Abstract
The uterus of virgin guinea-pigs is supplied with a well-developed system of adrenergic nerves, characterized by 50 nm diameter synaptic vesicles whose electron-density is enhanced following administration of 5-hydroxydopamine. In the course of pregnancy, an increasing number of nerves with signs of various stages of degeneration are seen, varying from a slight condensation of the axonal content or myelin figures, to highly osmiophilic dense bodies lacking plasma membrane and with no organelles discernible. Incipient degeneration in a small number of axons is evident already in early pregnancy (up to 10 days post coitum). At late pregnancy (40–50 days post coitum), almost all adrenergic nerve terminals have disappeared as a consequence of degeneration, so that only a few isolated heavily degenerated axon terminals remain visible. Neither normal nor degenerating axons are found in the myometrium at full term. The degenerative changes occur earlier and are, at the various pregnancy stages, more pronounced in that part of the uterus surrounding and expanded by the fetus, compared to those segments of the uterine wall separating the fetuses. Thus, the normal neuromuscular relationship in the uterus during such an entirely physiological condition as pregnancy is lost entirely, in contrast to other sympathetically innervated organs, where the nerve plexus usually keeps pace with volume changes in the effector tissue.
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