Research

Involvement of P311 in the affective, but not in the sensory component of pain

Yan-Gang Sun^1* , Yong-Jing Gao^1,6* , Zhong-Qiu Zhao¹ , Bing Huang^1,7 , Jun Yin¹ , Gregory A Taylor^4,5 and Zhou-Feng Chen^1,2,3

¹  Departments of Anesthesiology, Washington University School of Medicine Pain Center, St. Louis, Missouri 63110, USA

²  Psychistry, Washington University School of Medicine, St. Louis, Missouri 63110, USA

³  Developmental Biology, Washington University School of Medicine, St. Louis, Missouri 63110, USA

⁴  Departments of Medicine, Molecular Genetics and Microbiology, and Immunology, Division of Geriatrics, and Center for the Study of Aging and Human Development, Duke University Medical Center, Durham, NC 27710, USA

⁵  GRECC, VA Medical Center, Durham, NC 27705, USA

⁶  Institute of Nautical Medicine, Nantong University, Nantong, 226001, PR China

⁷  Department of Anesthesiology and Pain Management, Ministry of Health Beijing Hospital, Beijing, 100730, PR China

author email corresponding author email* Contributed equally

Molecular Pain 2008, 4:23doi:10.1186/1744-8069-4-23

Published:	12 June 2008

Abstract

Pain is comprised of the sensory and affective components. Compared to the well-investigated mechanisms of the sensory pain, much less is known about the mechanisms underlying the affective pain. In recent years, accumulating evidence suggests that the anterior cingulate cortex (ACC) is a key structure for pain affection. To identify the molecules that may be involved in the affective component of pain, we have searched the Allen Brain Atlas expression database for genes whose expression is enriched in the ACC, and found that P311, an 8-kDa peptide, showed the strong expression in the ACC. P311 is also expressed in other areas associated with pain affection including the amygdala, insular cortex and thalamus. To understand the role of P311 in pain perception, we have examined the pain behaviors of the mice lacking P311. P311^-/- mice showed normal heat and mechanical sensitivity, as well as normal formalin-induced inflammatory pain. In contrast, the formalin-induced avoidance behavior, which reflects pain-related negative emotion, was significantly attenuated in P311^-/- mice relative to the control mice. These results suggest that P311 is involved in the affective, but not in the sensory component of pain. Our study thus provides the first evidence suggesting that the affective and sensory pain may be regulated by distinct molecular mechanisms.