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Biomedical subjects

M A Soza

Publications and source records attributed to M A Soza.

7 recordsLinked to original sources
PubMed1988

Changes in contralateral synaptic acetylcholinesterase following motor nerve section in rats.

We report here that denervation of rat extensor digitorum longus, soleus and diaphragm muscle results in an increase of a subset of asymmetric acetylcholinesterase (class II A-forms) in the contralateral muscle, within a few days. This observation is interesting because it suggests a specific regulation of one asymmetric enzyme fraction, which is solubilized only in the presence of chelating agents and is thought to reside in the basal lamina.

Acetylcholinesterase↗
PubMed1988

Intramuscular pH and endurance are abnormal in skeletal muscles from rats with experimental myotonia.

The relation between resistance to fatigue and intramuscular pH was studied in fast muscles (anterior tibialis and extensor digitorum longus) from rats treated with 2,4-dichlorophenoxyacetic acid (2,4-D) to induce myotonia. Fatiguability was studied in muscles indirectly stimulated at 30 Hz (330 ms/s; 1 train/s) for 2 min. The resistance to fatigue decreased significantly 1 h after drug treatment and remained low 24 h later. The intramuscular pH was lower than normal in resting muscles from 2,4-D-treated rats. After 2 min of stimulation the pH decreased in both control and drug-treated muscles. However, this decrement was reduced in the experimental muscles. The pH of control and of 2,4-D-treated muscles were similar after the stimulation period, but only the drug-treated muscles were fatigued. Therefore, a decrease in intramuscular pH would not be the cause of the observed decrease in muscle resistance to fatigue after 2,4-D treatment. The reduced endurance of drug-treated muscles could not be attributed to impaired neuromuscular transmission.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1983

Increase of muscle peroxisomal enzymes and myotonia induced by nafenopin, a hypolipidemic drug.

The chronic administration of nafenopin, a hypolipidemic drug, induced an increase in catalase and acyl-CoA oxidase activities in various skeletal muscles, including the gracilis, diaphragm, soleus, and extensor digitorum longus. The magnitude of the increase was around 100% for both enzymes in each of the muscles studied in spite of the different basal level. These changes seem to be specific of the peroxisomal enzymes because acetylcholinesterase, which is not peroxisomal, did not follow the same pattern in all the muscles. Concomitant with the increase in muscle peroxisomal enzymes, the skeletal muscles presented an altered electromyogram with prolonged insertional activity, repetitive firing of action potentials, and myotonic runs characteristic of myotonia. Our results suggest a role for peroxisomes in the myotonic disorder.

Acetylcholinesterase↗
PubMed1983

Axonal transport dysfunction in dystrophia myotonica.

Axonal transport of acetylcholinesterase (AChE) was measured in the median and sural nerves of a subject who suffered from dystrophia myotonica and in a control subject. It was found that the basal activity of AChE was increased in myotonic nerves while its proximodistal transport was inhibited.

Acetylcholinesterase↗