Browsing by Author "RAMIREZ, BU"

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    AGE-RELATED RESPONSES OF SKELETAL-MUSCLE AFTER ECTOPIC INNERVATION, WITH PARTICULAR REFERENCE TO 16S ACETYLCHOLINESTERASE, IN ADULT-RATS
    (1984) MALDONADO, M; RAMIREZ, BU; RUIZ, G; YAMUY, J; INESTROSA, NC
    The formation of ectopic junctions between the foreign fibular nerve and the soleus muscle of young (35-day-old) and mature (200-day-old) adult rats was induced by severing the normal nerve 4 wk after implanting the foreign nerve. The various molecular forms of acetylcholinesterase (AChE) were studied both at the implanted region and at the original denervated endplates. The velocity of contraction was also studied. In young rats the 16S form was first detected in the ectopic junctions around day 5 after reinnervation; this form rapidly increased during the following weeks, reaching a plateau by day 20. By contrast, in mature rats the appearance of the 16S AChE was dramatically delayed; in fact, it could not be observed before day 80 after reinnervation. (The 16S AChE form appeared at day 20 after reinnervation in the original denervated endplates of young rats; however, at the same time, no effect was observed in mature animals.) The original, slow muscle fibers of the soleus became faster upon reinnervation; this change also occurred much earlier in younger than in mature rats. A loss of plasticity in the skeletal muscle of mature rats is indicated. Caution is suggested in the use of the ectopic innervation model to study development in mature adult rats.
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    AXOPLASMIC-TRANSPORT BLOCKAGE BY VANADATE
    (1982) RAMIREZ, BU; PUSCHEL, M; SAAVEDRA, R; PAVLOVIC, C
    The effect of vanadate on axoplasmic transport was studied. Vanadate was injected in adult cats under the epineurium of the hypoglossal nerve. After 24 h there was a significant increase of the AChE [acetylcholinesterase] content in a nerve segment proximal to the injection site of vanadate. This ion did not produce nerve degeneration. Vanadate blocks axoplasmic transport.
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    ENERGETIC METABOLISM AND FATIGABILITY IN EXPERIMENTAL MYOTONIA
    (1990) RAMIREZ, BU
    Experimental myotonia was induced in rats by 2,4-dichloro-phenoxyacetic acid (2,4-D). After 4 to 24 h of treatment, the anterior tibialis muscles exhibited increased fatigue at low frequency (30 Hz) nerve stimulation, but they developed normal tension at high-frequency (100 Hz) stimulation. Glycogen content and the activities of glycogen phosphorylase, lactate dehydrogenase and malate dehydrogenase remained normal. The absence of correlation between fatigability and energetic metabolism in this experimental model of myotonia suggests a dysfunction in excitation-contraction coupling.