Abstract
To examine the effects of peripheral nerve injury on second-order neurons in laminae I and II of the medullary dorsal horn, tooth pulps of all mandibular teeth in adult cats on one side were extirpated. This procedure severed and removed the receptors and terminal branches of the primary trigeminal neurons which innervate the tooth pulps of these teeth. The empty pulp chambers were then filled with dental cement to prevent regeneration. At 30 and 60 days postoperatively, membrane-lined cavities had formed inside many of the small-caliber dendrites of second-order neurons in laminae I and II. Cavity formation occurred mainly in dendritic shafts less than 2 micron in diameter and involved dendrites with synaptic vesicles as well as those without synaptic vesicles. The cavities extensively hollowed out these dendrites, often occupying more than half the cross-sectional diameter of the shafts and extending for appreciable distances in the long axis of the shaft. The process of cavitation ultimately resulted in the destruction of the affected dendrites. Many cavities became patent to the intercellular space with the cavity membrane establishing continuity with the dendritic membrane. Many cavities often formed in a single dendrite, and such severely cavitated dendrites became reduced to a trabeculated shell which ultimately fragmented into several small pieces. The presence of synaptic connections from a number of different kinds of axonal endings, including scalloped and dome-shaped endings, was not sufficient to prevent cavitation. The actual severing of synaptic connections on the cavitated dendrite appeared to be a relatively late event in the process since small pieces of dendritic debris could still be found clinging to their axodendritic synapses. Evidence that dendrites were being lost from the neuropil was most readily apparent in many of the disrupted glomeruli in lamina II in which many of the scalloped depressions in the central axonal endings that normally contained small dendrites were empty. Many central axonal endings remained in synaptic contact with only a single dendrite which often showed signs of cavitation. Such central endings showed only subtle remaining traces of their normal scalloped contours. This study demonstrates that injury to the distal branches of primary trigeminal neurons which innervate tooth pulps resulted in trans-synaptic degenerative changes in the dendritic arbors of second-order neurons which destroyed fine-caliber higher order dendrites.