Axoplasmic transport in zinc pyridinethione neuropathy: evidence for an abnormality in distal turn-around.
Axoplasmic transport studies were done in rats with a zinc pyridinethione-induced dying-back neuropathy characterized by the accumulation of branched interconnected tubulovesicular profiles in the motor nerve terminals. Fast anterograde transport studies in sensory and motor systems were significantly reduced compared to controls but there was a wide variation in results and a lack of correlation with clinical involvement. Retrograde transport studies showed a delay in the time of onset and a reduction in the amount of retrograde transported materials. Analysis of the integrals of retrograde transport indicated that the defect was related to a failure in the turn-around process in the distal axon as opposed to a decreased rate of retrograde transport. Similar changes were not present in the proximal morphologically normal portion of the axon where retrograde transport was provoked with a crush injury.
D000818:Animals; D001370:Axonal Transport / Q000187:drug effects*; D005727:Ganglia, Spinal / Q000187:drug effects / Q000503:physiopathology*; D007700:Kinetics; D007930:Leucine / Q000378:metabolism; D008297:Male; D009046:Motor Neurons / Q000502:physiology*; D009942:Organometallic Compounds; D011725:Pyridines / Q000494:pharmacology*; D051381:Rats; D013119:Spinal Cord Injuries / Q000503:physiopathology
D009942:Organometallic Compounds; D011725:Pyridines; D007930:Leucine; C010423:pyrithione zinc