Journal of Neuroscience, Vol 6, 899-906, Copyright © 1986 by Society for Neuroscience
A model of chronic pain in the rat: response of multiple opioid systems to adjuvant-induced arthritis
MJ Millan, MH Millan, A Czlonkowski, V Hollt, CW Pilcher, A Herz and FC Colpaert
Chronic arthritic pain was induced by intradermally inoculating rats at the
tail-base with Mycobacterium butyricum, which results in swelling,
inflammation, and hyperalgesia of the joints. These symptoms peak at 3
weeks after inoculation and disappear by 10 weeks. The following changes
were seen at 3 weeks. Immunoreactive dynorphin (ir-Dyn) and ir-
alpha-neo-endorphin (alpha-NE) manifested comparable patterns of change.
Their levels were increased in the anterior, but not neurointermediate,
pituitary. The thalamus showed a rise in ir-Dyn and ir-alpha-NE, but no
alterations were seen in other brain regions. In each case, cervical,
thoracic, and lumbosacral sections of the spinal cord showed a rise in
ir-Dyn and ir-alpha-NE: This was most pronounced in the lumbosacral region,
where the magnitude of these shifts correlated with the intensity of
arthritic symptoms. In addition, a moderate elevation in
ir-methionine-enkephalin (ME) was seen in lumbosacral spinal cord. In
brain, ir was not changed. The level of ir- beta-endorphin (beta-EP) was
elevated both in the plasma and the anterior, but not the
neurointermediate, pituitary. In addition, the content of messenger RNA
encoding the beta-EP precursor, proopiomelanocortin (POMC), was enhanced in
the anterior lobe. Thus, there was a selective activation of synthesis of
beta-EP in, and its secretion from, the anterior lobe. In no brain tissue
did levels of ir- beta-EP change. At 10 weeks postinoculation, the above
changes were no longer apparent, indicating their reversibility.(ABSTRACT
TRUNCATED AT 250 WORDS)
