It is known that the early environment affects the mental development in offspring of rodents and humans. However, it has not been determined whether early postpartum depressive state enhances depressive state in offspring. Using the learned helplessness (LH) as an animal model of depression, we examined the influence of early postpartum LH on the stress reactivity of offspring. Dam rats were judged as LH or non-helpless (nLH) on postnatal day (PN) 2-3, and maternal behavior was recorded during PN2-14. On PN 45-46, offspring were subjected to the LH test. The hippocampal levels of glucocorticoid receptor (GR) mRNA were measured before and after the LH test in the offspring using real-time quantitative PCR. Active nursing in LH dams was significantly lower than that in nLH dams. Susceptibility to the LH test in the offspring of LH dams was significantly higher than that in the offspring of nLH dams, and was negatively correlated with active nursing in the LH dams. The levels of GR mRNA in the offspring of LH dams were significantly lower than those in the offspring of nLH dams before and after the LH test. These findings suggested that early postpartum LH decreased active nursing and increased depression-like behavior in the offspring with the decreased expression of GR mRNA in the hippocampus.

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Selective serotonin reuptake inhibitors (SSRIs) have wide indications for the treatment of anxiety disorders, including panic disorder, generalized anxiety disorder, posttraumatic stress disorder, obsessive-compulsive disorder and social anxiety disorder in addition to depression. Until recently, no animal model has been available for screening the anxiolytic effect of SSRIs and studying its mechanism of action. We have investigated the relationship between serotonin neurotransmission and anxiety using conditioned fear stress (CFS), an animal model of anxiety. CFS increased serotonin neurotransmission in the medial prefrontal cortex and amygdala. In behavioral pharmacological studies, SSRIs, serotonin_<1A> agonists and monoamine oxidase inhibitors, which are assumed to facilitate serotonin neurotransmission, decreased conditioned freezing, an index of anxiety or fear, in CFS. In vivo microdialysis studies showed that serotonin neurotransmission in the medial prefrontal cortex increased after recovered from the freezing behavior. Microinjection of SSRI to the basolateral nucleus of the amygdala reduced conditioned freezing, indicating that the amygdala is one of target brain sites of anxiolytic action of SSRIs. Furthermore, CFS-induced c-Fos expression in the basolateral nucleus of the amygdala was reduced by SSRI pretreatment. Taken together, our animal studies suggest that facilitation of brain serotonin neurotransmission decreases anxiety in agreement with the clinical evidence, and that SSRI-induced inhibition of the neuronal activity of the basolateral nucleus of the amygdala is the mechanism of action of the anxiolytic efficacy of SSRIs.

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Psychosomatic disorders are the states with physical disorders, which are either organic or functional and originated from and/or aggravated by psychosocial stressors. The pathophysiology of psychosomatic disorders has been investigated mainly on autonomic nervous system and endocrine system. Recent advances in neuroscience enabled us to explore the brain mechanism of these disorders and emotion formation and typical example is irritable bowel syndrome. Noxious stimulation to the gut activates the anterior cingulate cortex, amygdala, insula, and so on. The activation of the anterior cingulate cortex is known to relate to depression, whereas the activation of the amygdala results in anxiety. Therefore, the common pathway between formation of visceral pain and that of negative emotion is suggested. Emotion is originated from the signal given to the peripheral sensory organs and initially it is perceived as olfaction, vision, audition, taste, and bodily sensation in the brain. Among these, role of bodily sensation whose prototype is visceral perception (interoception) in emotion formation will be clarified in the future.

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I will review the brain imaging studies on panic disorder (PD), and show the significance that they propose for the development of psychosomatic medicine. The major neuroanatomical models of PD have been proposed by Gorman and Coplan. The sufficient evidence has been accumulated these 5 years for supporting their hypotheses, and PD has come to be regarded as a brain disease. The studies include those showing brain functional abnormalities at rest, specific responses to the relevant tasks, and brain structural abnormalities. The results indicated the hypofunction and atrophy of prefrontal cortex besides the hyperfunction of amygdala, hippocampus, and periaqueductal grey that are the key structures of the above-mentioned models. On the other hand, PD could be treated successfully by a cognitive behavior therapy without the use of psychotropic drugs in a study, and the brain glucose metabolic changes were found not in amygdala but in bilateral dorsomedial prefrontal corteces related to mindful awareness. This result indicates that the change in mind brings the change in body, which is an important fact presenting a basis of mind/body interaction.

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Objectives: Recently, eating disorders and abnormal eating behaviors have been increasing among female college students. The purpose of this study was to develop the Abnormal Eating Behavior Scale (AEBS) and to examine the reliability and the validity of this scale. Subjects: The subjects of this study were 593 students and 31 patients with eating disorder. In these subjects, 429 (the mean age was 20.29±3.67) students and 27 patients with eating disorder (the mean age was 24.26±6.13) answered to these scales completely. Method: Firstly, we examined the structure of the AEBS by the factor analysis, and we also examined the reliability of this scale. Secondly, we tested the validity of this scale. The subjects were classified into 3 groups such as the high, the moderate and the low group according to each score of the EAT-26 and the EDI. The one-way analysis of variance (ANOVA) of 3 groups was performed on the factors of this scale. Thirdly, the cut-off point of this scale for discriminating eating disorder patients from normal subjects was examined by the receiver operating characteristic analysis. Results: The results of the factor analysis of 29 items for measuring an abnormal eating behavior were three factors (19 items) such as Factor 1: uncontrollability of excessive food intake, Factor 2: purging behavior and Factor 3: control of food intake. Cronbach's alpha coefficients demonstrated highly sufficient. The results of the examination for the EAT-26 indicated that all factor scores were higher in the high group than the moderate and low groups, and that all factors showed higher scores in the moderate group than the low group. In addition the results of the examination for the Binge-eating (EDI) indicated that Factor 3 score were higher in the high group than the moderate and low groups, and that Factor 2 and Factor 3 showed higher scores in the moderate group than the low group, while the examination for the Desire to be slim (EDI) indicated that Factor 2 and Factor 3 scores showed higher in the high group than the moderate and low groups. Moreover, the results of the receiver operating characteristic analysis were indicated the following cut-off points: Factor1: point of 16 (Sensitivity: 77.78%; 1-specificity: 83.46%), Factor2: point of 2 (Sensitivity 81.48%; 1-specificity: 92.91%), Factor 3: point of 7 (Sensitivity: 74.07%; 1-specificity: 70.08%). Conclusions: These results showed that the reliability and construct validity for this scale were acceptable. And, we can also say that this scale has criterion-referenced validity. Therefore, this scale may possibly be used to screen female college student for eating disorder.

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