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American Society for Action on Pain

UI - 000045

AU - Millan MJ

AU - Millan MH

AU - Czlonkowski A

AU - Hollt V

AU - Pilcher CW

AU - Herz A

AU - Colpaert FC

TI - A model of chronic pain in the rat: response of multiple opioid systems to adjuvant-induced arthritis

AB - 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


SO - Journal of Neuroscience 1986;6:899-906