PEPTIDERGIC AND MUSCARINIC EXCITATION AT AMPHIBIAN SYMPATHETIC SYNAPSES

PEPTIDERGIC AND MUSCARINIC EXCITATION AT AMPHIBIAN SYMPATHETIC SYNAPSES
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DOI:
10.1113/jphysiol.1983.sp014805
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发表时间:
1983-01-01
影响因子:
5.5
通讯作者:
SEJNOWSKI, TJ
SEJNOWSKI, TJ
中科院分区:
医学1区
文献类型:
--
作者:
KUFFLER, SW;SEJNOWSKI, TJ

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用单电极电压钳技术研究牛蛙椎旁交感神经节B细胞的慢毒蕈碱能和晚慢肽能兴奋性突触后电流(EPSC)。电导率下降,测定肽能EPSC在几乎所有的细胞在钳位电位附近的休息水平。在.apprx. 1/2的细胞的肽能EPSC的大小随着超极化而增加,并且在其中一些细胞中,在超极化水平下发现电导增加。在其余的细胞电导下降发生在所有水平的膜电位测试,并在其中的一些极性的EPSC逆转超极化电位。在毒蕈碱型EPSC中观察到类似的多样性。至少需要2个简单的离子机制来解释所观察到的异质电压依赖性:电导降低,主要是K+,占主导地位的去极化电位和电导增加,其他离子是更突出的超极化电位。这两种机制的比例在B细胞中似乎不同。在同一神经元中记录的2个慢EPSC具有相同的电压依赖性,并且尽管细胞之间存在差异,但在8个细胞中的每一个中都伴随着相同的电导变化。在肽能EPSC期间,在一系列膜电位范围内测试的25个神经元中的每一个中,毒蕈碱EPSC减少。外源性促黄体激素释放激素(LHRH)产生的电流具有相同的电压依赖性和电导变化的神经诱发的肽能EPSC在每个测试的15个细胞。氨甲酰胆碱,一种毒蕈碱激动剂,和LHRH产生的电流具有相同的电压依赖性和电导的变化,在每一个研究的12个细胞。在几个细胞中,对长时间应用LHRH的饱和反应完全阻断了对氨甲胆碱的反应,反之亦然。慢电流记录从解离的细胞体在响应于氨甲酰胆碱和LHRH,这些反应表现出相同的多样性的电压依赖性和电导的变化,在完整的神经节中观察到的。毒蕈碱受体和肽能受体的激活可以控制单个神经节细胞中共享的离子机制。
A single-electrode voltage clamp was used to study the slow muscarinic and late slow peptidergic excitatory post-synaptic currents (EPSC) in B cells of the paravertebral sympathetic ganglia of the bull-frog [Rana catesbeiana]. Conductance decreases were measured during peptidergic EPSC in nearly all cells at clamped potentials near the resting level. In .apprx. 1/2 of the cells the size of the peptidergic EPSC increased with hyperpolarization and in some of these cells conductance increases were found at hyperpolarized levels. In the remaining cells conductance decreases occurred at all levels of membrane potential tested, and in a few of these the polarity of the EPSC reversed at hyperpolarized potentials. A similar diversity was observed among muscarinic EPSC. At least 2 simple ionic mechanisms are required to explain the heterogeneous voltage dependencies observed: a conductance decrease primarily to K+ that dominates at depolarized potentials and a conductance increase to other ions that is more prominent at hyperpolarized potentials. The proportion of these 2 mechanisms appears to differ among B cells. The 2 slow EPSC recorded in the same neuron had the same voltage dependence and were accompanied by the same conductance changes in each of 8 cells despite differences between cells. The muscarinic EPSC was reduced during the peptidergic EPSC in each of 25 neurons tested over a range of membrane potentials. Externally-applied luteinizing hormone releasing hormone (LHRH) produced currents with the same voltage dependence and conductance changes as the nerve-evoked peptidergic EPSC in each of 15 cells tested. Bethanechol, a muscarinic agonist, and LHRH produced currents with the same voltage dependence and conductance changes in each of the 12 cells studied. In several cells a saturating response to a prolonged application of LHRH completely occluded the response to bethanechol, and vice versa. Slow currents were recorded from dissociated cell bodies in response to bethanechol and LHRH; these responses exhibited the same diversity of voltage dependence and conductance changes as was observed in intact ganglia. Activation of muscarinic and peptidergic receptors may control shared ionic mechanisms in single ganglion cells.