Abstract
In the isolated spinal cord of the newborn rat, methysergide and LSD-25 depressed the monosynaptic reflex discharge selectively. Cyproheptadine and dimethothiazine did not inhibit the monosynaptic reflex. The selective inhibitory effect of methysergide on the monosynaptic reflex was not due to a presumptive low safety factor of this reflex. The inhibition was restored under a condition such as the compound action potential in the dorsal root was enhanced by 4-aminopyridine. Methysergide did not decrease the sensitivity of the motoneuron to substance P and L-glutamic acid. It is suggested that methysergide acts at the presynaptic terminal of Ia afferent fibers and depresses evoked transmitter release.
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