Abstract: Abstract
Stress is a negative emotional experience accompanied by predictable biochemical, physiological, cognitive, and behavioral changes that are directed either toward altering the stressful event or to accommodating to its effects. Different types of stressful events might sometimes produce qualitatively different patterns of effects in behavior, suggesting that different central mechanisms may be involved. However, most of the molecules involved in central mechanisms of stress response, especially stress-induced behavioral disorders, are still unknown. Neurogranin (NG) is a brain-specific, postsynaptically located protein kinase C (PKC) substrate found by Watson and his colleagues in 1990. It is mainly distributed in the frontal cortex, hippocampus and amygdala of rodents that are considered as essential components of neural circuitry mediating stress responses. Numerous animal studies have demonstrated that NG is involved in several pathways of protein signal transduction in brain, long-term potentiation and long-term depression. NG-knockout animals exhibited deficits in learning and memory. These results implied that NG may be a mediator between stress and behavior. However, until recently, the cellular role of NG has not been clearly established. To understand more molecular events underlying central mechanisms of stress-induced behavioral changes, the purpose of the present study was to investigate the effects of acute emotional stress on behavior and protein levels of neurogranin in brain, and the correlation between protein levels of neurogranin and stress-induced behavioral changes.
Forty rats were randomly divided into emotional stressed group 1 (ES1), emotional stressed group 2 (ES2), handled-control 1 (C1) and handled-control 2(C2), with ten in each. Randomly giving empty water bottles at set times was used as an emotional stressor. Behavioral changes in rats after stress were observed by open-field test and elevated plus maze task, and protein levels and phosphorylation of neurogranin of hippocampus and forebrain were determined by Western blotting. The results showed that locomotor activity in open-field test in ES1 was increased more than that in C1 group (P<0.05). Protein levels and phosphorylation of Neurogranin of hippocampus and forebrain in ES1 were significantly higher than that in C1 (P<0.05, P<0.05) and C2 (P<0.05, P<0.05). Phosphorylation of Neurogranin level of forebrain in ES2 was significantly higher than that in C1 (P<0.05). The correlation was significant at 0.05 levels between locomotor activity and phosphorylation of neurogranin in the hippocampus. These results suggested that neurogranin is one of the stress-related substances in brain. Acute emotional stress can induce anxiety. Locomotor activity may be a sensitive behavioral index, and phosphorylation of neurogranin in the hippocampus may be an effective biological predictor for anxiety and/or depression induced by acute emotional stress. In summary, acute emotional stress induces behavioral changes and phosphorylation levels of neurogranin in frontal cortex of rats. Underlying mechanisms explaining the behavioral changes in stress effects are discussed, including the role of neurogranin in the hippocampus and frontal cortex.

Key words: acute stress, emotional stress, hippocampus, frontal cortex, behavior, neurogranin