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S Gomez

Publications and source records attributed to S Gomez.

65 records · Page 4Linked to original sources
PubMed1982

Discrepancies between spontaneous and evoked synaptic potentials at normal, regenerating and botulinum toxin poisoned mammalian neuromuscular junctions.

Amplitudes and times to peak of spontaneous miniature endplate potentials (m.e.p.ps) and evoked quantal endplate potentials (e.p.ps) were compared at normal, regenerating and botulinum toxin poisoned neuromuscular junctions of the extensor digitorum longus muscle of the rat. At normal junctions the mean time to peak of m.e.p.ps was longer and more variable than that of similar-sized e.p.ps. At endplates where nerve regeneration was induced by mechanical crushing of the motor nerve the frequency of m.e.p.ps was reduced and their amplitude distribution was broader than normal. The distribution of times to peak of m.e.p.ps was considerably broader than that of quantal e.p.ps recorded at the same endplates. At neuromuscular junctions poisoned with botulinum toxin type A, spontaneous and evoked transmitter release were greatly reduced. The amplitude distribution of m.e.p.ps was wider than that of e.p.ps and the time to peak of e.p.ps was about twice as fast as and less variable than that of m.e.p.ps. To explain the observed differences in time to peak among m.e.p.ps and between m.e.p.ps and quantal e.p.ps we suggest that some m.e.p.ps, but not e.p.ps, originate from transmitter quanta released from sites at a greater distance from postsynaptic receptors or that the release or diffusion process for acetylcholine is more prolonged when producing some of the m.e.p.ps. Such mechanisms produce at normal junctions a small population of m.e.p.ps with prolonged times to peak, at regenerating junctions a greater proportion of such m.e.p.ps and in botulinum toxin poisoning a majority.

Animals↗
PubMed1982

Effects of x-irradiation on axonal sprouting induced by botulinum toxin.

The effect of X-irradiation on axonal sprouting of motor nerves induced by botulinum toxin was examined. Muscles of one leg in the mouse were X-irradiated (15 Gy) prior to the injection of a locally paralysing dose of botulinum toxin. It was found that axonal sprouting occurred as expected, but the sprouts remained unmyelinated and many degenerated. Fewer new end-plates were formed, muscles remained more severely atrophied and supersensitive to acetylcholine and recovery of neuromuscular transmission was greatly delayed when compared with the effects of botulinum toxin alone. The experiments show that X-irradiation did not prevent sprouting but, probably by impairing Schwann cell proliferation, altered axon-Schwann cell relationships and prevented the maturation of newly-formed axons and the differentiation of new end-plates.

Acetylcholine↗
PubMed1982

Changes produced by a hypomyelinating neuropathy in muscle and its innervation. Morphological and physiological studies in the Trembler mouse.

The peripheral nerves of the Trembler mouse are hypomyelinated. The effects of the neuropathy on muscle and motor end-plate morphology, and on neuromuscular transmission in slow-twitch (soleus) and fast-twitch (extensor digitorum longus) muscle are reported. After forming normally, motor end-plates developed ultraterminal sprouts by about 18 days of age in deep, slow-twitch muscles. The only ultrastructural abnormality in muscle at this age was disruption of Z-lines. Ultraterminal sprouting progressed, and by about 3 months the innervation zone consisted of a mass of branching axons associated in places with cholinesterase activity. The ultrastructure of end-plates became abnormal. Fascicular atrophy was present in older Tremblers and the ultrastructural morphology of muscle fibres became disorganized with accumulation of subsarcolemmal granular material. Abnormal muscle fibres were innervated by axonal sprouts. The superficial, predominantly fast-twitch, muscles showed milder changes at all ages even though the nerves supplying them were hypomyelinated. Studies of neuromuscular transmission showed that soleus retained its slow-twitch and extensor digitorum longus its fast-twitch characteristics, and miniature end-plate potentials were of normal frequency and amplitude. The latency of end-plate potentials and the refractory period of transmission were prolonged in both soleus and extensor digitorum longus. With repetitive stimulation at 50 Hz a cyclical pattern of responses and failures occurred which was probably caused by intermittent conduction block along the peripheral nerve. Although the pathological changes in Trembler muscle were like those of partial denervation, atrophic muscles contained an abundance of axons and there was no evidence of axonal degeneration. The changes in muscle are therefore a consequence of hypomyelination without axonal loss. Since slow-twitch muscles are normally subjected to prolonged stimulation, failure of Trembler axons to conduct sustained trains of stimuli in vivo may contribute to the development of pathological changes in slow-twitch muscle. Hypomyelimated axons may be capable of conducting short bursts of impulses, however, which is the pattern of stimulation in fast-twitch muscle in vivo, so that fast-twitch muscle fibres and end-plates remain relatively spared.

Animals↗
PubMed1982

Giant miniature endplate potentials induced by 4-aminoquinoline.

