Activation Of Nerve Terminals Research Articles

Relative effects of streptomycin on motor nerve terminal and endplate

Using standard microphysiologic recording techniques, the effects of streptomycin on nerve terminal and endplates were evaluated using the isolated frog satorius muscle. Twitch tension studies were performed on the sciatic nerve sartorius muscle preparation. In low concentrations the agent increased mepp frequency and twitch strength and caused antidromic firing from the nerve terminal. In the concentration range causing inhibition of muscle twitch, nerve terminal activity remained elevated. In this range mepp amplitude and endplate sensitivity were markedly reduced. At high doses streptomycin finally inhibited nerve terminal function. The reduction in twitch height was explained by blockade of the post-junction membrane. It is postulated that streptomycin has three effects on the myoneural junction: (1) stimulation of the nerve terminal at low doses; (2) reduction of the endplate sensitivity to acetylcholine concomitant with a reduction in the twitch height at higher doses and (3) inhibition of nerve terminal function at the highest doses studied.

Sinus slowing produced by experimental ischemia of the sinus node in dogs

The effects on heart rate and rhythm of acutely impeding the blood supply to the sinus node were studied in 18 anesthetized dogs. In 8 dogs the blood supply to the sinus node appeared to originate from 1 main artery, whereas more than 1 source was found in the remaining animals. When the sinus node was supplied by a single main artery, ligation of this artery was followed by a decrease in heart rate whereas, when a multiple blood supply to the sinus node was observed, it was necessary to occlude all major arteries to affect sinus nodal function. The effects observed did not seem related to activation of coronary stretch-sensitive receptors or to local or reflex activation of cholinergic nerve terminals within the sinus node.

Effects of pancuronium bromide on the motor nerve terminal

The effect of pancuronium on miniature endplate potential (mepp) frequency and amplitude, on the sensitivity of the endplate to iontophoretically applied acetylcholine, and on muscle twitch were studied on the frog sartorius muscle. In addition, in separate experiments, electrodes were placed on the corresponding ventral root to monitor nerve terminal activity. In concentrations between 10 −12 and 10 −7 g/l there was an increase in twitch height and mepp frequency with no effect on amplitude. Antidromic action potentials from the terminal were also recorded following stimulation in this concentration range. Between 10 −6 and 10 −5 g/l there was a concomitant decrease in twitch height and mepp frequency. Mepp amplitude and sensitivity to acetylcholine were reduced by only 25%. In these high concentrations post-tetanic potentiation and post-tetanic repetitive activity in the nerve terminal were abolished. It is believed that the stimulation and inhibition of neuromuscular transmission by pancuronium are due to actions predominantly on the nerve terminal.

Actions of gallamine and tetraethylammonium at the frog neuromuscular junction.

Actions of gallamine and tetraethylammonium at the frog neuromuscular junction.

Antagonism of Digitalis Arrhythmia by Pronethalol : a Neural Phenomenon?

THE depression by pronethalol of ventricular arrhythmia induced by digitalis, and of ventricular escape during vagal stimulation, is apparently not related to the capacity of this drug to block the cardiac effects of exogenous catecholamines1–3. Roberts et al.3 pointed out that the actions of pronethalol on the digitalis-induced arrhythmia and on vagal escape closely resemble those of reserpine and β-TM10—agents which act on sympathetic nerve terminals—and suggested that pronethalol may also affect the activity of sympathetic post-ganglionic nerve terminals.