Morphometric evidence from C-synapses for phased Nissl body response in alpha-motoneurones retrogradely intoxicated with diphtheria toxin.
Diphtheria toxin (DTX) kills cells by inactivating ribosomal translocation and when used to retrogradely intoxicate cat intercostal motoneurones produces marked morphological alterations in Nissl bodies, including those specifically sited postsynaptic to C-type axon terminals. Here, qualitative examinations of 'intoxicated' postsynaptic Nissl bodies reveal a progressive structural alteration marked by rER dilatation, rER lamellae fragmentation but retention of both the highly ordered multilamellate organization and ribosomal attachment until final stages of Nissl body dissolution. Morphometric results identified 3 broad phases to the postintoxication response which differed in the degree of rER cisternal dilation, and the numerical and spatial relationships between rER-lamellae, rER-bound ribosomes and rER-associated polyribosomes. These phases reflect the known molecular basis of diphtheritic toxicity and contrast with the fast developing Nissl body reaction associated with the neurotoxin ricin which also invokes ribosomal dysfunction and has been used to mimic certain features of motor neurone disease. The cytopathology of DTX and ricin are compared in the Discussion.
Pullen
A H
AH
Sobell Department of Neurophysiology, Institute of Neurology, London, U.K.
D000818:Animals; D002415:Cats; D004167:Diphtheria Toxin / Q000494:pharmacology*; D007367:Intercostal Nerves / Q000187:drug effects / Q000648:ultrastructure*; D008297:Male; D009046:Motor Neurons / Q000187:drug effects / Q000648:ultrastructure*; D009410:Nerve Degeneration / Q000187:drug effects*; D013900:Thoracic Nerves / Q000648:ultrastructure*
D004167:Diphtheria Toxin