EARLY RESPONSE AFTER FACIAL NERVE DECOMPRESSION.
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Choline and neostigmine markedly antagonize the effect of acetylcholine (ACh) on the action potential of the venom-treated squid axon, although they themselves have no effect on conduction. Physostigmine also antagonizes the blocking action of ACh at a concentration well below that which has any effect on conduction. In contrast, d-tubocurarine (curare) increases the effect of ACh on the action potential. Choline, neostigmine, and physostigmine markedly decrease the penetration of C(14)-labeled ACh into the axoplasm of the squid axon. Curare, in contrast, increases the penetration of ACh, whereas dimethylcurare gives variable results. The results provide an explanation why physostigmine and neostigmine do not influence the action of ACh on axonal conduction in a way similar to that observed at the junction. The additive effect of curare and ACh on the action potential may be due either to the greater rate of penetration of ACh or to an additive effect of the two compounds on the receptor, or to a combination of both factors.
Field potentials evoked by mid-cervical vagal stimulation were systematically mapped in the dorsal motor and solitary nuclei of the pigeon. Since responses varied predictably with microelectrode position, they could be used for localization in the dorsal medulla. By varying stimulus intensity and monitoring the vagal compound action potential, contributions of the different compound action potential waves were then established. Activation of the Bl-wave, which includes cardioinhibitory fiber activity, has its most prominent effect in the intermediate rostrocaudal zone of the dorsal motor nucleus in the region of subnuxleus b. This is where the cells of origin of the vagal cardiac fibers have previously been anatomically localized. Single unit experiments then established that (a) vagal motoneurons with axonal conduction velocities in the cardioinhibitory fiber range (8.0-14.5 m/sec) are primarily localized to the intermediate rostrocaudal zone of the dorsal motor nucleus in the region of subnucleus b, and (b) motoneurons in this zone that conduct at 8.0-14.5 m/sec distribute their axons in the cardiac branches. Furthermore, no error is introduced by identifying such neurons with mid-cervical rather than midthoracic vagal stimulation. Thus, the following criteria establish a neuron as giving rise to a vagal cardioinhibitory fiber: (a) localizing it to the intermediate rostrocaudal zone of the dorsal motor nucleus on the basis of the field potential evoked by mid-cervical vagal stimulation; (b) antidromically activating it with mid-cervical vagal stimulation; and (c) demonstrating that its axon conducts at 8.8-14.5 m/sec.
Fibers that respond to distension of hollow viscera and to mechanical stimulation of somatic structures were found primarily near the ventromedian fissure of the upper lumbar spinal cord. These fibers could be directly excited by electrical stimulation at C(1). The average conduction velocity for these fibers was 68.6 meters per second.
1. Electrical activity accompanying motor activity can be recorded from the excised pharynx of Enchiridium punctatum. Multiple stimuli elicit behaviour which consists of an initial aperture closure followed by extension and then peristalsis. If the stimulus parameters are increased the preparation bends from side to side instead of proceeding through the behavioural sequence. Bending appears to inhibit other movements differentially. 2. The conduction involved with peristalsis is polarized and proceeds in a proximal direction. 3. With stimulus intensities greater than those needed to produce the behavioural response an initial muscle potential (IMP) is evoked. The IMP is frequency sensitive. Maximum facilitation occurs within 100 ms and drops to 50% of maximum within 250 ms. 4. Conduction velocities of the IMP range from 0-05 m s-1 to 1-9 m s-1. Conduction velocities appear to increase with facilitation.