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Synaptic plasticity in the molluscan peripheral nervous system: physiology and role for peptides

机译:软体动物外周神经系统中的突触可塑性:肽的生理和作用

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摘要

The plasticity of a synapse in the molluscan peripheral nervous system was examined under a variety of experimental, physiological, and pharmacological conditions. These studies employed the isolated salivary glands and attached buccal ganglia of the freshwater snail Helisoma. Action potentials evoked in buccal neuron 4 normally evoke a large excitatory postsynaptic potential (EPSP) which drives an action potential in gland secretory cells. In order to measure modulation of the EPSP, action potential generation in gland cells was prevented by bathing the preparation in low calcium, high magnesium salines. The relationship between the gland EPSP amplitude and specific physiological properties of neuron 4 was analyzed. In common with some central molluscan synapses, the EPSP was found to be strongly influenced by the membrane potential of neuron 4. Specifically, its amplitude was reduced by hyperpolarization of the neuron 4 soma. The relationship between EPSP amplitude and somatic potential of neuron 4 was linear in the range from resting potential (-47 +/- 6mV) to -100 mV. Furthermore, the EPSP amplitude was directly proportional to the action potential half-width of neuron 4. In order to evaluate the possible physiological role of this action potential/EPSP relationship, we examined whether gland EPSPs are modulated during the spike broadening that occurs in both spontaneous burst activity and imposed impulse trains. The preceding action potential/EPSP relationship was maintained under both of these conditions, i.e., EPSP magnitude increased as spikes broadened during bursts or trains. The peptidergic modulation of neuroglandular transmission was also examined. The molluscan peptide SCPB was found to depolarize neuron 4 and an increase in EPSP amplitude was concomitantly observed.(ABSTRACT TRUNCATED AT 250 WORDS)
机译:在各种实验,生理和药理条件下检查了软体动物外周神经系统中突触的可塑性。这些研究采用了淡水蜗牛Helisoma的孤立唾液腺和颊神经节。颊神经元4诱发的动作电位通常会引起大的兴奋性突触后电位(EPSP),从而驱动腺体分泌细胞的动作电位。为了测量EPSP的调节,通过将制剂浸入低钙,高镁盐溶液中来防止腺体细胞中动作电位的产生。分析了腺EPSP振幅与神经元4特定生理特性之间的关系。与某些中央软体动物突触相同,发现EPSP受神经元4的膜电位的强烈影响。特别是,其振幅由于神经元4体的超极化而降低。 EPSP振幅与神经元4的体细胞电位之间的关系在静息电位(-47 +/- 6mV)至-100 mV的范围内呈线性关系。此外,EPSP振幅与神经元4的动作电位半宽成正比。为了评估该动作电位/ EPSP关系的可能的生理作用,我们检查了腺体EPSPs是否在两个峰发生的尖峰加宽过程中被调节自发爆发活动并施加冲动火车。在这两个条件下都保持了先前的动作电位/ EPSP关系,即,在爆发或训练期间,随着尖峰变宽,EPSP幅度增加。还检查了神经腺传递的肽能调节。发现软体动物肽SCPB使神经元4脱极化,并同时观察到EPSP振幅增加。(摘要截断为250字)

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