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.
Bibliographical noteFunding 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.
- Depression-related behavior
- Plasticity-related genes
- Psychophysical stress
- Psychosocial stress
ASJC Scopus subject areas
- Neuropsychology and Physiological Psychology
- Endocrine and Autonomic Systems
- Psychiatry and Mental health
- Behavioral Neuroscience