Tetanic Nerve Stimulation Research Articles

The effect ofHabrobracon venom on excitatory neuromuscular transmission in insects

1. The action of the venom of the braconid waspHabrobraconhebetor was studied in nerve-muscle preparations of its host the mealmoth larva (Ephestia kuhniella) and of the locust (Locusta migratoria) by comparing physiological properties of normal and paralysed preparations. 2. The venom neither had an effect on nervous conduction nor on membrane potential, current-voltage relationship, graded electrogenesis and contraction of the muscle fibres. 3. Inhibitory transmission was not blocked. Excitatory junction potentials were either greatly diminished or absent during paralysis. They could not be restored to normal size by increasing the external Ca concentration. 4. The postjunctional sensitivity to L-glutamic acid was not significantly altered by the venom. 5. In paralysed locust preparations miniature excitatory junction potentials were still observed, but their frequency was reduced to as little as 1% of controls. Their amplitude distributions were similar to controls, except that the proportion of very large mejps was somewhat higher. 6. In weakly paralysed preparations tetanic nerve stimulation caused facilitation and posttetanic potentiation of the reduced ejps. With more extensive paralysis, tetanic stimulation increased the frequency of the mejps and a few of the stimuli were followed by mejp-like ejps. 7. Raising the osmolarity of the saline increased the mejp-frequenoy of paralysed preparations significantly less than in control preparations. 8. The thiol oxidizing compound diamide caused a large increase of mejpfrequency in controls but completely blocked spontaneous release in paralysed preparations. These effects could be quickly reversed by a subsequent application of the disulfide reducing agent dithiothreitol. 9. It is unlikely that the purely presynaptic effect ofHabrobracon venom is on the electrical properties of the excitatory nerve terminals. It is discussed whether the release mechanism or the supply of transmitter are affected. There may be a specific affinity of the venom to glutaminergic synapses.

ASSESSMENT OF RECOVERY FROM CURARE

The major hazard in the use of curare-like drugs in anesthesia is the failure to antagonize residual muscle weakness. We have shown that the head-raising test is not always a reliable index of curare recovery. On the other hand, a sustained muscular contraction in response to tetanic nerve stimulation could always be correlated with greater than 90% recovery in vital capacity and maximum voluntary ventilation. We recommend that in the event a patient cannot maintain a tetanic contracture, residual effects from the administration of curare should be treated with an anticholinesterase drug.

The effect of type D botulinum toxin on frog neuromuscular junctions.

1. Botulinum toxin type D blocks neuromuscular transmission in frogs. Motor nerve impulses continue to invade the nerve terminals but cease to evoke the phasic release of transmitter normally associated with them.2. Sensory receptors in the muscle continue to generate impulses even after 4 days of continuous exposure to botulinum toxin.3. Contrary to expectations, spontaneous miniature end-plate potentials did not disappear completely after botulinum intoxication; they still occurred, although with reduced frequency, in most end-plates. These miniature potentials had a skew amplitude distribution instead of the bell-shaped distribution of normal end-plates.4. The electron-microscopic appearance of botulinum-poisoned end-plates was not obviously altered.5. Even though after botulinum nerve impulses fail to release transmitter, tetanic nerve stimulation causes an increase in the frequency of miniature end-plate potentials. Many of the unit potentials which appear during the tetanic period are of an amplitude which is larger than that of spontaneous potentials, indicating that a different class of unit is being released preferentially. Some implications of this finding are briefly discussed.

Ionic mechanism of post-tetanic potentiation at the neuromuscular junction of the frog.

1. Transmitter release at the frog neuromuscular junction was studied after sodium influx in nerve and muscle was abolished by tetrodotoxin (TTX).2. In the presence of TTX, transmitter release evoked by electrotonic depolarization of the nerve terminal was potentiated following presynaptic stimulation by a train of depolarizing pulses.3. Post-tetanic potentiation (PTP) in the presence of TTX appeared no different from that observed in control (TTX-free) muscles. The magnitude as well as the time course of PTP was dependent on the number of tetanic stimuli and on temperature of the medium when sodium influx was inhibited by TTX.4. When external sodium was replaced by an isotonic calcium chloride solution PTP was still present. Ionophoretic application of calcium during tetanic nerve stimulation and increase in the intensity of the depolarizing pulse of the train, which presumably enhances calcium movements into nerve endings, caused a large increase in the duration of PTP.5. It is concluded that PTP does not require sodium but depends on movement of calcium from the external medium into the nerve terminal.

Assessment of Recovery From Curare

The major hazard in the use of curare-like drugs in anesthesia is the failure to antagonize residual muscle weakness. We have shown that the head-raising test is not always a reliable index of curare recovery. On the other hand, a sustained muscular contraction in response to tetanic nerve stimulation could always be correlated with greater than 90% recovery in vital capacity and maximum voluntary ventilation. We recommend that in the event a patient cannot maintain a tetanic contracture, residual effects from the administration of curare should be treated with an anticholinesterase drug.

Acetylcholine-releasing effects of some nicotinic agents on chick biventer cervicis nerve muscle preparation.

SummaryThe mechanism of action of some nicotinic agents has been studied on the baby chick biventer cervicis nerve muscle preparation. The effects of various nicotinic agents on this preparation were blocked by 1.2 × 10—2M triethylcholine (TEC) or by neuromuscular blockade achieved by TEC treatment with interrupted tetanic nerve stimulation, whereas the dose-responsive curve of acetylcholine (ACh) was not altered. These results suggest that the nicotinic agents tested are presumably acting primarily at the nerve terminals rather than at the receptor sites on the postjunctional membrane. After the effects of the nicotinic agents were completely blocked by TEC alone, the muscle was still responsive to nerve stimulation. This suggests that the TEC blockade of the nicotinic effects of the drugs tested may be at the membrane site of the nerve terminal since ACh is still available in the storage site for release after TEC blockade. In the same preparation, the responses to most of the nicotinic agents were mark...

Effects of curare-like agents on the block of tetanic contractions produced by neostigmine in the rat

The effects of some curare-like agents on the failure of the muscle to respond to tetanic nerve stimulation in the presence of neostigmine were examined. Investigations were carried out on the sciatic nerve - anterior tibial muscle preparation of the rat. The ability of the muscle to respond with sustained tetanic contractions was restored by curare-like agents and the time of recovery was shortened by these agents.

Transmitter release in the rat diaphragm during tetanic nerve stimulation.

Am isolierten Phrenicus-Zwerchfellpraparat der Ratte wurden, nach transversaler Durchschneidung der Muskelfasern auf jeder Seite der Endplattenregion, Endplatten-Potentiale, ohne Zusatz von modifizierenden Substanzen, intrazellular registriert. Wahrend kurzdauernder tetanischer Nervenreizung erwies sich der Abfall der EPP-Amplituden als unerheblich und die Freisetzung des neuro-muskularen Ubertragers Acetylcholin bei Saugetieren wahrend des Tetanus, entgegen der gewohnlichen Auffassung, als offenbar anhaltender.