Satterlie R A, Norekian T P
Department of Zoology, Arizona State University, Tempe 85287-1501, USA.
J Exp Biol. 1995 Apr;198(Pt 4):917-30. doi: 10.1242/jeb.198.4.917.
Swim acceleration in Clione limacina can occur via central inputs to pattern generator interneurons and motor neurons and through peripheral inputs to the swim musculature. In the previous paper, peripheral modulation of the swim muscles was shown to increase wing contractility. In the present paper, central inputs are described that trigger an increase in swim frequency and an increase in motor neuron activity. In dissected preparations, spontaneous acceleration from slow to fast swimming included an increase in the cycle frequency, a baseline depolarization in the swim interneurons and an increase in the intensity of motoneuron firing. Similar effects could be elicited by bath application of 10(-5) mol l-1 serotonin. Two clusters of cerebral serotonin-immunoreactive interneurons were found to produce acceleration of swimming accompanied by changes in neuronal activity. Posterior cluster neurons triggered an increase in swim frequency, depolarization of the swim interneurons, an increase in general excitor motoneuron activity and activation of type 12 interneurons and pedal peripheral modulatory neurons. Cells from the anterior cerebral cluster also increased swim frequency, increased activity in the swim motoneurons and activated type 12 interneurons, pedal peripheral modulatory neurons and the heart excitor neuron. The time course of action of the anterior cluster neurons did not greatly outlast the duration of spike activity, while that of the posterior cluster neurons typically outlasted burst duration. It appears that the two discrete clusters of serotonin-immunoreactive neurons have similar, but not identical, effects on swim neurons, raising the possibility that the two serotonergic cell groups modulate the same target cells through different cellular mechanisms.
海若螺的游泳加速可通过对模式发生器中间神经元和运动神经元的中枢输入以及对游泳肌肉组织的外周输入来实现。在前一篇论文中，已表明游泳肌肉的外周调节可增加翅膀收缩力。在本文中，描述了引发游泳频率增加和运动神经元活动增强的中枢输入。在解剖制备中，从慢速游泳到快速游泳的自发加速包括周期频率增加、游泳中间神经元的基线去极化以及运动神经元放电强度增加。通过在浴液中施加10(-5) mol l-1血清素可引发类似效果。发现两簇脑血清素免疫反应性中间神经元可产生游泳加速并伴有神经元活动变化。后簇神经元引发游泳频率增加、游泳中间神经元去极化、一般兴奋性运动神经元活动增加以及12型中间神经元和足周缘调节神经元激活。前脑簇的细胞也增加游泳频率、增加游泳运动神经元活动并激活12型中间神经元、足周缘调节神经元和心脏兴奋性神经元。前簇神经元的作用时程并不比动作电位活动的持续时间长得多，而后簇神经元的作用时程通常比爆发持续时间长得多。看来这两簇血清素免疫反应性神经元对游泳神经元有相似但不完全相同的作用，这增加了两个血清素能细胞群通过不同细胞机制调节相同靶细胞的可能性。
