Evans Colin G, Jing Jian, Rosen Steven C, Cropper Elizabeth C
Department of Physiology and Biophysics, Mount Sinai School of Medicine, New York, New York 10029, USA.
J Neurosci. 2003 Apr 1;23(7):2920-31. doi: 10.1523/JNEUROSCI.23-07-02920.2003.
Afferent transmission can be regulated (or gated) so that responses to peripheral stimuli are adjusted to make them appropriate for the ongoing phase of a motor program. Here, we characterize a gating mechanism that involves regulation of spike propagation in Aplysia mechanoafferent B21. B21 is striking in that afferent transmission to the motor neuron B8 does not occur when B21 is at resting membrane potential. Our data suggest that this results from the fact that spikes are not actively propagated to the lateral process of B21 (the primary contact with B8). When B21 is peripherally activated at its resting potential, electrotonic potentials in the lateral process are on average 11 mV. In contrast, mechanoafferent activity is transmitted to B8 when B21 is centrally depolarized via current injection. Our data suggest that central depolarization relieves propagation failure. Full-size spikes are recorded in the lateral process when B21 is depolarized and then peripherally activated. Moreover, changes in membrane potential in the lateral process affect spike amplitude, even when the somatic membrane potential is virtually unchanged. During motor programs, both the lateral process and the soma of B21 are phasically depolarized via synaptic input. These depolarizations are sufficient to convert subthreshold potentials to full-size spikes in the lateral process. Thus, our data strongly suggest that afferent transmission from B21 to B8 is, at least in part, regulated via synaptic control of spike initiation in the lateral process. Consequences of this control for compartmentalization in B21 are discussed, as are specific consequences for feeding behavior.
传入性传递可以被调节（或门控），以便对外周刺激的反应得到调整，使其适合运动程序的进行阶段。在这里，我们描述了一种门控机制，它涉及对海兔机械感觉传入神经元B21中动作电位传播的调节。B21的显著之处在于，当B21处于静息膜电位时，不会发生向运动神经元B8的传入性传递。我们的数据表明，这是由于动作电位不会主动传播到B21的侧突（与B8的主要接触部位）。当B21在其静息电位时受到外周激活，侧突中的电紧张电位平均为11毫伏。相比之下，当通过电流注入使B21发生中枢去极化时，机械感觉传入活动会传递到B8。我们的数据表明，中枢去极化可缓解传播失败。当B21去极化然后受到外周激活时，在侧突中记录到全尺寸的动作电位。此外，即使体细胞的膜电位实际上没有变化，侧突中的膜电位变化也会影响动作电位的幅度。在运动程序期间，B21的侧突和体细胞都会通过突触输入发生阶段性去极化。这些去极化足以将阈下电位转换为侧突中的全尺寸动作电位。因此，我们的数据有力地表明，从B21到B8的传入性传递至少部分是通过对侧突中动作电位起始的突触控制来调节的。我们讨论了这种控制对B21中分隔的影响，以及对摄食行为的具体影响。
