Lead uptake in motor axons

Abstract

In an attempt to determine whether lead (Pb) in striated muscle can be taken up by motor axon, mice were injected intramuscularly with a 5% Pb nitrate solution, and the passage of Pb through the tissues was traced with electron microscopy. Thirty minutes after injection in the tibialis anterior muscle, Pb was seen at the sarcolemma and axolemma of the neuromuscular junction (NMJ) and in the adjacent sarcoplasmic reticulum (SR). Pb was also present in the axoplasm and mitochondria of terminal and preterminal motor axons. The presence of Pb was confirmed with x-ray elemental microanalysis. The results indicate that there is a pathway for intramuscular Pb to enter terminal motor axons. This supports the hypothesis that some forms of motor neuron disease (MND) may be due to axonal uptake and retrograde transport of Pb.

Mitochondria Initiate and Regulate Sarcopenia

“…This has been known for several decades, because when toxins or other compounds are injected into muscles, the compounds undergo retrograde transport to the neuromuscular junction (105), deposit in motor neurons (11), and sometimes contributes to motor neuronal dysfunction (reviewed in (33, 39). This communication is also seen when spinal cord injury or denervation induces large-scale muscle wasting (57, 76, 107, 129, 131, 137), and denervation is a condition often seen as part of sarcopenia.…”

Experimental neurotoxicity of mercury Autometallographic and stereologic studies on rat dorsal root ganglion and spinal cord

“…These findings are noteworthy because this transport mechanism represents a pathway into the nervous system that bypasses the blood-brain barrier. The metals that have been demonstrated to be transported retrogradely in axons include: iron, using Perls Prussian blue reaction in mice (Malmgreen et a1 1978); lead, using either 203Pb in rats (Baruah et a1 1981) or X-ray elemental microanalysis in mice (Pamphlett and Bayliss 1992); cadmium, using lo9Cd in mice (Arvidson 1985) and pikes (Tjalve and Gottofrey 1986); thallium, using 204Tl in frogs (Bergquist et a1 1983); and silver (Danscher 1982b) and zinc, using autometallography in rats (Danscher 1982a; Slomianka et a1 1990).…”

Nerve‐dependent regulation of succinate dehydrogenase in junctional and extrajunctional compartments of rat muscle fibres.

“…Together, these studies are coherent with the notion that renewal of postsynaptic membrane proteins is achieved via a mechanism of local transcription of genes encoding synaptic proteins, and of focal insertion of newly synthesized molecules at the endplate. Despite these recent advances in our understanding of neuromuscular junction structure and function, information concerning the distribution, density and biochemical composition of mitochondria located within the postsynaptic sarcoplasm is still rudimentary and conflicting (see Couteaux, 1960;Kelly & Zacks, 1969;Miledi & Slater, 1970;Padykula & Gauthier, 1970;Lentz, 1972;Manolov, 1974;Uehara, Campbell & Burnstock, 1976;Pamphlett & Bayliss, 1992). This is surprising, given that mitochondria assume a crucial role in cellular metabolism and demonstrate, in both nerve and muscle, a remarkable plasticity in meeting specific metabolic 3300 requirements associated with chronic alterations in neuromuscular activity.…”