Stress impairs healing and in part this effect is thought to be mediated by glucocorticoids. However, the brain systems that underlie the effects of stress on healing remain to be determined. Since the central nucleus of the amygdala (CeA) plays a role in mediating an individual's behavioral and physiological reactivity to stress, we investigated, in rhesus monkeys, whether selective lesions of the CeA altered the gene expression of chemokines (IL-8 and MIP-1α) that are associated with early dermal healing. We used rhesus monkeys because they provide an excellent animal model to investigate brain mechanisms relevant to human stress, anxiety, and psychopathology. Hypothalamic-pituitary-adrenal (HPA) activity was assessed in the monkeys prior to the wound healing experiment demonstrating that the CeA lesions reduce HPA activity. In the healing experiment, stress decreased IL-8 and MIP-1α gene expression in both CeA lesioned and non-lesioned animals. Conversely, the CeA lesions increased the tissue expression of IL-8 and MIP-1α mRNA prior to and after stress exposure. These results demonstrate that in primates the CeA is a key brain region involved in the regulation of processes associated with wound healing. Because of brain and behavioral similarities between rhesus monkeys and humans, these results are particularly relevant to understanding brain mechanisms that influence healing in humans.
|Number of pages||5|
|Journal||Brain, Behavior, and Immunity|
|Publication status||Published - Nov 2006|
Bibliographical noteFunding Information:
We are grateful to H. Van Valkenberg, T. Johnson, J. King, and the staff at the Harlow Center for Biological Psychology and the National Primate Research Center at the University of Wisconsin for their technical support. This work was supported by Grants P50 DE-13749, MH46729, MH52354, MH61083, the Health Emotions Research Institute, and Meriter Hospital.
- HPA axis
- Rhesus monkey
- Wound healing
- Stress, Psychological
- Macaca mulatta