Original article

Scand J Work Environ Health 1977;3(1):36-42    pdf

doi:10.5271/sjweh.2792

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

by Juntunen J, Linnoila I, Haltia M

Myoneural junctions in the tibialis anterior muscle of rats with clinical signs of polyneuropathy induced with carbon disulfide were studied by light and electron microscopy. Histochemically demonstrable acetylcholinesterase (AChE; E.C. 3.1.1.7) activity was distributed similarly in the myoneural junctions of both the exposed and the control rats. In both groups intense enzyme activity was localized at the level of the post-synaptic membrane of the myoneural junction. The postsynaptic infoldings of the myoneural junctions of the exposed rats appeared normal. No enzyme activity was seen outside the zone of the myoneural junctions. The ultrastructure of the sub-sarcolemmal space, as well as 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. It thus seems that systemic carbon disulfide poisoning 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.