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J Neurophysiol 58: 276-287, 1987;
0022-3077/87 $5.00
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Journal of Neurophysiology, Vol 58, Issue 2 276-287, Copyright © 1987 by APS


ARTICLES

Retrograde effects of target atrophy on submandibular ganglion neurons

M. D. Womble and S. Roper
Department of Anatomy, University of Colorado Health Sciences Center, Denver 80262.

1. To study the retrograde effects of changes in target tissue upon the innervating nerve supply, we have examined the parasympathetic submandibular ganglion of the adult rat. Neurons of this ganglion innervate the submandibular and sublingual salivary glands. 2. Ligating the salivary ducts leads to rapid and prolonged salivary gland cell atrophy. 3. Duct ligations, without direct injury to the glandular nerve supply, initially produced few alterations in the ganglion. After 8 wk, however, neuron number was reduced by 50%. The numbers of presynaptic inputs/neuron and synapses/neuron perimeter were not affected by the cell loss. 4. After 1 wk of duct ligation in which the glandular nerve supply was intentionally damaged, some ganglionic neurons have lost all presynaptic inputs, suggesting synaptic disjunction. This is followed at 3 wk by a 40% decrease in neuron number and an increase in the number of inputs per (remaining) ganglion cell. However, the number of synapses/neuronal profile was unchanged. 5. Thus axotomy plus target atrophy causes synaptic disjunction, neuron cell death, and input rearrangement, presumably due to a combination of direct injury effects and an abrupt loss of peripheral trophic supplies. 6. In contrast, target atrophy alone produced more gradual changes in submandibular ganglion neurons. Only prolonged target atrophy leads to a decrease in the number of ganglionic neurons, perhaps due to the gradual loss of peripheral trophic supplies. However, other features, such as the number of inputs/cell and the number of synapses/neuron perimeter, remain unaltered. Evidently, the gradual loss of trophic support does not result in synaptic disjunction to the degree needed to produce presynaptic input rearrangement.





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