Histochemical and electron microscopic observations on the myoneural junctions of rats with carbon disulfide induced polyneuropathy.

Open Access
Publisher Website
Google Scholar
Abstract
Myoneural junctions in the tibialis anterior muscle of rats with clinical signs of polyneuropathy induced with carbon disulfide were studied by light microscopy and EM. Histochemically demonstrable acetylcholinesterase (AChE; E.C. 3.1.1.7) activity was distributed similarly in the myoneural junctions of both exposed and control rats. In both groups intense enzyme activity was localized at the level of the postsynaptic membrane of the myoneural junction. The postsynaptic infoldings of the myoneural junctions of exposed rats appeared normal. No enzyme activity was seen outside the zone of the myoneural junctions. The ultrastructure of the subsarcolemmal space, and the postsynaptic membranes of the myoneural junctions of the exposed animals, was normal. In the terminal axons signs of various degrees of degeneration were present, e.g., disappearance of the preterminal axoplasmic neurotubules, partial disappearance of synaptic vesicles, appearance of dense bodies, and even total disappearance or destruction of the terminal axons. Synaptic clefts were often widened with Schwann cell interposition. Systemic carbon disulfide poisoning probably primarily alters the presynaptic structures of the myoneural junctions, while the postsynaptic side remains relatively intact, especially since the histochemical distribution of AChE in myoneural junctions was normal.