Weimann J M, Skiebe P, Heinzel H G, Soto C, Kopell N, Jorge-Rivera J C, Marder E
Department of Biology, Brandeis University, Waltham, Massachusetts 02254, USA.
J Neurosci. 1997 Mar 1;17(5):1748-60. doi: 10.1523/JNEUROSCI.17-05-01748.1997.
The modulation of the pyloric rhythm of the stomatogastric ganglion of the crab, Cancer borealis, by crustacean cardioactive peptide (CCAP) is described. CCAP activated pyloric rhythms in most silent preparations, and altered the phase relationships of pyloric motor neuron firing in all preparations. In CCAP, the pyloric rhythms were characterized by long lateral pyloric (LP) neuron bursts of action potentials. The threshold for CCAP action was approximately 10(-10) M, with increasing effects at higher CCAP concentrations. The changes in motor pattern evoked by CCAP produced significant changes in LP-innervated muscle movement. These movements were additionally potentiated by CCAP applications to isolated nerve-muscle preparations. Thus, enhanced motor neuron firing and increase of the gain of the neuromuscular junctions are likely to operate coordinately in response to hormonally released CCAP. High CCAP concentrations sometimes resulted in modification of the normal 1:1 alternation between the pyloric dilator (PD) and LP neurons to patterns of 2:1, 3:1, or 4:1 alternation. CCAP seems to activate slow intrinsic oscillations in the LP neuron, as well as enhance faster oscillations in the pacemaker group of PD/anterior burster (AB) neurons. Simulations of fast and slow oscillators with reciprocal inhibitory coupling suggest mechanisms that could account for the mode switch from 1:1 alternation to multiple PD bursts alternating with one LP neuron burst.
本文描述了甲壳类动物心脏活性肽(CCAP)对北方黄道蟹口胃神经节幽门节律的调节作用。CCAP在大多数静止的标本中激活了幽门节律,并改变了所有标本中幽门运动神经元放电的相位关系。在CCAP作用下,幽门节律的特征是外侧幽门(LP)神经元动作电位的长时间爆发。CCAP作用的阈值约为10^(-10) M,随着CCAP浓度的升高,作用效果增强。CCAP诱发的运动模式变化导致LP支配的肌肉运动发生显著改变。在分离的神经肌肉标本中应用CCAP,这些运动进一步增强。因此,运动神经元放电增强和神经肌肉接头增益增加可能协同作用以响应激素释放的CCAP。高浓度的CCAP有时会导致幽门扩张肌(PD)和LP神经元之间正常的1:1交替模式改变为2:1、3:1或4:1交替模式。CCAP似乎激活了LP神经元中的缓慢内在振荡,同时增强了PD/前爆发神经元起搏器组中的较快振荡。对具有相互抑制耦合的快速和慢速振荡器的模拟表明了一些机制,这些机制可以解释从1:1交替模式到多个PD爆发与一个LP神经元爆发交替模式的转换。