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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.

细胞内记录来自位于胶状质（SG，板层II的Rexed）在切片的成年大鼠脊髓保留一个附加的背根的神经元。刺激初级传入A δ纤维诱发甘氨酸能和/或GABA能IPSP，持续时间小于100 ms。士的宁和荷包牡丹碱阻断这些IPSP后，一个额外的慢IPSP与一个非常长的时间过程，持续30- 180 s后，一个单一的刺激，出现。单独刺激A δ纤维，不包括C纤维，可以产生全尺寸的慢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极性反转。缓慢的IPSP被CNQX（10 μ M）消除，表明多突触起源。已对脊髓中间神经元中所含的几种肽进行了测试，但除生长抑素和脑啡肽外，它们对SG神经元没有明显的影响。脑啡肽产生膜超极化。然而，阿片受体拮抗剂纳洛酮（2 μ M）对慢IPSP无明显影响，提示脑啡肽可能不是慢IPSP的递质。在生长抑素诱导的超极化过程中，慢IPSP被阻断。这些观察结果表明，甘氨酸能和GABA能中间神经元通常抑制一个子集的中间神经元或其终端释放的递质负责生产的慢IPSP.The问题的递质可能是生长抑素，但这仍有待进一步研究。