Honmou O, Sakatani K, Young W
Department of Neurosurgery, New York University Medical Center, NY 10016.
Neuroscience. 1993 May;54(1):93-104. doi: 10.1016/0306-4522(93)90385-s.
The neurotransmitter GABA markedly depresses action potential conduction in neonatal rat spinal dorsal columns. However, GABA sensitivity of the dorsal columns declines with maturation and myelination. At seven to 14 days after birth, the corticospinal tract component of the dorsal columns is immature and unmyelinated compared to the cuneate-gracilis fasciculi. GABA and isoguvacine (a GABAA receptor agonist) were applied to isolated neonatal (seven to 14 days old) dorsal columns during recordings of conducted cuneate-gracilis fasciculi and corticospinal tract action potentials. GABA (10(-4) to 10(-3) M) significantly reduced amplitudes (-28.9% to -69.7%) and increased latencies (+4.8% to +23.9%) of cuneate-gracilis fasciculi responses but had less effect on corticospinal tract response amplitudes (-1.1% to -14.7%) and latencies (+0.9% to +6.2%). Likewise, isoguvacine (10(-5) to 10(-4) M) reduced amplitudes (-26.7% to -37.5%) and increased latencies (+11.2% and +24.0%) of cuneate-gracilis fasciculi responses but had little or no effect on corticospinal tract response amplitudes (-6.2% to -3.8%) or latencies (-0.8% to +1.5%). At 10(-4) and 10(-3) M, GABA rapidly increased extracellular K+([K+]e) from baseline levels of 3.0 mM to 3.7 +/- 0.4 and 6.6 +/- 1.4 mM in cuneate-gracilis fasciculi and increased corticospinal tract [K+]e to 3.9 +/- 0.4 and 4.4 +/- 0.4 mM (mean +/- S.D.). [K+]e declined during drug application and fell below baseline after drug washout. Cuneate-gracilis fasciculi responses, however, did not recover until several minutes after [K+]e returned to baseline. In separate experiments, increasing bath [K+]e concentrations to 3.7 and 6.6 mM reduced cuneate-gracilis fasciculi response amplitudes by only -7.6% and -29.6%. Latencies increased by +1.3% and +3.6% respectively. The results indicate that the cuneate-gracilis fasciculi are more sensitive to GABA than the corticospinal tract and that the GABA effect is not entirely due to [K+]e changes.
神经递质γ-氨基丁酸（GABA）可显著抑制新生大鼠脊髓背柱的动作电位传导。然而，随着成熟和髓鞘形成，背柱对GABA的敏感性会下降。出生后7至14天，与楔束-薄束相比，背柱的皮质脊髓束部分尚未成熟且无髓鞘。在记录楔束-薄束和皮质脊髓束动作电位时，将GABA和异鹅肌肽（一种GABAA受体激动剂）应用于分离的新生（7至14日龄）背柱。GABA（10^(-4)至10^(-3) M）显著降低了楔束-薄束反应的幅度（-28.9%至-69.7%）并增加了潜伏期（+4.8%至+23.9%），但对皮质脊髓束反应幅度（-1.1%至-14.7%）和潜伏期（+0.9%至+6.2%）的影响较小。同样，异鹅肌肽（10^(-5)至10^(-4) M）降低了楔束-薄束反应的幅度（-26.7%至-37.5%）并增加了潜伏期（+11.2%和+24.0%），但对皮质脊髓束反应幅度（-6.2%至-3.8%）或潜伏期（-0.8%至+1.5%）几乎没有影响。在10^(-4)和10^(-3) M时，GABA使楔束-薄束中的细胞外钾离子（[K+]e）从基线水平3.0 mM迅速增加到3.7±0.4 mM和6.6±1.4 mM，并使皮质脊髓束的[K+]e增加到3.9±0.4 mM和4.4±0.4 mM（平均值±标准差）。在药物应用期间[K+]e下降，药物洗脱后降至基线以下。然而，楔束-薄束反应直到[K+]e恢复到基线后几分钟才恢复。在单独的实验中，将浴液[K+]e浓度增加到3.7 mM和6.6 mM时，楔束-薄束反应幅度仅降低了-7.6%和-29.6%。潜伏期分别增加了+1.3%和+3.6%。结果表明，楔束-薄束对GABA比皮质脊髓束更敏感，且GABA的作用并不完全归因于[K+]e的变化。
