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.

细胞内记录是由位于成年大鼠脊髓切片中的质明明胶（SG，Rexed lamina II）的神经元制成的，该切片保留了附着的背根。刺激初级传入的三角洲纤维引起的甘油能和/或GABA能IPSP，持续时间小于100 ms。在通过士宁宁和二美瓜阻止这些IPSP之后，出现了一个额外的慢速IPSP，具有异常长的时间，持续了30-180，在一次刺激之后，出现了30-180。仅刺激三角洲纤维，不包括C纤维，就会产生全尺寸的慢速IPSP。慢速IPSP与输入电阻的降低有关，并在钾平衡电位附近的极性逆转。慢速IPSP被CNQX（10 MUM）废除，表明多突触起源。儿茶酚胺能，血清素能或胆碱能拮抗剂对慢速IPSP没有显着影响。据报道，这些肽已被测试，这些肽已被测试，但它们对SG神经元没有明显的影响，除SG神经元没有明显的影响。 Enkephalin产生了膜超极化。然而，阿片受体拮抗剂纳洛酮（2 MUM）对慢速IPSP没有显着影响，这表明enkephalin可能不是SG神经元中慢速iPSP.somatatin的发射机，而SG神经元中产生的慢性超极化响应在缓慢的超极化反应上与慢速生理相对于慢速IPSP.In添加了慢速生理学。在生长抑素诱导的超极化期间，慢速IPSP被阻塞。这些观察结果表明，甘氨酸能和GABA能中间神经元通常抑制中间神经元或其末端的子集，从而释放了负责慢速IPSP产生的发射机。相关的发射器可能是生物结构化蛋白，但这仍然可以进一步研究。