IPSP of full size. The slow IPSP was associated with a decrease in input resistance and reversed in polarity near the potassium equilibrium potential. The slow IPSP was abolished by CNQX (10 muM), suggesting polysynaptic origin. Catecholaminergic, serotonergic or cholinergic antagonists had no significant effect on the slow IPSP.Several peptides which are reported to be contained in spinal interneurons have been tested, but they showed no appreciable effects on SG neurons, except for somatostatin and enkephalin. Enkephalin produced a membrane hyperpolarization. However, the opiate receptor antagonist, naloxone (2 muM) had no significant effect on the slow IPSP,suggesting that enkephalin may not be a transmitter for the slow IPSP.Somatostatin produced in SG neurons a slow hyperpolarizing response that was electrophysiologically analogous to the slow IPSP.In addition. the slow IPSP was occluded during somatostatin induced hyperpolarization. These observations suggest that glycinergic and GABAergic interneurons normally suppress a subset of interneurons or their terminals which liberate the transmitter responsible for production of the slow IPSP.The transmitter in question might possible be somatostatin, but this remains to be investigated further.

在保留背根的成年大鼠脊髓切片上，对位于胶状质(SG，Rexed的II层)的神经元进行了细胞内记录。刺激初级传入A三角纤维可诱发持续时间小于100ms的甘氨酸和/或GABA能IPSP。在用士的宁和荷包牡丹碱阻断这些IPSP后，出现了另一种缓慢的IPSP，其病程非常长，在一次刺激后持续30-180秒。单独刺激A-Delta纤维(不包括C-纤维)可产生全尺寸慢的IPSP。缓慢的IPSP与输入电阻的降低有关，并且在钾平衡电位附近的极性反转。慢的IPSP可被CNQX(10微米)取消，提示多突触起源。儿茶酚胺能、5-羟色胺和胆碱能拮抗剂对慢IPSP无明显影响。已有研究表明，脊髓中间神经元中含有几种多肽，但除生长抑素和脑啡肽外，对SG神经元无明显影响。脑啡肽引起细胞膜超极化。然而，阿片受体拮抗剂纳洛酮(2um)对慢IPSP无明显影响，提示脑啡肽可能不是慢IPSP的递质。生长抑素在SG神经元产生与慢IPSP类似的慢超极化反应。生长抑素引起的超极化可阻断慢的IPSP。这些观察表明，甘氨酸能和GABA能中间神经元通常抑制中间神经元或其终末的子集，从而释放负责产生慢速IPSP的递质。所讨论的递质可能是生长抑素，但这仍有待进一步研究。