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Anti–nerve growth factor does not change physical activity in normal young or aging mice but does increase activity in mice with skeletal pain

Majuta, Lisa A.a; Mitchell, Stefanie A.T.a; Kuskowski, Michael A.b; Mantyh, Patrick W.a,c,*

doi: 10.1097/j.pain.0000000000001330
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Anti–nerve growth factor (anti-NGF) therapy has shown significant promise in attenuating several types of skeletal pain. However, whether anti-NGF therapy changes the level of physical activity in individuals with or without skeletal pain is largely unknown. Here, automated day/night activity boxes monitored the effects of anti-NGF treatment on physical activity in normal young (3 months old) and aging (18-23 months old) mice and mice with bone fracture pain. Although aging mice were clearly less active and showed loss of bone mass compared with young mice, anti-NGF treatment had no effect on any measure of day/night activity in either the young or aging mice. By contrast, in mice with femoral fracture pain, anti-NGF treatment produced a clear increase (10%-27%) in horizontal activity, vertical rearing, and velocity of travel compared with the Fracture + Vehicle group. These results suggest, just as in humans, mice titrate their level of physical activity to their level of skeletal pain. The level of skeletal pain may in part be determined by the level of free NGF that seems to rise after injury but not normal aging of the skeleton. In terms of bone healing, animals that received anti-NGF showed an increase in the size of calcified callus but no increase in the number of displaced fractures or time to cortical union. As physical activity is the best nondrug treatment for many patients with skeletal pain, anti-NGF may be useful in reducing pain and promoting activity in these patients.

Anti–nerve growth factor does not increase physical activity in young or aging naive mice but attenuates the decline in physical activity in mice with skeletal pain.

aDepartment of Pharmacology, University of Arizona, Tucson, AZ, United States

bDepartment of Psychiatry, University of Minnesota, Minneapolis, MN, United States

cCancer Center, University of Arizona, Tucson, AZ, United States

Corresponding author. Address: Department of Pharmacology, University of Arizona, 1501 N. Campbell Ave, PO Box 245050, Tucson, AZ 85724, United States. Tel.: (520) 626-0742; fax: (520) 626-8869. E-mail address: pmantyh@email.arizona.edu (P.W. Mantyh).

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.painjournalonline.com).

Received February 28, 2018

Received in revised form May 09, 2018

Accepted May 25, 2018

© 2018 International Association for the Study of Pain
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