Sodium-mediated plateau potentials in an identified decisional neuron contribute to feeding-related motor pattern genesis in Aplysia.

IF 3.4 3区 医学 Q2 NEUROSCIENCES
Alexis Bédécarrats, John Simmers, Romuald Nargeot
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Abstract

Motivated behaviors such as feeding depend on the functional properties of decision neurons to provide the flexibility required for behavioral adaptation. Here, we analyzed the ionic basis of the endogenous membrane properties of an identified decision neuron (B63) that drive radula biting cycles underlying food-seeking behavior in Aplysia. Each spontaneous bite cycle arises from the irregular triggering of a plateau-like potential and resultant bursting by rhythmic subthreshold oscillations in B63's membrane potential. In isolated buccal ganglion preparations, and after synaptic isolation, the expression of B63's plateau potentials persisted after removal of extracellular calcium, but was completely suppressed in a tetrodotoxin (TTX)- containing bath solution, thereby indicating the contribution of a transmembrane Na+ influx. Potassium outward efflux through tetraethylammonium (TEA)- and calcium-sensitive channels was found to contribute to each plateau's active termination. This intrinsic plateauing capability, in contrast to B63's membrane potential oscillation, was blocked by the calcium-activated non-specific cationic current (ICAN) blocker flufenamic acid (FFA). Conversely, the SERCA blocker cyclopianozic acid (CPA), which abolished the neuron's oscillation, did not prevent the expression of experimentally evoked plateau potentials. These results therefore indicate that the dynamic properties of the decision neuron B63 rely on two distinct mechanisms involving different sub-populations of ionic conductances.

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钠介导的高原电位在一个确定的决策神经元有助于进食相关的运动模式的发生在澳大利亚。
进食等动机行为依赖于决策神经元的功能特性,以提供行为适应所需的灵活性。在这里,我们分析了一个已确定的决策神经元(B63)的内源性膜特性的离子基础,该决策神经元驱动radula咬循环,在澳大利亚寻找食物的行为。每个自发的咬循环都是由不规则的高原电位触发和B63膜电位阈下振荡的节律性破裂引起的。在分离的颊神经节制剂中,在突触分离后,B63平台电位的表达在去除细胞外钙后仍然存在,但在含河豚毒素(TTX)的浴液中被完全抑制,从而表明跨膜Na+内流的贡献。钾通过四乙基铵(TEA)和钙敏感通道向外流出,导致了每个高原的主动终止。与B63的膜电位振荡相反,这种固有的稳定能力被钙激活的非特异性阳离子电流(ICAN)阻滞剂氟芬那酸(FFA)阻断。相反,SERCA阻滞剂环吡肟酸(CPA)虽然可以消除神经元的振荡,但并不能阻止实验诱发的平台电位的表达。因此,这些结果表明,决策神经元B63的动态特性依赖于涉及不同亚群离子电导的两种不同机制。
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来源期刊
CiteScore
6.00
自引率
5.70%
发文量
135
审稿时长
4-8 weeks
期刊介绍: Frontiers in Neural Circuits publishes rigorously peer-reviewed research on the emergent properties of neural circuits - the elementary modules of the brain. Specialty Chief Editors Takao K. Hensch and Edward Ruthazer at Harvard University and McGill University respectively, are supported by an outstanding Editorial Board of international experts. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics and the public worldwide. Frontiers in Neural Circuits launched in 2011 with great success and remains a "central watering hole" for research in neural circuits, serving the community worldwide to share data, ideas and inspiration. Articles revealing the anatomy, physiology, development or function of any neural circuitry in any species (from sponges to humans) are welcome. Our common thread seeks the computational strategies used by different circuits to link their structure with function (perceptual, motor, or internal), the general rules by which they operate, and how their particular designs lead to the emergence of complex properties and behaviors. Submissions focused on synaptic, cellular and connectivity principles in neural microcircuits using multidisciplinary approaches, especially newer molecular, developmental and genetic tools, are encouraged. Studies with an evolutionary perspective to better understand how circuit design and capabilities evolved to produce progressively more complex properties and behaviors are especially welcome. The journal is further interested in research revealing how plasticity shapes the structural and functional architecture of neural circuits.
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