|Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1995: ¥1,900,000 (Direct Cost: ¥1,900,000)
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.