Study of motor units innervated by common peroneal nerve in monkey

The average number and size of motor units were assessed by investigating the components of motor units supplied by Common Peroneal Nerve in monkey [macaca mulatta]. The motoneurons forming the common peroneal nerve [CPN] localized by horseradish peroxidase neuronal tracing technique extended from the caudal part of L[4] to the caudal part of L[6] segments of the spinal cord. The average somal diameter of motoneurons ranged between 14 and 78 m. The motoneurons measuring more than 38 [micro]m [presumably the alpha neurons] were 69.23%. The motor end-plates on skeletal myofibres of muscles supplied by the CPN were localized by using Bromo-indigo and urea-silver technique. The average number of motor units was assessed as the ratio between the number of motoneurons and the motor endplates. The total of 992 motor units with the size of 157 of the muscles innervated by the CPN have been observed in the present study

Efflux of acetylcholine in dimorphic skeletal muscle from castrated male rats

The effect of testosterone on motor neurons of dimorphic muscles is demostrable by increased frequency of miniature end-plate potentials (mepp) and decreased end-plate acetylcholinesterase activity observed in castrated rats. No change occurs in induced acetylcholine (ACh release. Although these muscles atrophy after castration there is no loss of muscle fibers. In the present study we reinvestigate the neuromuscular transmission in levator ani (LA) muscles from normal (N) adult (120 days) male rats and from rats castrated (C) 30 days before. The measurement of radioactive [3H]-choline was used to evaluate ACh release since it permits simultaneous estimation of quantal and non-quantal and non-quantal ACh release. The LA muscle was incubated with [3H]-choline (1µCi/ml) for 30 min and ACh efflux was measured after washout. The basal release of [3H]-choline (dpm total tissue radioactivity-1 number of fibers-1) was 296 ñ 33 and 156 ñ 24 in N and C, respectively. Induced ACh release (25 Hz, 5 min) was the same in N and C (653.19 ñ 66.46) and 496.62 ñ 68.67, respectively). These results indicate that castration increased nepp frequency buth reduced the total spontaneous release of ACh

Androgen regulation of the nicotinic acetylcholine receptor-ionic channel in a hormone-dependent skeletal muscle

The trophic influence of testosterone on the nicotinic acetylcholine receptor-ionic channel (AChR) was studied in the levator ani (LA) muscle of adult malr rats (120 days) intact (C) or gonadectomized when 90 days old (G). In the indirectly elicited muscle twitch, the LA from G rats was less sensitive to d-tubocurarine (0.1-1µM) than control muscles (IC25:C = 0.30µM,G=0.46µM). In G rats, the amplitude of neurally evoked endplate currents (EPC) was reduced by 70%, but the EPC time constant was not changed. Maximal junctional binding of [125I] alfa-bungarotoxin in the LA(C: 72.5 ñ 13.2 amol/endplate) was reduced by 18.8-fold in LA from G rats, with no change of the association rate constant (C: 5.64 ñ 1.29 10**6 M-1 min**-1). The results indicate that testosterone deprivation reduces the junctional AChR density in the rat LA without modifying the binding properties of the receptor

Phentonium induces a transient increase of acetylcholine efflux from motor nerve terminals

Phenthonium (10-50 µM), a quaternary derivative of 1-hyoscyamine, increases the frequency of miniature end-plate potentials (205 fold) and blocks the nicotinic receptor-ionic channel in skeletal muscles. When tested on rat diaphragms previously incubated with [3H] choline, phenthonium (50µM) increased the spontaneous release of radiolabelled acetylcholine (ACh) from 11.6 ñ 6.4 to 110.5 ñ 40.2 x 10**3 dpm/g within 15 min. The effect was transient, declining to 24.6 ñ 14.7 after 50 min. Subsequent electrical stimulation still in the prsence of phenthonium increased the efflux to 164.7 ñ 45.3. The fractional release relative to the level before stimulation did not differ from controls. Phenthonium (20 µM) did not increase the spontaneous ACh release but doubled the efflux induced by nerve stimulation. The present results, compared to previous electrophysiological findeings, indicate that quantal and nonquantal release are increased by phenthonium. They also show that the transient effect is not due to ACh depletion in nerve terminals

Ca-independent augmentation of endplate potential during repetitive stimulation

Con objetivo de elucidar la función del Ca intracelular en la transmisión neuromuscular investigamos en preparaciones de músculo de rana los efectos del ácido 1,2-bis (o-aminofenoxi)etano-N,N,N',N'-tetraacético (BAPTA) sobre el aumento-potenciación por frecuencia (anteriormente llamdo facilitación por frecuencia) el que ha sido de utilidad para identificar-los sitios de acción de varios agentes colinérgicos. La disminución de los iones Ca del espacio intracelular por BAPTA sólo suprimió el componente dependiente de Ca del fenómeno (mo) sin modificar el factor de estimulación dependiente de frecuencia (K). La depresión causada por BAPTA en la facilitación de corto plazo del potencial de placa (EPP) fue la misma tanto en reposo como en la estimulación. El efecto del BAPTA fue parcialmente antagonizado, por el ionóforo de Ca A23187. Esto sugiere que la capacidad de "buffer" de Ca del BAPTA se mantiene durante la estimulación repetitiva de baja frecuencia. BAPTA no modificó la potenciación post-tetánica de los EPP miniatura en medio libre de Ca. Estos resultados indican que los iones Ca son esenciales para la liberación de transmisor y para la facilitación de corto plazo, pero no son responsables de todos los cambios en la liberación de transmisor