Sah P, McLachlan E M
Department of Physiology & Pharmacology, University of Queensland, Australia.
J Auton Nerv Syst. 1995 May 17;53(1):1-15. doi: 10.1016/0165-1838(94)00161-c.
Intracellular recordings were made from neurons in the intermediolateral column and adjacent white matter in horizontal slices of upper thoracic spinal cord from rats aged 21-28 days. Membrane properties were studied in the presence of picrotoxin (100 microM) to block ongoing inhibitory synaptic potentials. 37 neurons were identified as sympathetic preganglionic neurons (SPNs) by their electrical behaviour, anatomical location and/or morphology. SPNs had resting potentials of -57 +/- 2 mV and input resistances of 254 +/- 31 M omega (n = 14). Following a hyperpolarising voltage step, a transient outward current was activated which had a time constant of decay of approx. 400 ms. The inflection in the repolarising phase of the action potential and the following prolonged AHP were both abolished by Cd2+ (50 microM). The current underlying the AHP had two components with kinetic properties similar to the two calcium-activated potassium conductances, gKCa1, and gKCa2, characterized in other autonomic neurons. Noradrenaline (10-100 microM) caused a small depolarization and blocked the calcium component of the action potential suppressing the AHP. This revealed an afterdepolarization (ADP) with an underlying inward current with a decay time constant of approx. 150 ms. All effects of noradrenaline were blocked by phentolamine (10 microM). Graded stimulation of the lateral funiculus 0.5-1 mm rostral to the recording site evoked in all cells monosynaptic fast excitatory synaptic potentials (fEPSPs) which were graded in amplitude. fEPSPs decayed with a time constant identical to the cell input time constant and were reduced in amplitude by CNQX (10-20 microM). In 7 cells, higher stimulus voltages elicited slow EPSPs with a time to peak of 1.1 +/- 0.1 s and a half decay of 2.8 +/- 0.3 s (n = 7) which were not reduced by alpha-adrenoceptor antagonists. The AHP was not blocked when the action potential was initiated during the slow EPSP. We conclude that excitatory bulbospinal inputs to SPNs involve at least one fast transmitter which is likely to be glutamate and one slow transmitter which is not noradrenaline.
对21至28日龄大鼠上胸段脊髓水平切片中间外侧柱及相邻白质中的神经元进行细胞内记录。在存在印防己毒素（100微摩尔）的情况下研究膜特性，以阻断正在进行的抑制性突触电位。根据其电行为、解剖位置和/或形态，37个神经元被鉴定为交感神经节前神经元（SPN）。SPN的静息电位为-57±2毫伏，输入电阻为254±31兆欧（n = 14）。在超极化电压阶跃后，激活了一个瞬时外向电流，其衰减时间常数约为400毫秒。动作电位复极化阶段的拐点及随后的延长的后超极化（AHP）均被Cd2 +（50微摩尔）消除。AHP的基础电流有两个成分，其动力学特性类似于在其他自主神经元中表征的两种钙激活钾电导gKCa1和gKCa2。去甲肾上腺素（10 - 100微摩尔）引起小的去极化，并阻断动作电位的钙成分，抑制AHP。这揭示了一个后去极化（ADP），其基础内向电流的衰减时间常数约为150毫秒。去甲肾上腺素的所有效应均被酚妥拉明（10微摩尔）阻断。在记录部位前方0.5 - 1毫米处对侧索进行分级刺激，在所有细胞中诱发单突触快速兴奋性突触电位（fEPSP），其幅度呈分级变化。fEPSP以与细胞输入时间常数相同的时间常数衰减，并被CNQX（10 - 20微摩尔）降低幅度。在7个细胞中，更高的刺激电压诱发慢兴奋性突触后电位（slow EPSP），其峰值时间为1.1±0.1秒，半衰时间为2.8±0.3秒（n = 7），且不被α - 肾上腺素能拮抗剂降低。当动作电位在慢EPSP期间起始时，AHP未被阻断。我们得出结论，向SPN的兴奋性延髓脊髓输入至少涉及一种可能是谷氨酸的快速递质和一种不是去甲肾上腺素的慢速递质。
