TY - JOUR
T1 - Physical stress differs from psychosocial stress in the pattern and time-course of behavioral responses, serum corticosterone and expression of plasticity-related genes in the rat
AU - Kavushansky, Alexandra
AU - Ben-Shachar, Dorit
AU - Richter-Levin, Gal
AU - Klein, Ehud
N1 - Funding Information:
This work was supported by the Research grant of the Chief Scientist Office of the Ministry of Health, Israel, #3000003141, by a post-doctoral fellowship from the Lady Davis’s fellowship trust, by a post-doctoral fellowship from the National Institute for Psychobiology in Israel and by the EU’s PROM-EMORIA Grant #512012.
PY - 2009
Y1 - 2009
N2 - Stressors differ in their physiological and behavioral outcomes. One of the major mechanisms by which stressors affect the brain and behavior is alteration in neuronal plasticity. We investigated in the rat the effects of a single exposure to psychophysical (electrical foot shock) vs. psychological (social defeat) stressors on anxiety-and depression-related behaviors, serum levels of corticosterone and the expression of plasticity-related genes CAM-L1, CREB, GAP-43, and laminin in the prefrontal cortex (PFC), the amygdala and the hippocampus. Rats were examined for 24 h or 1 week after the exposure to stress. Footshocks enhanced anxiety-related behaviors, whereas social defeat induced depression-related behaviors at both time points and less pronounced anxiety 1 week post-exposure. Serum corticosterone concentrations were enhanced 24 h after shocks, but only 1 week after exposure to the social stressor. Moreover, the shock-stressed rats exhibited decreased CAM-L1 protein level in the hippocampus 24 h post-exposure and decreased GAP-43 protein level in the PFC 1 week post-exposure. By contrast, the social stressor enhanced expression of the plasticity-related proteins in the amygdala and the hippocampus, mostly 1 week after the exposure. These results indicate stressor-specific time-dependent changes in different neuronal pathways, and suggest consideration of a cause-specific approach to the treatment of stress-related disorders.
AB - Stressors differ in their physiological and behavioral outcomes. One of the major mechanisms by which stressors affect the brain and behavior is alteration in neuronal plasticity. We investigated in the rat the effects of a single exposure to psychophysical (electrical foot shock) vs. psychological (social defeat) stressors on anxiety-and depression-related behaviors, serum levels of corticosterone and the expression of plasticity-related genes CAM-L1, CREB, GAP-43, and laminin in the prefrontal cortex (PFC), the amygdala and the hippocampus. Rats were examined for 24 h or 1 week after the exposure to stress. Footshocks enhanced anxiety-related behaviors, whereas social defeat induced depression-related behaviors at both time points and less pronounced anxiety 1 week post-exposure. Serum corticosterone concentrations were enhanced 24 h after shocks, but only 1 week after exposure to the social stressor. Moreover, the shock-stressed rats exhibited decreased CAM-L1 protein level in the hippocampus 24 h post-exposure and decreased GAP-43 protein level in the PFC 1 week post-exposure. By contrast, the social stressor enhanced expression of the plasticity-related proteins in the amygdala and the hippocampus, mostly 1 week after the exposure. These results indicate stressor-specific time-dependent changes in different neuronal pathways, and suggest consideration of a cause-specific approach to the treatment of stress-related disorders.
KW - Anxiety
KW - Corticosterone
KW - Depression-related behavior
KW - Plasticity-related genes
KW - Psychophysical stress
KW - Psychosocial stress
UR - http://www.scopus.com/inward/record.url?scp=70549094416&partnerID=8YFLogxK
U2 - 10.1080/10253890802556081
DO - 10.1080/10253890802556081
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C2 - 19929444
AN - SCOPUS:70549094416
SN - 1025-3890
VL - 12
SP - 412
EP - 425
JO - Stress
JF - Stress
IS - 5
ER -