Sakuma J, Ciporen J, Abrahams J, Young W
Department of Neurosurgery, New York University Medical Center, NY 10016, USA.
Neuroscience. 1996 Dec;75(3):927-38. doi: 10.1016/0306-4522(96)00268-0.
We compared the effect of GABA and the serotonin receptor agonist (+/-)-8-hydroxy-dipropylaminotetralin hydrobromide (8-OH-DPAT) on compound action potential amplitudes, latency, and conduction velocity in the spinal cord isolated from young (eight to 13-day-old) Long-Evans hooded rats. Supramaximally activated conducting action potentials and extracellular K+ activity were recorded with microelectrodes from the cuneatus-gracilis fasciculi and corticospinal tract. In the cuneatus-gracilis fasciculi, 8-OH-DPAT (10(-4) M) significantly reduced response amplitudes by 26.1 +/- 10.3% (mean +/- S.D., P < 0.0001, paired t-test, n = 27) and increased latencies by 20.3 +/- 7.9% (P < 0.0001). GABA (10(-4) M) reduced/amplitudes by 31.7 +/- 15.0% (P < 0.0001, n = 28) and increased latencies by 6.1 +/- 5.4% (P < 0.0001). However, neither GABA nor 8-OH-DPAT significantly altered conduction velocities, suggesting that the latency shifts are due to changes in activation time and not conduction velocity. In cortical spinal tract, 8-OH-DPAT (10(-4) M) depressed response amplitudes by 18.9 +/- 9.6% (P < 0.05, n = 5), increased latencies by 23.3 +/- 7.2% (P < 0.0001), but reduced conduction velocities by 19.9 +/- 10.2%. GABA (10(-4) M) reduced amplitudes by 16.4 +/- 7.5% (P < 0.01, n = 5), increased latencies by 5.3 +/- 2.3% (P < 0.05), and did not change conduction velocities. Bicuculline or picrotoxin blocked the GABA effects but did not affect the 8-OH-DPAT effects on both tracts. The potassium channel blocker tetraethylammonium did not alter the 8-OH-DPAT effects. The Na+/K(+)-ATPase inhibitor ouabain (10(-6) M) markedly enhanced the depressive GABA effects from 27.9 +/- 12.0% to 49.4 +/- 24.5% (P < 0.01, n = 9), but had no effect on 8-OH-DPAT-mediated effects. These results suggest that GABA and serotonin agonists depress axonal excitability through different and independent mechanisms.
我们比较了γ-氨基丁酸（GABA）和5-羟色胺受体激动剂（±）-8-羟基二丙基氨基四氢萘溴化物（8-OH-DPAT）对从幼年（8至13日龄）Long-Evans有帽大鼠分离出的脊髓中复合动作电位幅度、潜伏期和传导速度的影响。用微电极从楔束-薄束和皮质脊髓束记录超最大激活的传导动作电位和细胞外钾离子活性。在楔束-薄束中，8-OH-DPAT（10⁻⁴ M）使反应幅度显著降低26.1±10.3%（平均值±标准差，配对t检验，P<0.0001，n = 27），潜伏期增加20.3±7.9%（P<0.0001）。GABA（10⁻⁴ M）使幅度降低31.7±15.0%（P<0.0001，n = 28），潜伏期增加6.1±5.4%（P<0.0001）。然而，GABA和8-OH-DPAT均未显著改变传导速度，这表明潜伏期的变化是由于激活时间的改变而非传导速度的改变。在皮质脊髓束中，8-OH-DPAT（10⁻⁴ M）使反应幅度降低18.9±9.6%（P<0.05，n = 5），潜伏期增加23.3±7.2%（P<0.0001），但传导速度降低19.9±10.2%。GABA（10⁻⁴ M）使幅度降低16.4±7.5%（P<0.01，n = 5），潜伏期增加5.3±2.3%（P<0.05），且不改变传导速度。荷包牡丹碱或印防己毒素可阻断GABA的作用，但不影响8-OH-DPAT对两条束的作用。钾通道阻滞剂四乙铵不改变8-OH-DPAT的作用。钠钾ATP酶抑制剂哇巴因（10⁻⁶ M）显著增强了GABA的抑制作用，从27.9±12.0%增强至49.4±24.5%（P<0.01，n = 9），但对8-OH-DPAT介导的作用无影响。这些结果表明，GABA和5-羟色胺激动剂通过不同且独立的机制降低轴突兴奋性。
