TY - JOUR
T1 - Serotonin accumulation by skeletal muscle
AU - Stahl, S. M.
AU - Meltzer, H. Y.
N1 - Funding Information:
Recent evidence suggests that serotonin may be linked to the etiology and/or pathophysiology of Duchenne-type muscular dystrophy. In rats, aortic ligation plus small doses of serotonin produces the scattered skeletal muscle necrosis and increases in serum creatine phosphokinase activity characteristic of this disease (11, 12). Murphy et al. (13) have reported that the initial rate of uptake of serotonin into blood platelets from patients with Duchenne-type muscular dystrophy is less than in normal controls or patients with other neuromuscular disorders. Parker and Mendell (15) attempted to reproduce this biochemical abnormality in rats by administer- 1 Supported by USPHS Grant No. MH18396 and MH25116. Dr. Stahl is a Medical Fellow, NIGMS Fellowship No. 56040. Dr. Meltzer is the recipient of Research Career Scientist Award No. MH47,808.
PY - 1977/1
Y1 - 1977/1
N2 - The properties of serotonin accumulation by rat extensor digitorum longus muscles have been characterized. No evidence was found for an active transport process because serotonin accumulation was unaffected by ouabain, metabolic inhibitors, or structural analogs. Serotonin transport was dependent on temperature and the external concentration of serotonin, was not saturable, and accumulated two- to threefold higher than urea. These findings suggest that serotonin transport into skeletal muscle is mediated via passive diffusion followed by tissue binding. In vivo imipramine and chlorpheniramine, drugs which given with serotonin produce an acute myopathy, also inhibited its accumulation by rat extensor digitorium longus muscles. This supports the notion that the myopathy produced by serotonin plus membrane-active drugs may be mediated by the action of serotonin upon the sarcolemma or upon the skeletal muscle vasculature in combination with the membrane action of imipramine and chlorpheniramine upon skeletal muscle membranes.
AB - The properties of serotonin accumulation by rat extensor digitorum longus muscles have been characterized. No evidence was found for an active transport process because serotonin accumulation was unaffected by ouabain, metabolic inhibitors, or structural analogs. Serotonin transport was dependent on temperature and the external concentration of serotonin, was not saturable, and accumulated two- to threefold higher than urea. These findings suggest that serotonin transport into skeletal muscle is mediated via passive diffusion followed by tissue binding. In vivo imipramine and chlorpheniramine, drugs which given with serotonin produce an acute myopathy, also inhibited its accumulation by rat extensor digitorium longus muscles. This supports the notion that the myopathy produced by serotonin plus membrane-active drugs may be mediated by the action of serotonin upon the sarcolemma or upon the skeletal muscle vasculature in combination with the membrane action of imipramine and chlorpheniramine upon skeletal muscle membranes.
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U2 - 10.1016/0014-4886(77)90233-3
DO - 10.1016/0014-4886(77)90233-3
M3 - Article
C2 - 832697
AN - SCOPUS:0017331882
SN - 0014-4886
VL - 54
SP - 42
EP - 53
JO - Experimental Neurology
JF - Experimental Neurology
IS - 1
ER -