In adult rats very few dorsal root ganglion neurones (DRG) express NPY; however, following injury to their peripherally projecting axons many large DRG neurones start to synthesise this peptide. In the spinal cord increased expression of NPY is seen in dorsal horn LIÐLIII in the somatotopic region corresponding to an injured nerve. In these regions abnormal myelinated afferent sprouts have been observed. The present study has examined whether this new expression of NPY results in altered function of LII neurones.

Unilateral sciatic nerve section was carried out in rats between 12 and 14 days postnatally under aseptic conditions and short duration halothane anaesthesia. Sham-operated litter mates acted as controls. Seven to fifteen days later they were anaesthetised with ketamine (200 mg kg^-1 I.M.) and decapitated. Parasaggital lumbar spinal cord slices were prepared with intact L4, L5, L6 dorsal roots, DRG and peripheral nerves, and intracellular recordings made from LII neurones. The effects of bath-applied NPY and nerve stimulation were examined. Neurones were labelled by intracellular injection of neurobiotin and subsequently slices were stained with IB4 lectin to reveal the relationship of the injected neurones to the denervated zone and LII.

Bath application of NPY (100 nMÐ10 µM) caused mainly hyperpolarisation of LIÐLIII neurones. In the denervated zone, nine (64 %) of the intrinsic LII neurones tested with 1 µM NPY were hyperpolarised (mean amplitude -8.14 mV ± 4.18, S.D.), whereas in sham-operated animals and non-denervated regions, five (54 %) of these were hyperpolarized (mean amplitude -10.6 mV ± 4.82, S.D.) (n.s., P > 0.5, unpaired t test). In a sample of 39 neurones from LIIÐLIII (based on electrode targeting, not intracellular labelling) studied in neonatal animals not subject to prior operation, 28 (72 %) were hyperpolarized by NPY (mean amplitude -6.4 mV). Intrinsic LII neurones in either the denervated area or innervated regions were not depolarised by NPY. Immunocytochemical studies revealed that LIIIÐIV neurones and their dendrites projecting into LII are probably a target for myelinated primary afferents, which synthesise NPY following nerve injury. The distribution of the NPY Y1 receptor shown by immunochemistry corresponded to neurones inhibited by NPY and showed no change following nerve section. The responses to nerve stimulation suggested that no new myelinated afferent sprouts had grown following nerve section which targeted intrinsic LII neurones.

These studies suggest that the changes that occur in myelinated primary afferents following nerve injury do not result in NPY-mediated excitation of LII neurones via aberrant myelinated afferent sprouts.

This work was supported by Action Research.

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