In experiments on the isolated extensor digitorum longus muscle of the rat it was shown that 4-aminoquinoline (125-250 micro M) altered the amplitude distribution of spontaneous miniature endplate potentials to include a large portion of giant miniature endplate potentials with slow rise and decay times. Similar, slow-rising giant miniature endplate potentials were induced by the drug at neuromuscular junctions with regenerating nerve terminals, i.e. in a condition where spontaneous as well as evoked transmitter release is depressed. The appearance of giant miniature endplate potentials was not correlated with inhibition of cholinesterase since neostigmine (3 micro M) failed to induce such potentials. Nerve impulse evoked endplate potentials of amplitudes similar to the spontaneous giant miniature endplate potentials had a faster and more uniform rise time. The results suggest that 4-amino-quinoline, by a direct action on the nerve terminal, causes the release of larger than normal quanta of acetylcholine. Quantitative assays of acetylcholine released before and in the presence of 4-aminoquinoline gave similar values showing that the amounts of acetylcholine which give rise to the giant miniature potentials contribute little to the total amount of acetylcholine liberated.

Action Potentials↗
PubMed1982

The effects of black widow spider venom on the innervation of muscles paralysed by botulinum toxin.

Botulinum toxin (BoTx) was injected into the muscles of one leg in mice causing local paralysis. Black widow spider venom (b.w.s.v.) was then injected into the paralysed muscles 3 or 15 d later. In both groups b.w.s.v. destroyed the nerve terminals poisoned by BoTx. In the 15 d group axonal sprouts, which had former due to the block of neuromuscular transmission by BoTx, were also destroyed. Within a few days the motor nerve terminal regenerated and the muscles recovered from paralysis at a faster rate than after BoTx alone. Recovery seemed to begin earlier in muscles where axonal sprouting was already advanced when b.w.s.v. was injected. The normal pattern of innervation was re-established in both groups, which was in marked contrast with muscles after BoTx alone where numerous sprouts and many ectopic end-plates had formed.

Acetylcholine↗
PubMed1981

The neuromuscular junction of the mouse after black widow spider venom.

1. A sublethal quantity of black widow spider venom was injected into the calf muscles of mice. After 30 min to 6 weeks soleus muscles were examined by light and electron microscopy and by electrophysiological techniques. 2. Within 30 min motor nerve terminals were swollen and depleted for synaptic vesicles and by 6 h were disrupted and engulfed by Schwann cells. By 24 h every end-plate examined was denervated. Some preterminal myelinated axons also showed degenerative changes. 3. Re-innervation was first seen at 2 days. By 3 days axon terminals were present at most end-plates and by 8 days their morphology was nearly normal. The normal pattern of innervation of the muscle was re-established in that axons re-innervated their original end-plates and very few ultraterminal axonal sprouts were found. 4. Physiological study showed complete failure of transmission and absence of miniature end-plate potentials (m.e.p.p.s) and end-plate potentials (e.p.p.s) until day 3, when muscles responded weakly to indirect stimulation and m.e.p.p.s were recorded at 30% and e.p.p.s at 40% of fibres. The mean quantal content of e.p.p.s was low and there was rapid fatigue on repetitive stimulation. Extrajunctional sensitivity to acetylcholine developed within 1 day, was maximal at 3 days and declined to normal at 12-14 days. 5. The proportion of fibres at which m.e.p.p.s and e.p.p.s were recorded returned to normal by day 6 and mean quantal content was normal by day 9. 6. These findings show that the re-innervation of original end-plates is of importance in facilitating the rapid return of transmission to normal levels and limiting the extent of axonal growth.

Animals↗
PubMedDate not supplied

Fever and neutropenia in children with cancer in one pediatric hospital in Argentina.

The authors retrospectively analyzed 863 episodes of neutropenia and fever in 635 children with cancer or hematological disease hospitalized between October 1988 and November 1994. The most frequent underlying diseases were solid tumors (45%) and acute lymphoblastic leukemia (29%). Clinical site of infection could be determined in 454 (53%) episodes. Bacteremia was documented in 114 (13%) cases. Gram-positive cocci were the microorganisms most frequently isolated (47% of the cases). Noninfectious complications could be determined in 140 (16%) episodes, and were mainly severe bleeding and metabolic impairment. The episodes were divided in two groups for comparative evaluation: group A, 404 episodes, study period 1988-1991, and group B, 459 episodes, 1992-1994. According to the results, more patients in group A than group B were younger than 1 year old and had profound neutropenia; fewer patients in group A than group B had an endovascular catheter, a higher frequency of manifest clinical site of infection at admission, and a prevalence of isolation of gram-negative bacilli. A higher percentage of patients in group B had neutropenia of more than 14 days, gram-positive cocci in culture, and lower mortality. Multivariate analysis by logistic regression in 340 patients revealed that the presence of a severe noninfectious complication, severe neutropenia, and positive blood culture correlated with high mortality rate (p < or = 0.001).

Adolescent↗