Synaptic relationships between induced neuropeptide Y-like immunoreactive terminals and cuneothalamic projection neurons in the rat cuneate nucleus following median nerve transection

J Chem Neuroanat. 2008 Sep;36(1):27-32. doi: 10.1016/j.jchemneu.2008.05.006. Epub 2008 May 28.

Abstract

Previous studies have demonstrated that following complete median nerve transection (CMNT), neuropeptide Y-like immunoreactive (NPY-LI) fibers were dramatically increased and predominantly expressed in the ventral portion of the middle cuneate nucleus (CN), reaching maximum numbers at four weeks. Ultrastructurally, NPY-LI terminals made axodendritic synapses, but the postsynaptic elements are unknown. In the present study, using retrograde tract-tracing of wheat germ agglutinin conjugated with horseradish peroxidase (WGA-HRP) and NPY immunocytochemistry we examined the synaptic relationships between cuneothalamic projection neurons (CTNs) and NPY-LI terminals in the rat CN following CMNT. The injury-induced NPY-LI fibers were distributed throughout the rostrocaudal extent of the CN. Further, the greatest number of HRP-labeled CTNs was observed in the ventral portion of the middle CN. Ultrastructurally, the NPY-LI terminals made asymmetric axodendritic synaptic contact with the HRP-labeling CTN dendrites. These data suggest that injury-induced NPY may modulate the excitability of CTNs, and thus, play a role in the transmission of neuropathic sensation following median nerve injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axotomy
  • Immunohistochemistry
  • Male
  • Median Nerve / physiology
  • Medulla Oblongata / metabolism
  • Medulla Oblongata / ultrastructure*
  • Microscopy, Electron, Transmission
  • Neural Pathways / metabolism
  • Neural Pathways / ultrastructure*
  • Neurons / metabolism
  • Neurons / ultrastructure*
  • Neuropeptide Y / metabolism*
  • Presynaptic Terminals / metabolism
  • Presynaptic Terminals / ultrastructure*
  • Rats
  • Rats, Wistar
  • Synapses / metabolism
  • Synapses / ultrastructure*

Substances

  • Neuropeptide Y