Hormonal modulation of sensorimotor integration.
Hormonal modulation of sensorimotor integration.
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DOI：
10.1523/jneurosci.5533-09.2010
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发表时间：
2010-02-17
期刊：
影响因子：
--
通讯作者：
Nusbaum MP
中科院分区：
文献类型：
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作者：
DeLong ND;Nusbaum MP
神经元回路通常从下行、上行和荷尔蒙系统同时接受输入。然而，到目前为止，大多数这样的输入都是单独研究的，以确定它们对给定电路的影响。在此，我们研究了激素甲壳动物心脏活性多肽(CCAP)和胃幽门受体(GPR)本体感受器神经元在由投射神经元MCN1(调制连合神经元1)驱动的双相胃磨(咀嚼)节律中的整合作用。在对照生理盐水中，GPR刺激通过突触前抑制MCN1选择性地延长胃磨机牵引器阶段。在没有GPR刺激的情况下，CCAP不改变牵拉持续时间，并适度延长牵拉。在这里，我们使用计算模型和动态钳制操作显示，CCAP的存在减弱或消除了GPR对胃磨机节律的影响。这种CCAP作用的结果是，它能够激活胃磨回路神经元胃外侧(LG)中与MCN1相同的调制器激活的电导(GMI)。由于GPR通过削弱LG中GMI的MCN1激活来延长收缩，CCAP对GMI的平行激活减少了GPR调节这一电导的影响。CCAP激活的GMI因此抵消了GPR介导的由MCN1激活的LG GMI的减少，并降低了GPR调节胃磨节律的能力。因此，尽管CCAP既不改变MCN1的收缩持续时间，也不改变GPR对MCN1的抑制，但它激活了关键下游回路神经元中由调制器激活的电导，使CCAP能够减弱或消除对运动回路输出的感觉调节。
Neuronal circuits commonly receive simultaneous inputs from descending, ascending and hormonal systems. Thus far, however, most such inputs have been studied individually to determine their influence on a given circuit. Here, we examine the integrated action of the hormone crustacean cardioactive peptide (CCAP) and the gastropyloric receptor (GPR) proprioceptor neuron on the biphasic gastric mill (chewing) rhythm driven by the projection neuron MCN1 (modulatory commissural neuron 1) in the isolated crab stomatogastric ganglion. In control saline, GPR stimulation selectively prolongs the gastric mill retractor phase, via presynaptic inhibition of MCN1. In the absence of GPR stimulation, CCAP does not alter retraction duration and modestly prolongs protraction. Here we show, using computational modeling and dynamic clamp manipulations, that the presence of CCAP weakens or eliminates the GPR effect on the gastric mill rhythm. This CCAP action results from its ability to activate the same modulator-activated conductance (GMI) as MCN1 in the gastric mill circuit neuron lateral gastric (LG). Because GPR prolongs retraction by weakening MCN1 activation of GMI in LG, the parallel GMI activation by CCAP reduces the impact of GPR regulation of this conductance. The CCAP-activated GMI thus counteracts the GPR-mediated decrease in the MCN1-activated GMI in LG and reduces the GPR ability to regulate the gastric mill rhythm. Consequently, although CCAP neither changes retraction duration nor alters GPR inhibition of MCN1, its activation of a modulator-activated conductance in a pivotal downstream circuit neuron enables CCAP to weaken or eliminate sensory regulation of motor circuit output.