Ryan G P, Hackman J C, Wohlberg C J, Davidoff R A
Brain Res. 1984 Jun 3;301(2):331-41. doi: 10.1016/0006-8993(84)91102-8.
Spontaneous dorsal root potentials (sDRPs) were recorded from the dorsal roots of the isolated frog spinal cord using sucrose gap techniques. sDRPs were always negative (depolarizing) in sign and ranged in size from about 100 microV to 6.0 mV. The largest sDRPs were 25-40% of the amplitude of DRPs evoked by stimulation of adjacent dorsal roots. Hypoxia or accumulation of extracellular K+ ions did not appear responsible for the generation of this spontaneous activity since exposing the cord to unoxygenated Ringer's solution decreased sDRPs and K+-sensitive microelectrodes indicated that only small changes in extracellular K+ (approximately 0.15 mM) were produced coincidently with the largest sDRPs. Chemically-mediated synaptic transmission was found to be necessary for the production of sDRPs because the addition of Mn2+ or Mg2+ ions or tetrodotoxin to the Ringer's solution or reduction of its Na+ concentration blocked sDRPs, whereas application of 4-aminopyridine enhanced them. It did not seem that a direct action of GABA on afferent fiber terminals was responsible for the generation of spontaneous potentials since an increase in sDRPs was seen after: application of the GABA antagonists, bicuculline and picrotoxin; exposure to the glutamic acid decarboxylase inhibitor, semicarbazide (which significantly reduced the concentration of GABA in the cord); and lowering of the external Cl- concentration. Similarly taurine is probably not significant since the taurine antagonist, TAG, increased the amount of spontaneous activity. On the other hand, (--)-baclofen, which is thought to reduce excitatory amino acid release, D,L-alpha-aminoadipic acid, alpha, epsilon-diaminopimelic acid, and 2-amino-4-phosphonobutyric acid, which are believed to be selective postsynaptic excitatory amino acid antagonists, and [D-Pro2-D-Phe7-D-Trp9]-substance P, a postsynaptic blocker of the action of substance P, markedly and reversibly reduced sDRPs. Experiments were performed on isolated cords without supraspinal or afferent input; therefore sDRPs must be generated by intraspinal structures. It would seem that interneurons are responsible because addition of mephenesin or pentobarbital--compounds which inhibit polysynaptic reflex transmission involving interneurons--reduced the production of sDRPs. sDRPs may result from the action of excitatory transmitters such as L-glutamate, L-aspartate, or substance P released by interneuronal firing in the spinal cord. Moreover, because sDRPs were increased by application of yohimbine, corynanthine and propanolol and reduced by haloperidol, such interneurons may be under descending control of adrenergic and dopaminergic fibers.
采用蔗糖间隙技术，从离体蛙脊髓的背根记录自发背根电位（sDRPs）。sDRPs在信号上总是负性的（去极化），大小范围约为100微伏至6.0毫伏。最大的sDRPs为刺激相邻背根诱发的背根电位（DRPs）幅度的25% - 40%。缺氧或细胞外K⁺离子的积累似乎并非这种自发活动产生的原因，因为将脊髓暴露于无氧的林格氏液中会使sDRPs降低，且K⁺敏感微电极表明，在出现最大的sDRPs时，细胞外K⁺仅产生了小的变化（约0.15毫摩尔）。发现化学介导的突触传递是产生sDRPs所必需的，因为向林格氏液中添加Mn²⁺或Mg²⁺离子、河豚毒素或降低其Na⁺浓度会阻断sDRPs，而应用4 - 氨基吡啶则会增强它们。似乎GABA对传入纤维终末的直接作用并非自发电位产生的原因，因为在应用GABA拮抗剂荷包牡丹碱和印防己毒素后、暴露于谷氨酸脱羧酶抑制剂氨基脲（这会显著降低脊髓中GABA的浓度）以及降低细胞外Cl⁻浓度后，sDRPs均增加。同样，牛磺酸可能也不显著，因为牛磺酸拮抗剂TAG增加了自发活动的量。另一方面，据认为可减少兴奋性氨基酸释放的（ - ） - 巴氯芬、被认为是选择性突触后兴奋性氨基酸拮抗剂的D,L - α - 氨基己二酸、α,ε - 二氨基庚二酸和2 - 氨基 - 4 - 膦酰丁酸，以及P物质的突触后作用阻断剂[D - Pro² - D - Phe⁷ - D - Trp⁹] - P物质，均显著且可逆地降低了sDRPs。实验是在没有脊髓以上或传入输入的离体脊髓上进行的；因此，sDRPs必定是由脊髓内结构产生的。似乎中间神经元是原因所在，因为添加美芬新或戊巴比妥——抑制涉及中间神经元的多突触反射传递的化合物——会减少sDRPs的产生。sDRPs可能是由脊髓中中间神经元放电释放的兴奋性递质如L - 谷氨酸、L - 天冬氨酸或P物质的作用导致的。此外，由于应用育亨宾、柯楠碱和普萘洛尔会增加sDRPs，而氟哌啶醇会降低sDRPs，所以此类中间神经元可能受肾上腺素能和多巴胺能纤维的下行控制。
