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Biomedical subjects

J B Pickett

Publications and source records attributed to J B Pickett.

At least 19 recordsLinked to original sources
PubMed1992

Insulin increases amino acid transport into rat soleus motor axons.

Hyperosmotic neurosecretion was used to measure basal and insulin-stimulated amino acid and myoinosital transport into rat motor nerve terminals. L-Alanine and alpha(methylamino)-isobutyric acid (a nonmetabolizable system A-specific analog) transport was rapid into motor nerve terminals innervating a fast-twitch muscle, the extensor digitorum longus, and slow into motor nerve terminals innervating the soleus, a slow-twitch muscle. A physiological concentration of insulin, 10 microU/mL, increased L-alanine and alpha(methylamino)-isobutyric acid transport into motor nerve terminals in the soleus. Large doses of insulin, 100 or 1000 microU/mL, had no effect on L-alanine or alpha(methylamino)-isobutyric acid transport into nerve terminals in the extensor digitorum longus. There was negligible basal or insulin-stimulated transport of D-alanine or myoinositol into nerve terminals of the soleus or extensor digitorum longus. These studies show that insulin regulates sterospecific amino acid transport into soleus motor axons, but has no effect on the rapid amino acid transport into extensor digitorum longus motor axons. Differences in basal and insulin-stimulated transport suggest that motor axons differ in their metabolism, and might be selectively vulnerable to disease processes.

Amino Acids↗
PubMed1988

AAEE case report #16: Botulism.

Botulinal toxin causes a marked reduction in the number of quanta released by autonomic and motor nerve terminals. As a result it causes blurred vision, inability to move the eyes, weakness of other cranial nerve-innervated muscles, dyspnea progressing to apnea, and generalized weakness. Electrodiagnostic findings in severe botulism can be relatively nonspecific, with low amplitude and short duration motor unit action potentials and small M wave amplitudes. A modest increment in M wave amplitude with rapid repetitive nerve stimulation may help to localize the disorder to the neuromuscular junction. Identification of the toxin in the patient's serum is diagnostic. The treatment of botulism is mainly supportive.

Adolescent↗
PubMed1988

Insulin improves rat soleus axon function by increasing glucose transport.

The effect of varying glucose and insulin concentration on neuromuscular transmission was investigated in rat soleus and extensor digitorum longus (EDL) nerve-muscle preparations using conventional microelectrode techniques. Soleus and EDL axons were similar in that both failed after approximately 70 min of glucose deprivation and often did not recover from glucose deprivation. Soleus and EDL axons differed in the following ways: 1) soleus axons required greater than 7.64 mM of glucose to give sustained function vs. greater than 2.78 mM of glucose for the EDL; 2) 30 microU/ml of insulin improved soleus axon function over a range of glucose concentrations from 4.17 to 9.72 mM vs. no effect of 1,000 microU/ml on EDL axons; 3) resting glucose transport was slow into soleus axons and rapid into EDL axons; and 4) 10 microU/ml of insulin increased glucose transport into soleus axons vs. no effect of 1,000 microU/ml of insulin on glucose transport into EDL axons. These results suggest that insulin improves soleus axon function by increasing glucose transport, whereas insulin has no effect on EDL axons.

Animals↗
PubMed1985

Localizing peroneal nerve lesions.

The main result of a peroneal nerve lesion, foot drop, is so obvious that few patients can ignore its presence. However, the detailed knowledge of peroneal nerve anatomy needed to localize the lesion may tax even a seasoned clinician. Examination of the strength of five muscles--the tibialis anterior, peroneus longus and brevis, posterior tibial, gluteus medius and quadriceps--provides information necessary to localize the site of the neuropathy. This tentative localization can be confirmed by electromyography. Treatment is directed to the cause of the lesion and stabilization of the ankle if necessary.

Electromyography↗
PubMed1984

Localizing peroneal nerve lesions to the knee by motor conduction studies.

We studied peroneal motor conduction in 186 normal patients (206 nerves) and in 36 patients with 38 peroneal nerve lesions localized to the knee by electromyography. The efficiency of the test, or percentage of times the test results were true, was used to find the optimal point to separate the normal patients from patients with peroneal nerve lesions at the knee. This analysis revealed that the best indicator for localizing a peroneal nerve lesion to the knee was a greater than 20% drop in peroneal motor amplitude across the knee. This gave a calculated efficiency of 99.52% and detected 60% to 70% of peroneal nerve lesions at the knee.

Adult↗
PubMed1984

Some effects of lead at mammalian neuromuscular junction.

The effect of lead on transmitter release was investigated in a rat phrenic nerve-hemidiaphragm preparation using conventional microelectrode techniques. Lead reduced the number of quanta released by a nerve stimulus (m) in a dose-dependent fashion. As extracellular Ca2+ concentration ([Ca2+]o) was varied in the absence of lead, a linear relationship between ln(m) and ln([Ca2+]o) was obtained. Lead shifted the relationship between ln(m) and ln([Ca2+]o) to the right without altering the slope. This suggested lead competed with Ca2+, which was confirmed by using a modified Lineweaver-Burk plot. Lead inhibits Ca2+ entry into frog sympathetic preganglionic nerve terminals, and a similar mechanism may underlie this present finding; such a mechanism, however, could not explain all the observed actions of lead. Lead increased the frequency of spontaneous quantal release in a dose-dependent manner, and 10(-4) M lead doubled the magnitude of facilitation of evoked release seen with five stimuli at 60 Hz. It is suggested that these effects result from inhibition of some, or all, of the nerve terminal's Ca2+ sequestration mechanisms.

Animals↗
PubMed1982

Infant botulism--the first five years.

In 1976 physicians in California reported the presence of botulism in infancy. Over a period of a few days infants developed generalized weakness and lost autonomic functions. The severity of infant botulism has varied from feeding difficulties to paralysis. No toxin was found in the infants' food, but it was detected in the stool along with C. botulinum spores and organism. This suggested that infants consumed the spores, which germinated into organisms, which produced the toxin.

Animals↗
PubMed1980

Nerve terminals are as metabolically different as the muscle fibers they innervate.

The rate at which glucose enters nerve terminals in muscle was estimated indirectly by measuring changes in miniature end-plate potential frequency D-Glucose entered nerve terminals in muscles with a fast twitch more rapidly than it entered those with a slow twitch. This suggests that nerve terminals in fast- and slow-twitch muscles differ in their rate of metabolism.

Animals↗
PubMed1980

Sputtering positive potentials in the EMG: an artifact resembling positive waves.

Sputtering positive potentials (SPPs) in the electromyogram are small, irregularly occurring waveforms recorded in normal distal muscles. They represent cannula-recorded "nerve" potentials, but may be mistaken for the positive waves seen in denervation. Differences in amplitude, regularity, and duration help in distinguishing SPPs.

Action Potentials↗
PubMed1979

Inhibition of the evoked release of acetylcholine by the porphyrin precursor delta-aminolevulinic acid.

The effect of delta-aminolevulinic acid (ALA) on neuromuscular transmission were studied. High concentrations (0.6 to 18 mM) of ALA caused significant reductions in the amplitudes of curarized end-plate potentials (epps). Changing the ratio of calcium to magnesium in the bathing solution allowed the quantal content of the epps to be directly measured. Under these conditions, ALA reduced the quantal content of epps without affecting the depolarization produced by a single quantum of acetylcholine. It was concluded that ALA, in high concentrations, inhibits the release of acetylcholine evoked by a nerve impulse but is unlikely to be the cause of the neurological defects of acute porphyria.

Acetylcholine↗