Neural control of muscle movements in feeding behavior

进食行为中肌肉运动的神经控制

基本信息

  • 批准号:
    06671860
  • 负责人:
  • 金额:
    $ 1.41万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
  • 财政年份:
    1994
  • 资助国家:
    日本
  • 起止时间:
    1994 至 1995
  • 项目状态:
    已结题

项目摘要

Major goal of our research is to know the neural mechanism generating feeding behavior in Aplysia which has simple nervous system. Jaw-closing (JC) muscle in a specific portion is doubly innervated by excitatory (JC) and inhibitory motor neurons (MAl) , which release glutamate (Glu) and acetylcholine (ACh) , respectively. On the other hand, redula-closer (ARC) muscle is innervated by cholinergic excitatory motor neurons. The purpose of this research is to know the characteristics the receptor and channels producing junction potentials, and also the modulatory mechanism of their function by central neurons. The muscle fibers were dissociated by using papain, and whole-cell patch clamp was performed on isolated single muscle cells to study the ionic mechanism associated with ACh or Glu reception. Iontophoretically applied ACh hyperpolarized the JC muscle cells while applied Glu depolarized the same cells, suggesting that ACh and Glu receptors coexist on the membrane of the single cell in the JC muscle. The experiments with different cation and anion compositions in the pipette solution showed that ACh-induced response in the JC muscle cells is caused by Cl^- currents while the response in the ARC muscle cells is cause by Na^+ and partly K^+ currents. These results suggest that the ACh receptors associated with a Cl^- channel in the JC muscle cells, and with a cation channel permeable to both Na+ and K+ in the ARC muscle cells. The effects of peptides (FMRF,Myomodulin A,SCP_A) widely found in Aplysia neurons and muscles on the inhibitory junction potentials (IJPs) were also explored. Application of these peptides reduced the size of IJPs produced in the JC muscle fibers by the MAl firing. In the whole cell clamp experiments, FMRF reduced Cl^- current induced by ACh application, suggesting that FMRF can modulate the function of ACh receptor channels.
本研究的主要目的是了解具有简单神经系统的食饵类动物产生摄食行为的神经机制。特定部位的下颌闭合(JC)肌肉由兴奋性(JC)和抑制性运动神经元(MAl)双重支配,其分别释放谷氨酸(Glu)和乙酰胆碱(ACh)。另一方面,红核关闭肌(ARC)由胆碱能兴奋性运动神经元支配。本研究的目的是了解产生连接电位的受体和通道的特性,以及中枢神经元对它们功能的调节机制。用木瓜蛋白酶分离肌纤维,在分离的单个肌细胞上进行全细胞膜片钳,以研究与ACh或Glu接收相关的离子机制。离子电渗应用ACh超极化JC肌细胞,而应用Glu去极化相同的细胞,这表明ACh和Glu受体共存于JC肌的单细胞膜上。用不同阳离子和阴离子组成的移液管溶液进行的实验表明,JC肌细胞中ACh诱导的反应是由Cl^-电流引起的,而ARC肌细胞中ACh诱导的反应是由Na^+和部分K^+电流引起的。这些结果表明,ACh受体与JC肌细胞中的Cl^-通道相关,与ARC肌细胞中的Na+和K+都可渗透的阳离子通道相关。本研究还探讨了广泛存在于脊髓神经元和肌肉中的肽(FMRF、Myomodulin A、SCP_A)对抑制性连接电位(IJPs)的影响。这些肽的应用降低了通过MAl放电在JC肌纤维中产生的IJP的大小。在全细胞钳夹实验中,FMRF可降低ACh诱导的Cl^-电流,提示FMRF可调节ACh受体通道的功能。

项目成果

期刊论文数量(30)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
T.Nagahama: "Ionic basis of acetylcholine-induced currents mediating hyperpolarization of Aplysia jaw-closing muscles." The Japanese Journal of Physiology. 43(S). S169 (1993)
T.Nagahama:“乙酰胆碱诱导电流介导海兔下颌闭合肌超极化的离子基础。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
T.Nagahama: "Acetylcholine-activated chloride channels produce an inhibitory junction potential in buccal muscle cells of Aplysia." Proceedings of the Royal Society of London Series B. 254. 275-280 (1993)
T.Nagahama:“乙酰胆碱激活的氯离子通道在海兔颊肌细胞中产生抑制性连接电位。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
I.Inoue: "Cl^- channels as a cholinergic ACh receptor responsible for generation of inhibitory junction potential in Aplysia buccal muscle cells." The Japanese Journal of Physiology. 44. S149-S155 (1994)
I.Inoue:“Cl^- 通道作为胆碱能 ACh 受体,负责在海兔颊肌细胞中产生抑制性连接电位。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
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NAGAHAMA Tatsumi其他文献

NAGAHAMA Tatsumi的其他文献

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{{ truncateString('NAGAHAMA Tatsumi', 18)}}的其他基金

Study on functional roles of a single neuron in animal behaviors by functional transplant of channel rhodopsin 2
视紫红质2通道功能移植研究单个神经元在动物行为中的功能作用
  • 批准号:
    21570082
  • 财政年份:
    2009
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
ACh recognition and modulation of the inhibitory nicotinic ACh receptor
抑制性烟碱 ACh 受体的 ACh 识别和调节
  • 批准号:
    08680723
  • 财政年份:
    1996
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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