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[Abstract Title]. - Society for Neuroscience

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Support: Supported by CIHR<br />

<strong>Title</strong>: Bone cancer pain: A new way to fight pain ?<br />

Authors: *V. V. OTIS, L. GENDRON;<br />

Physiologie et Biophysique, Univ. de Sherbrooke, Sherbrooke, QC, Canada<br />

<strong>Abstract</strong>: In North America, cancer appears in one third of the population and leads to bone<br />

tumour invasion in 60% of cases. Bone metastasis are usually seen in advance stages of cancer<br />

especially those originating from breast or prostate cancer. Chronic pain due to osteosarcoma can<br />

achieve high levels of background and breakthrough pain, there<strong>for</strong>e increasing the difficulty to<br />

treat patients. As of today, morphine and its derivatives are among the most powerful and<br />

commonly used opioids to alleviate pain. Even with their strong analgesic potency, opioids<br />

acting at mu opioid receptors are often accompanied by various side-effects, possibly including<br />

increased osteolytic activity and bone loss. Over the past few years, compounds activating the<br />

delta opioid receptor (DOPR) were shown to have significant analgesic effects without any<br />

significant side-effects usually associated with narcotics. The aim of this study is to evaluate the<br />

potential roles of selective DOPR agonists <strong>for</strong> the treatment of bone cancer pain induced by<br />

injection of 30 000 syngenic MRMT-1 cells (mammary carcinoma) in the femur of Sprague-<br />

Dawley rats. As other mammary tumours, our results revealed the presence of DOPR mRNA in<br />

MRMT-1, although at low levels. Thus, DOPR agonists might potentially have an influence on<br />

tumour progression. Fourteen days after cancer induction, rats had develop significant allodynia<br />

in their ipsilateral hindpaw, an effect accompanied by an unilateral activation of glial cells<br />

(astrocyte and microglia) in L2-L4 lumbar spinal cord segments. Our results suggest that this<br />

bone cancer model might be a promising tool to evaluate the role of DOPR agonists <strong>for</strong> the<br />

treatment of bone cancer-induced pain.<br />

Disclosures: V.V. Otis, None; L. Gendron, None.<br />

Poster<br />

267. Pain: Pain Models II<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 267.7/FF13<br />

Topic: D.08.j. Pain models<br />

Support: NIH R21 NS 055896<br />

P32 NS07375

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