Aa. Cameron et al., THE ENDOGENOUS LECTIN RL-29 IS TRANSSYNAPTICALLY INDUCED IN DORSAL HORN NEURONS FOLLOWING PERIPHERAL NEUROPATHY IN THE RAT, Brain research, 620(1), 1993, pp. 64-71
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.