Captivity alters neuroendocrinology of house sparrows


Meeting Abstract

4-4  Monday, Jan. 4 08:45  Captivity alters neuroendocrinology of house sparrows. DURANT, S.E.*; LOVE, A.C.; BELIN, B.; TAMAYO-SANCHEZ, D.; SANTOS-PACHECO, M; DICKENS, M.J.; CALISI, R.M.; Oklahoma State Univ; Oklahoma State Univ; Barnard College, Columbia University; Barnard College, Columbia University; Barnard College, Columbia University; UC Berkely; Barnard College, Columbia University/UC Davis sarah.durant@okstate.edu

Captivity causes stress in most wild-caught vertebrates. While many species eventually acclimate to captive conditions, some species never adjust to their new environment. Wild-caught house sparrows are commonly-used in captive studies, yet physiological data from our lab suggest they do not acclimate to captivity within 9 weeks of capture. We examined whether neuroendocrine changes in the hypothalamus of house sparrows coincided with plasma corticosterone (an avian glucocorticoid) and immune responses. We measured mRNA expression of glucocorticoid receptor (GR; binds to corticosterone), corticotropin releasing hormone (CRH; neurohormone involved in the stress response), and gonadotropin inhibitory hormone (GnIH; inhibits reproduction) immediately upon capture (controls) or after 24, 45, or 66 days in captivity. We also quantified cells immunoreactive for GnIH (GnIH-ir) using immunohistochemistry. We found that GR expression and GnIH-ir cell counts initially increased in response to captivity but did not differ from control birds after 66 days in captivity. CRH and GnIH expression exhibited similar responses to captivity, but this was not statistically significant. We did not detect significant correlations between changes in neuroendocrine measurements and corticosterone or immune responses. However, control birds with high CRH expression also had greater capacity to secrete corticosterone. Captivity affected physiological measures of birds throughout the entire period of captivity; however, these effects are likely not driven by changes in expression of the neuroendocrine endpoints we measured.

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