Pharmacological characterization of ionic currents that regulate high-frequency spontaneous activity of electromotor neurons in the weakly electric fish, Apteronotus leptorhynchus.
Pharmacological characterization of ionic currents that regulate high-frequency spontaneous activity of electromotor neurons in the weakly electric fish, Apteronotus leptorhynchus.
复制标题
调节弱电鱼 Apteronotus leptorhynchus 电动神经元高频自发活动的离子电流的药理学特征。
DOI：
10.1002/neu.20202
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Smith,GTroy
中科院分区：
文献类型：
--
作者：
Smith,GTroy
控制褐鬼刀鱼（Apteronotus leptorhynchus）器官放电（EOD）的神经回路包含两个自发振荡器。髓质中的起搏神经元和脊髓中的电动神经元 (EMN) 都会以 500-1000 Hz 的频率自发放电来控制 EOD。这些神经元继续以与体内 EOD 频率高度相关的频率在体外放电。先前的研究使用通道阻断药物来药理学表征控制起搏神经元高频放电的离子电流。本研究的目标是使用类似的技术来研究 EMN 中的离子电流，EMN 是电动机回路中另一种类型的自发活动神经元。与起搏器神经元一样，EMN 的高频放电主要受河豚毒素敏感的钠电流和对 4-氨基吡啶和 κA-芋螺毒素 SIVA 敏感但对四乙铵具有抗性的钾电流调节。然而，EMN 与起搏神经元的不同之处在于它们对某些通道阻断药物的敏感性。 α-树突毒素可阻断 Kv1 钾通道的子集，增加 EMN 的放电率，但不会增加起搏神经元的放电率；钠通道阻滞剂 μO-芋螺毒素 MrVIA 可降低起搏神经元的放电率，但对 EMN 没有影响。这些结果表明，类似但不相同的离子电流调节 EMN 和起搏神经元的高频放电。起搏神经元和 EMN 中表达的离子电流的差异可能与这两种细胞类型的形态、连接性或功能的差异有关。 © 2005 Wiley periodicals, Inc. J Neurobiol，2006
The neural circuit that controls the electric organ discharge (EOD) of the brown ghost knifefish (Apteronotus leptorhynchus) contains two spontaneous oscillators. Both pacemaker neurons in the medulla and electromotor neurons (EMNs) in the spinal cord fire spontaneously at frequencies of 500–1000 Hz to control the EOD. These neurons continue to firein vitroat frequencies that are highly correlated within vivoEOD frequency. Previous studies used channel blocking drugs to pharmacologically characterize ionic currents that control high‐frequency firing in pacemaker neurons. The goal of the present study was to use similar techniques to investigate ionic currents in EMNs, the other type of spontaneously active neuron in the electromotor circuit. As in pacemaker neurons, high‐frequency firing of EMNs was regulated primarily by tetrodotoxin‐sensitive sodium currents and by potassium currents that were sensitive to 4‐aminopyridine and κA‐conotoxin SIVA, but resistant to tetraethylammonium. EMNs, however, differed from pacemaker neurons in their sensitivity to some channel blocking drugs. Alpha‐dendrotoxin, which blocks a subset of Kv1 potassium channels, increased firing rates in EMNs, but not pacemaker neurons; and the sodium channel blocker μO‐conotoxin MrVIA, which reduced firing rates of pacemaker neurons, had no effect on EMNs. These results suggest that similar, but not identical, ionic currents regulate high‐frequency firing in EMNs and pacemaker neurons. The differences in the ionic currents expressed in pacemaker neurons and EMNs might be related to differences in the morphology, connectivity, or function of these two cell types. © 2005 Wiley Periodicals, Inc. J Neurobiol, 2006