Control of locomotion in marine mollusc Clione limacina

Control of locomotion in marine mollusc Clione limacina
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海洋软体动物 Clione limacina 的运动控制

DOI:
10.1007/bf00235652
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发表时间:
2004
影响因子:
2
通讯作者:
Lyudmila B. Popova
Lyudmila B. Popova
中科院分区:
医学4区
文献类型:
--
作者:
Arshavsky YuI;T. Deliagina;G. Orlovsky;Panchin YuV;Pavlova Ga;Lyudmila B. Popova

文献摘要

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在先前对翼足类软体动物Clionelimacina的离体足神经节进行的工作中,我们描述了神经元元件(12型神经元)的活动,并研究了其在运动节律产生中的作用(Arshavasky等,1985 d)。正如我们后来了解到的那样,活动是从通过足神经节的神经元轴突记录下来的,而神经元索马位于胸膜神经节中,因此在足神经节分离过程中被切断。因此,有必要通过减少中枢神经系统的制备来重新研究这种神经元的特性及其在运动节律产生中的作用。获得了以下结果。(1)每个胸膜神经节仅包含一个这种类型的神经元,因此该细胞被认为是所识别的神经元。神经元的轴突通过侧足连接到达足神经节。然后轴突分成两个分支,终止于两个足神经节的外侧区域。来自左侧和右侧胸膜神经节的神经元12彼此没有直接连接;它们在运动周期中的同步操作由共同的输入确定。(2)完整的神经元12和没有索马的神经元的电特性大致相同。在任一种情况下,神经元产生“平台”电位,即,它可以在去极化状态下持续很长时间。平台电位可由去极化电流脉冲或EPSP诱导,并由超极化电流或IPSP终止。在平台电位产生期间,神经元输入电阻下降约两倍。(3)记录在胸膜神经节的神经元12表明,其活动在“虚构的游泳”并没有不同的somadeprived轴突记录在孤立的足神经节。神经元在运动周期的V相产生平台电位(Arshavsky等,1985 b)。该电位由8d亚群足神经元诱发的EPSP触发。在第7组神经元诱发的IPSP的影响下,平台电位终止于D相。神经元12对足神经节中运动发生器的其它神经元元件的影响也不依赖于细胞索马的存在。(4)当正常周期与某些神经元组的活动受到抑制的减少周期交替时,足神经节运动发生器有时会产生“异常节律”。来自两个神经元12的同时记录表明,交替节律的产生是由其中一个神经元12的异常行为引起的:神经元在去极化状态下持续一个半周期而不是半个周期,如在运动发电机的正常操作期间。
SummaryIn previous work carried out on the isolated pedal ganglia of the pteropod mollusc Clione limacina we described the activity of a neuronal element (type 12 neuron) and looked into its role in the locomotor rhythm generation (Arshavasky et al. 1985d). As we learned subsequently, the activity was recorded from the neuron axon passing in the pedal ganglia, while the neuron soma was located in the pleural ganglia and consequently was cut off in the course of pedal ganglia isolation. It thus became necessary to reinvestigate the properties of this neuron and its role in locomotory rhythm generation by using less reduced preparation of the central nervous system. The following results were obtained. (1) Each pleural ganglion contains only one neuron of this type, this cell is thus to be considered as the identified neuron. The neuron's axon reaches into the pedal ganglion via the pleuro-pedal connective. Then the axon divides into two branches terminating in the lateral regions of both pedal ganglia. The neurons 12 from the left and right pleural ganglia have no direct connections with one another; their synchronous operation in the locomotor cycle is determined by common inputs. (2) The electrical properties of an intact neuron 12 and one without a soma are about the same. In either case the neuron generates “plateau” potentials, i.e., it may persist for a long time in the depolarized state. Plateau potentials can be induced by a depolarizing current pulse or by an EPSP, and terminated by hyperpolarizing current or by an IPSP. The neuron input resistance drops about twofold during generation of the plateau potential. (3) Recording of the neuron 12 in the pleural ganglia showed that its activity during “fictive swimming” does not differ from that of somadeprived axon recorded in the isolated pedal ganglia. The neuron generates a plateau potential in the V-phase of the locomotor cycle (definitions for the phases of the cycle were given in Arshavsky et al. 1985b). This potential is triggered by an EPSP evoked by subgroup 8d pedal neurons. The plateau potential terminates in the D-phase under the influence of an IPSP evoked by group 7 neurons. The effects of the neuron 12 on other neuronal elements of the locomotor generator in pedal ganglia do not depend on the presence of the cell soma either. (4) The pedal ganglia locomotor generator sometimes generates an “anomalous rhythm” when normal cycles alternate with reduced ones in which the activity of some groups of neurons is inhibited. Simultaneous recording from two neurons 12 demonstrated that the alternating rhythm generation was caused by the anomalous behaviour of one of the neurons 12: the neuron persisted in the depolarized state for one cycle and a half and not for half a cycle, as during the normal operation of the locomotor generator.