| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Research Abstract |
It has been suggested that early adverse life events including childhood abuse, neglect, and parental loss may predispose individuals for the development of affective disorders in response to extreme stress exposure in adulthood. Recently, we have demonstrated that the prenatal saline injection stress produced an enhanced adrenocortical response to conditioned fear stress and a prolonged immobility duration in forced swimming stress, indicating that the prenatally stressed offspring seemed to be susceptive to an acute stress in adulthood endocrinologically and behaviorally. It is still unclear whether prenatally stressed rats can habituate to chronic stress in adulthood. We have investigated the stress response of c-fos mRNA expression in brain and of corticosterone secretion in prenatally stressed adult male rats during 14 days repeated restraint stress. To an acute restraint stress, prenatally stressed rats showed significantly increased response of c-fos mRNA expression, to the same extent, compared to control rats, in brain regions including para-ventricular nucleus, amygdala, locus ceruleus, raphe nucleus, cingulate cortex, piriform cortex, and seputum. Repeated restraint stress for 14 days induced significant reduction of c-fos response, compared to the expession of c-fos mRNA during acute restraint stress, in all investigated brain regions except septum of prenatally stressed rats. In septum, prenatally stressed rats showed significant increase in c-fos expression in response to repeated restraint stress, compared to control rats. In addition, control rats showed reduction of plasma corticosterone level at 120min after the beginning of restraint stress from the 7th day of stress, whereas prenatally stressed rats did not show such habituation. These findings indicate that the neural circuit including septum may be responsible to the vulnerabillty of prenatally stressed rats to chronic stress in adulthood.
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