Browsing by Author "BEHRENS, MI"

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    COLCHICINE ALTERS APAMIN RECEPTORS, ELECTRICAL-ACTIVITY, AND SKELETAL-MUSCLE RELAXATION
    (1993) VERGARA, C; RAMIREZ, B; BEHRENS, MI
    A low conductance calcium-activated K+ channel is thought to regulate the rate of firing of several excitable cells. In skeletal muscle the expression of this channel is under nerve control. Previously, we reported that axonal flow blockade of rat nerves, induced by colchicine, caused a transient increase in muscle apamin receptors, determined by I-125-apamin binding to membrane fractions. The increase in apamin receptors was correlated with repetitive discharges resembling myotonic potentials in the electromyogram, that were blockable by apamin. Here we show that the increase in muscle apamin receptors and the alteration of the electromyogram are followed closely by a slowing of the twitch relaxation, that in turn, is decreased by apamin. Furthermore, the presence of myotonic-like alterations in the electromyogram and a slowing of muscle relaxation when muscle apamin receptors are increased suggests that these channels may participate, among other factors, in the generation of some kinds of myotonia. (C) 1993 John Wiley & Sons, Inc.
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    INCREASE OF MUSCLE PEROXISOMAL ENZYMES AND MYOTONIA INDUCED BY NAFENOPIN, A HYPOLIPIDEMIC DRUG
    (1983) BEHRENS, MI; SOZA, MA; INESTROSA, NC
    The chronic administration of nafenopin, a hypolipidemic drug, induced an increase in catalase and acyl-CoA oxidase activities in various rat 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. A role for peroxisomes in the myotonic disorder is suggested.
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    NEURAL 16S ACETYLCHOLINESTERASE IS SOLUBILIZED BY HEPARIN
    (1983) TORRES, JC; BEHRENS, MI; INESTROSA, NC
    The effect of heparin, a sulfated glycosaminoglycan, on the solubilization of rat sciatic-nerve acetylcholinesterase (acetylcholine acetylhydrolase; AChE; EC 3.1.1.7) was studied. Heparin solubilized esterase activity from ligated nerves. Sedimentation analysis revealed this activity to be mainly the 16S form. Chondroitin sulfate did not solubilize AChE activity, and protamine eliminated the solubilizng effect. The results suggest the involvement of sulfated glycosaminoglycans in the intra-axonal localization and transport of 16S AChE.
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    ROSENBLUETH PHENOMENON
    (1979) BEHRENS, MI; LORENZO, D; FERNANDEZ, O; LUCO, JV
    Rosenblueth and Luco (1939) showed that, during prolonged stimulation of a motor nerve, neuromuscular fatigue is followed by a rise of tension that has been called the Rosenblueth Phenomenon. The Rosenblueth Phenomenon was investigated in a cat neuromuscular preparation in which the nerves were severed at different levels and stimulated at 60 Hz for several hours. In the longer nerve preparation the Rosenblueth Phenomenon starts earlier and its maximal tension is higher. Acetylcholine sensitivity was studied in the superior cervical ganglion preparation and no change was observed when tested before stimulation, during fatigue and during the Rosenblueth Phenomenon. The onset and amplitude of the Rosenblueth Phenomenon depend on the length of the peripheral nerve stump: the longer the stump, the earlier and higher the response. The Rosenblueth Phenomenon is apparently produced by an increase in the transmitter release which would be due to axonal progression of molecules along the nerve.