THE ENDOGENOUS LECTIN RL-29 IS TRANSSYNAPTICALLY INDUCED IN DORSAL HORN NEURONS FOLLOWING PERIPHERAL NEUROPATHY IN THE RAT

Neurons containing immunoreactivity to the endogenous lactose-binding lectin, RL-29, were examined in the L4 segment of the spinal cord of r ats with an experimental neuropathy. The cells appeared by 5 days and were also present at 14 and 28 days postoperatively. All neurons were found in the dorsal horn ipsilateral to the injury. The neurons were m ultipolar and the reaction product revealed the morphology of the prim ary and secondary dendrites and some axons. Most of the neurons were l ocated in the reticulated region of the dorsal horn, corresponding to Rexed's lamina V. In 14-day neuropathy animals treated with the NMDA-r eceptor antagonist MK-801, the number of RL-29 cell profiles observed was significantly reduced. Double labeling experiments revealed that s pinothalamic tract neurons did not contain RL-29. The results suggest that the neuropathic injury produces a long term, transynaptic change in a subpopulation of dorsal horn neurons, that is mediated by excitat ory amino acid transmitters acting at NMDA receptors.