Journal of Neuroscience, Vol 14, 3958-3968, Copyright © 1994 by Society for Neuroscience
Some sensory neurons express neuropeptide Y receptors: potential paracrine inhibition of primary afferent nociceptors following peripheral nerve injury
PW Mantyh, CJ Allen, S Rogers, E DeMaster, JR Ghilardi, T Mosconi, L Kruger, PJ Mannon, IL Taylor and SR Vigna
Molecular Neurobiology Laboratory, Veterans Administration Medical Center, Minneapolis, Minnesota 55417.
Neuropeptide Y (NPY) has been suggested to exert antinociceptive actions by
inhibiting the release of neurotransmitters from trigeminal and dorsal root
ganglia (DRG) neurons, but the site of direct NPY action in vivo and the
NPY receptor subtype mediating these effects are unknown. 125I-peptide YY
(PYY) was used to localize and characterize NPY receptor binding sites in
trigeminal ganglia, DRG, and spinal cord of the rat, rabbit, and monkey. In
the rat, rabbit, and monkey, 5-20% of trigeminal ganglia and DRG neurons
express NPY binding sites. Unilateral cuff-induced neuropathy or
transection of the rat sciatic nerve did not significantly alter the
density or number of DRG neurons expressing NPY receptors. A unimodal size
distribution for L4 and L5 DRG neurons expressing NPY binding sites in the
rat was determined, with a mean cross-sectional area of 947 microns 2. In
the spinal cord the highest concentration of NPY receptors is found in
laminae I, II, V, X, and Onuf's nucleus. Pharmacological experiments using
selective Y1 and Y2 receptor antagonists suggest that Y2 is the prominent
NPY receptor subtype expressed in trigeminal ganglia neurons, DRG neurons,
and spinal cord. Previous studies have demonstrated that a population of
large-diameter, presumably myelinated primary afferents express NPY after
peripheral nerve injury. NPY released from these injured large- diameter
DRG neurons may act in a paracrine fashion to block the transmission of
nociceptive information from the small- and medium- diameter DRG neurons
that constitutively express NPY receptors. NPY receptors are therefore
uniquely positioned to inhibit primary afferent nociceptors directly,
especially after peripheral nerve injury.
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