Activity-dependent peptidergic modulation of the plateau-generating neuron B64 in the feeding network of Aplysia

Activity-dependent peptidergic modulation of the plateau-generating neuron B64 in the feeding network of Aplysia
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DOI:
10.1152/jn.01230.2006
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发表时间:
2007-02-01
影响因子:
2.5
通讯作者:
Weiss, Klaudiusz R.
Weiss, Klaudiusz R.
中科院分区:
医学3区
文献类型:
--
作者:
Koh, Hae-Young;Weiss, Klaudiusz R.

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许多行为表现出各种形式的活动依赖性可塑性。这种可塑性的一个例子是,当反复引发进食反应时,海兔进食反应的延长期持续时间会逐渐缩短。当通过长时间刺激命令样神经元CBI-2引起进食样运动程序时,在孤立的神经节中观察到类似的延长持续时间缩短。在这里,我们调查的细胞机制,可能是这种活动依赖性的缩短延长持续时间的喂养电机程序的基础。CBI-2含有两种神经肽,CP 2和FCAP。先前的工作表明,CP 2缩短了CBI-2引起的程序的延长持续时间。我们在这里表明,同样的情况也适用于FCAP。我们还表明,CP 2和FCAP调制的高原生成神经元,B64的生物物理特性,这起着重要的作用,在终止延长阶段的喂养运动程序。我们发现,预刺激的CBI-2,以及灌流的CP 2和FCAP,降低了阈值激活的平台电位在B64。CBI-2预刺激的阈值降低作用被FCAP和CP 2灌流阻断。此外,在升高的温度下,在这种条件下,肽释放被阻止在失智症,预刺激CBI-2不降低平台电位阈值,而灌流的CP 2和FCAP。我们的研究结果是一致的假设,从CBI-2释放的肽降低激活的平台电位在B64的阈值,从而有助于缩短延长持续时间时,CBI-2被反复激活。
Many behaviors display various forms of activity-dependent plasticity. An example of such plasticity is the progressive shortening of the duration of protraction phase of feeding responses of Aplysia that occurs when feeding responses are repeatedly elicited. A similar protraction-duration shortening is observed in isolated ganglia of Aplysia when feeding-like motor programs are elicited through a prolonged stimulation of the command-like neuron CBI-2. Here, we investigate a cellular mechanism that may underlie this activity-dependent shortening of protraction duration of feeding motor programs. CBI-2 contains two neuropeptides, CP2 and FCAP. Previous work showed that CP2 shortens protraction duration of CBI-2 elicited programs. We show here that the same is true for FCAP. We also show that both CP2 and FCAP modulated the biophysical properties of a plateau-generating neuron, B64, that plays an important role in terminating the protraction phase of feeding motor programs. We find that prestimulation of CBI-2, as well as superfusion of CP2 and FCAP, lowered the threshold for activation of the plateau potential in B64. The threshold-lowering actions of CBI-2 prestimulation were occluded by superfusion of FCAP and CP2. Furthermore, at elevated temperature, conditions under which peptide release is prevented in Aplysia, prestimulation of CBI-2 does not lower the plateaupotential-threshold, whereas superfusion of CP2 and FCAP does. Our findings are consistent with the hypothesis that peptides released from CBI-2 lower the threshold for activation of plateau potential in B64, thereby contributing to the shortening of protraction duration when CBI-2 is repeatedly activated.