Yoshimura M, Polosa C, Nishi S
Brain Res. 1987 Jun 23;414(1):138-42. doi: 10.1016/0006-8993(87)91334-5.
Intracellular recordings were made from sympathetic preganglionic neurons of the lateral horn in slices of cat thoracic cord maintained in vitro. Focal electrical stimulation of the slice evoked, in addition to the already described fast EPSPs, EPSPs of several seconds duration. The slow EPSPs, like the fast EPSPs, were graded with stimulus intensity and were abolished by TTX or low Ca and high Mg superfusion. The slow EPSP decreased in amplitude with membrane hyperpolarization and was nullified at -90 mV but did not reverse with further hyperpolarization. The slow EPSP was abolished by phentolamine or prazosin but not by yohimbine. Noradrenaline NA, 10-50 microM) caused in 30% of neurons a TTX-resistant depolarization. The NA-evoked depolarization had the same characteristics as the slow EPSP with respect to sensitivity to membrane potential and to adrenergic blockers. These results suggest that NA, acting on an alpha 1-receptor, may be the mediator of the slow EPSP evoked in this neuron by focal stimulation.
在体外保存的猫胸段脊髓切片中，对侧角交感神经节前神经元进行细胞内记录。对切片进行局部电刺激，除了已描述的快速兴奋性突触后电位（fast EPSPs）外，还诱发了持续数秒的兴奋性突触后电位。慢兴奋性突触后电位（slow EPSPs）与快速兴奋性突触后电位一样，随刺激强度分级，并被河豚毒素（TTX）或低钙高镁灌流消除。慢兴奋性突触后电位的幅度随膜超极化而降低，在-90 mV时消失，但不会随进一步超极化而反转。慢兴奋性突触后电位被酚妥拉明或哌唑嗪消除，但不被育亨宾消除。去甲肾上腺素（NA，10 - 50 microM）在30%的神经元中引起了对TTX耐药的去极化。NA诱发的去极化在对膜电位和肾上腺素能阻滞剂的敏感性方面与慢兴奋性突触后电位具有相同的特征。这些结果表明，作用于α1受体的NA可能是该神经元局部刺激诱发慢兴奋性突触后电位的介质。
