認知の発達 Development of Cognition
P1-1-187 思春期の慢性疲労による報酬知覚時の線条体の活性低下 Low striatal activity during reward perception caused by adolescent chronic fatigue ○水野敬1,2, 田島華奈子1, 川谷淳子3, 上土井貴子3, 米田哲也3, 友田明美4, 渡辺恭良1,2 ○Kei Mizuno1,2, Kanako Tajima1, Junko Kawatani3, Takako Joudoi3, Tetsuya Yoneda3, Akemi Tomoda4, Yasuyoshi Watanabe1,2 理化学研究所分子イメージング科学研究センター1, 大阪市立大学大学院医学研究科2, 熊本大学大学院生命科学研究部3, 福井大学大学院医学系研究科4 RIKEN Center for Molecular Imaging Science (CMIS)1, Osaka City University Graduate School of Medicine2, Faculty of Life Sciences, Kumamoto University3, Graduate School of Medicine, University of Fukui4 There is negative correlation between fatigue and motivation to learn in adolescents. Reward is a driving force to muster up the motivation. In our previous study using functional magnetic resonance imaging (fMRI), we found that mental fatigue score, which was calculated by Chalder's fatigue scale, was negatively correlated with the activity of the striatum during monetary reward perception. This result suggests that decreased motivation on mental fatigue of adolescents may be induced by decrease in reward processing of the striatum based on the decreased dopaminergic function. However, it is unclear the neural relationship between chronic fatigue and the striatal activity in adolescents. Therefore, we conducted fMRI study using the same monetary reward task in patients with childhood chronic fatigue syndrome (CCFS) which is an illness characterized by profound disabling fatigue that persists for at least 3 months. We found that during reward perception, the striatal activity of CCFS patients was also decreased as compared with healthy adolescents. These results indicate that low reward processing in the striatum is commonly caused by acute and chronic fatigue in adolescence. Decreased reward processing of adolescent chronic fatigue may induce decrease in motivation to learn and lower academic performance.	P1-1-188 幼弱時手綱核破壊の前頭前野ドーパミン・セロトニン放出とオープンフィールド行動間相関の発達的変化 The developmental changes in correlations between prefrontal dopamine/serotonin release and open-field behaviors in rats with neonatal habenula lesion ○瀧田正寿1, 李英娥2, 後藤幸織3 ○Masatoshi Takita1, Young-A Lee2, Yukiori Goto3 産総研・認知行動システムRG1, 富山大和漢研・神経機能学分野2, 京大霊長研・行動神経研究部門・認知学習分野3 Cognition and Action Research Grp, Natl Inst of Adv Indl Sci and Tech (AIST), Japan1, Div of Neuromedical Sci, Inst of Natural Med, Univ of Toyama, Toyama, Japan2, Cognition & Learning Section, Dept Behav & Brain Sci, Kyoto Univ Primate Res Inst, Inuyama, Japan3 The habenula presumably engages in inhibitory feedback control of midbrain monoamines such as dopamine (DA) and serotonin (5HT). Neonatal habenula lesion (NHL) given at postnatal days (PD) 6-8 increased locomotor activity at PD28-35 but not at PD56 or older in rats (Lee and Goto, 2011). This developmental feature resembles attention deficit/hyperactivity disorder (ADHD) symptoms. In this study, we conducted microdialysis in the prefrontal cortex and HPLC assay to measure DA/5HT release during locomotor activity/rearing for 2 days (d1 or d2) in the open field chamber. We found the higher basal DA/5HT releases on d1 in PD28-35 NHL rats than in control ones, which was likely to cause a ceiling effect and thereby make indifference of DA/5HT release between NHL and control rats. On the other hand, the DA/5HT release on d2 tended to correlate positively with locomotor activity and/or rearing in NHL rats while the negative correlation was found in control rats. This opposition of correlation may be explained by an inverted-U shaped profile of prefrontal monoamine control on exploratory behaviors. We are currently analyzing DA/5HT release-behavior relationship in adult NHL and control rats, to further investigating the ADHD-like developmental feature and the inverted-U feature on their relationship.
P1-1-189 環境適応としての胎児期ストレスによる脳発達の変化 Prenatal stress-induced neurodevelopmental alterations as environmental adaptation ○李英娥1, 後藤幸織2 ○Young-A Lee1, Yukiori Goto2 富山大学和漢医薬学総合研究所神経機能学分野1, 京都大学霊長類研究所認知学習分野2 Div of Neuromedical Sci, Inst of Natural Med, Univ of Toyama, Toyama, Japan1, Cognition & Learning Section, Dept Behav & Brain Sci, Kyoto Univ Primate Res Inst, Aichi, Japan2 Stress is the best known environmental factor that affects brain function. Severe, chronic stress yield adverse effects, causing various cognitive and affective dysfunction. Moreover, stress has been also shown to have impacts on brain development. Animals exposed to prenatal stress have been reported to exhibit behavioral and associated brain alterations. Indeed, stress is usually not a single life event, but its exposure can be multiple times throughout life over different ages. However, the effects of multiple times of stress exposure on brain function have not been unexplored. In this study, we examined whether and how behavioral alterations caused by prenatal stress interact with postnatal stress in mice. Mice exposed to prenatal stress for 1 week from gestational days 14-15 to 19-20 were re-exposed to chronic stress for 2 weeks during juvenile period at postnatal days (PD) 28-42 or during adulthood at PD 56-70. The effects of stress on spatial and non-spatial memories were examined with modified object recognition tests. We found that mice exposed to only prenatal stress exhibited impaired spatial memory. However, when mice exposed to prenatal stress were re-exposed to postnatal stress during juvenile period or adulthood, these mice exhibited spatial memory comparable to that in normal mice. In contrast, none of prenatal stress as well as prenatal x postnatal stress interaction affected non-spatial memory. These results suggest that behavioral alterations including memory caused by prenatal stress may not be deficits, but rather considered as environmental adaptation to prepare for expected postnatal stressful environment. As such, mismatch of prenatal and postnatal environments results in behavioral changes considered as deficits.

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