G protein signaling in a neuronal network is necessary for rhythmic motor pattern production
G protein signaling in a neuronal network is necessary for rhythmic motor pattern production
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DOI：
10.1152/jn.00765.2002
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发表时间：
2003-02-01
影响因子：
2.5
通讯作者：
Katz, PS
中科院分区：
文献类型：
--
作者：
Clemens, S;Katz, PS
G蛋白偶联受体被广泛认为在介导外源性神经调节输入到运动网络的行为中起重要作用。然而，它们直接参与有节奏运动模式产生的潜力却很少受到关注。本研究的结果表明，G蛋白信号传导似乎是软体动物Tritonia diomedea逃避游泳的核心模式发生器（CPG）运作的组成部分。通过胞内离子导入鸟嘌呤核苷酸类似物鸟嘌呤5′- o -（2-硫代二磷酸）（gdp - β - s），阻断单个CPG神经元（大脑神经元C2）中的G蛋白信号传导，可阻止游泳运动程序的产生。此外，通过离子导入GTP类似物鸟苷5′- o -（3-硫代三磷酸）（GTP- γ - s）和5′-鸟酰亚胺二磷酸对该神经元G蛋白信号传导的强直性激活也抑制了运动模式的产生。对这些鸟嘌呤核苷酸类似物的可能作用位点进行了检查，以评估它们干扰运动模式产生的潜在机制。胞内gdp - β - s离子导入C2不影响C2基底突触强度。然而，它确实降低了背游中间神经元（DSIs）（一组血清素能游泳CPG神经元）引起的C2突触异突触易化。相比之下，gtp - γ - s直接增强C2突触强度到DFN上，模仿dsi的神经调节作用。GTP类似物抑制了C2的兴奋性，而GTP类似物抑制了DSI刺激增加C2兴奋性的能力，而GTP类似物抑制了C2兴奋性。gdp - β - s引起的C2兴奋性下降不太可能是抑制游泳运动模式的原因，因为通过注入超极化电流降低C2放电率并不能阻止节律运动模式的产生。综上所述，这些数据表明G蛋白信号是Tritonia逃避游泳CPG的必要组成部分，G蛋白信号介导DSI对C2的异突触促进，但可能不介导DSI引起的C2兴奋性增强。
G protein-coupled receptors are widely recognized as playing important roles in mediating the actions of extrinsic neuromodulatory inputs to motor networks. However, the potential for their direct involvement in rhythmic motor pattern generation has received considerably less attention. Results from this study indicate that G protein signaling appears to be integral to the operation of the central pattern generator (CPG) underlying the escape swim of the mollusk Tritonia diomedea. Blocking G protein signaling in a single CPG neuron, cerebral neuron C2, with intracellular iontophoresis of the guanine nucleotide analogue guanosine 5'-O-(2-thiodiphosphate) (GDP-beta-S), prevented the production of the swim motor program. Moreover, tonic activation of G protein signaling in this neuron by iontophoresis of the GTP analogues guanosine 5'-O-(3-thiotriphosphate) (GTP-gamma-S) and 5'-guanylyl-imidodiphosphate also inhibited motor pattern production. The possible sites of action of these guanine nucleotide analogues were examined to assess potential mechanisms by which they interfered with motor pattern production. Intracellular iontophoresis of GDP-beta-S into C2 did not affect C2 basal synaptic strength. However, it did reduce heterosynaptic facilitation of C2 synapses caused by the dorsal swim interneurons (DSIs), a set of serotonergic swim CPG neurons. In contrast, GTP-gamma-S directly enhanced C2 synaptic strength onto DFN, mimicking the neuromodulatory effect of the DSIs. GDP-beta-S, but not the GTP analogues, decreased C2 excitability, whereas both GTP analogues, but not GDP-beta-S, blocked the ability of DSI stimulation to increase C2 excitability. The decrease in C2 excitability caused by GDP-beta-S is not likely to be responsible for the inhibition of the swim motor pattern because decreasing C2 firing rate, by injecting hyperpolarizing current, did not prevent the production of the rhythmic motor pattern. Taken together, these data suggest that G protein signaling is a necessary and integral component of the escape swim CPG in Tritonia and that G protein signaling mediates DSI heterosynaptic facilitation of C2 but may not mediate the DSI-evoked enhancement of C2 excitability.