TY - JOUR
T1 - Corticotropin releasing hormone receptor alterations elicited by acute and chronic unpredictable stressor challenges in stressor-susceptible and resilient strains of mice
AU - Anisman, Hymie
AU - Prakash, Priya
AU - Merali, Zul
AU - Poulter, Michael O.
N1 - Funding Information:
This research was supported by the Canadian Institutes of Health Research and by the Natural Sciences and Engineering Research Council of Canada. HA holds a Canada Research Chair in Neuroscience and MOP holds a NARSAD Fellowship. The assistance of Marzena Sieczkos, Nathalie Lukenbill and Katie Cleland is much appreciated.
PY - 2007/8/6
Y1 - 2007/8/6
N2 - Stressors increase corticotropin releasing hormone (CRH) functioning in hypothalamic and frontal cortical brain regions, and thus may contribute to the provocation of anxiety and depressive disorder. As the effects of stressors on these behavioral changes are more pronounced in some strains of mice (e.g., BALB/cByJ) than in others (e.g., C57BL/6ByJ), the present investigation assessed whether acute and chronic stressors would differentially influence CRH receptor immunoreactivity (ir-CRHr) and CRH receptor mRNA expression (CRH1 and CRH2) in the orbital frontal cortex (OFC) of these strains. An acute noise stressor, and to a greater extent a chronic, variable stressor regimen reduced ir-CRHr in BALB/cByJ mice. In contrast, in the hardier C57BL/6ByJ mice the acute stressor increased ir-CRHr in portions of the OFC, whereas a chronic stressor tended to reduce ir-CRHr. However, whereas the acute stressor did not influence CRH1 mRNA expression, the chronic stressor increased CRH1 mRNA expression in both mouse strains. The CRH2 expression appeared in low abundance in both strains and was unaltered by the stressor. In addition to the OFC variations, quantitative immunohistochemistry indicated that the chronic stressor treatment increased CRH immunoreactivity in the median eminence of C57BL/6ByJ mice, but co-expression of CRH and arginine vasopressin (AVP) immunoreactivity was not provoked by the stressors. The data support the view that stressors provoke marked variations of ir-CRHr in the OFC that might contribute to the differential anxiety/depression-like profiles ordinarily apparent in the stressor-vulnerable and -resilient mouse strains.
AB - Stressors increase corticotropin releasing hormone (CRH) functioning in hypothalamic and frontal cortical brain regions, and thus may contribute to the provocation of anxiety and depressive disorder. As the effects of stressors on these behavioral changes are more pronounced in some strains of mice (e.g., BALB/cByJ) than in others (e.g., C57BL/6ByJ), the present investigation assessed whether acute and chronic stressors would differentially influence CRH receptor immunoreactivity (ir-CRHr) and CRH receptor mRNA expression (CRH1 and CRH2) in the orbital frontal cortex (OFC) of these strains. An acute noise stressor, and to a greater extent a chronic, variable stressor regimen reduced ir-CRHr in BALB/cByJ mice. In contrast, in the hardier C57BL/6ByJ mice the acute stressor increased ir-CRHr in portions of the OFC, whereas a chronic stressor tended to reduce ir-CRHr. However, whereas the acute stressor did not influence CRH1 mRNA expression, the chronic stressor increased CRH1 mRNA expression in both mouse strains. The CRH2 expression appeared in low abundance in both strains and was unaltered by the stressor. In addition to the OFC variations, quantitative immunohistochemistry indicated that the chronic stressor treatment increased CRH immunoreactivity in the median eminence of C57BL/6ByJ mice, but co-expression of CRH and arginine vasopressin (AVP) immunoreactivity was not provoked by the stressors. The data support the view that stressors provoke marked variations of ir-CRHr in the OFC that might contribute to the differential anxiety/depression-like profiles ordinarily apparent in the stressor-vulnerable and -resilient mouse strains.
KW - AVP
KW - CRH
KW - CRH
KW - Corticotropin releasing hormone
KW - Orbital frontal cortex
KW - Stress
UR - http://www.scopus.com/inward/record.url?scp=34250168662&partnerID=8YFLogxK
U2 - 10.1016/j.bbr.2007.04.002
DO - 10.1016/j.bbr.2007.04.002
M3 - Article
C2 - 17517441
AN - SCOPUS:34250168662
SN - 0166-4328
VL - 181
SP - 180
EP - 190
JO - Behavioural Brain Research
JF - Behavioural Brain Research
IS - 2
ER -