Journal of Neuroscience, Vol 12, 1716-1725, Copyright © 1992 by Society for Neuroscience
Neonatal capsaicin treatment attenuates spinal Fos activation and dynorphin gene expression following peripheral tissue inflammation and hyperalgesia
JL Hylden, K Noguchi and MA Ruda
Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892.
An animal model of nociception involving unilateral hindpaw inflammation
has been used to examine behavioral, molecular, and biochemical aspects of
well-characterized spinal cord neural circuits involved in pain
transmission. The neurotoxin capsaicin administered neonatally was used to
modify this neuronal system by producing a selective destruction of most
small, unmyelinated primary afferent axons. Capsaicin had minimal effects
on the behavioral hyperalgesia and edema associated with the hindpaw
inflammation and on the constitutive expression of preprodynorphin (PPD)
mRNA and preproenkephalin mRNA in the spinal cord. However, the
inflammation-induced increases in Fos- like immunoreactivity (Fos-LI) and
in PPD mRNA were greatly attenuated by neonatal capsaicin treatment. The
data indicate that input from small-diameter unmyelinated primary afferents
is important for the stimulus-induced increase in Fos-LI and PPD mRNA. Our
finding that neonatal capsaicin reduces the levels of Fos-LI and PPD mRNA
in a related fashion in the spinal dorsal horn provides further evidence
for a relationship between the protein product of the c-fos protooncogene
and regulation of dynorphin gene transcription.
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