A neuroendocrinological study for rats exposed to emotional stress as a model of anorexia nervosa.

对暴露于情绪压力的大鼠作为神经性厌食症模型的神经内分泌学研究。

• 批准号: 06670980
• 负责人: SUZUKI Mari
• 金额: $ 1.22万
• 依托单位: Tokyo Women's Medical College
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06670980/
• 关键词: anorexia nervosa; emotional stress; communication box system; paraventricular nucleus; in situ hybridization; corticotropin-releasing factor; microdialysis; noradrenaline; ACTH; β-エンドルフィン; コルチゾール; 自発行動; 生殖機能

The chronic exposure to emotional stress using by a communications box system (1.5mA/sec, 2times/min, 1hr/time, 2times/day for 7day) significantly reduced total amount of food intake as well as body weight gain in Wister strain's rats. That stress also decreased blood sugar and increased plasma levels of ACTH and corticosterone. Rats chronically exposed to emotional stress showed increased locomotor activity in a familiar environment and decreased exploratory behaivior in a novel environment. The content of immunoreactive corticotropin-releasing factor (CRF) significantly increased in hypothalamus in rats chronically exposed to emothinal stress. It was observed by in situ hybridization that the emotinal stress for 5days induced CRF m RNA expression only in parvocellulr neurons of paraventricular nucleus in rats. The exposure to emotional stress increased noradrenaline release of paraventricular nucleus examined by intracerebral microdialysis. The increase of noradrenaline induced by emotional stress for 5min on the first day of the experiment did not change when the same stress was repeated on the 7th day, which indicated that desensitization of noradrenaline neurons dose not occur. These changes induced by chronic exposure to emotional stress were smaller than those by electric footshock.The emotional stress used in our study induced the similar findings in rats to those in patients with anorexia nervosa except for hypogonadism, which was accompanied by activation of CRF and noradrenaline releases in paraventricular nucleus.

用交流盒系统对Wister系大鼠进行慢性情绪应激（1.5mA/sec，20次/min，1hr/次，20次/天，共7 d），可显著降低大鼠的摄食量和体重增长。这种压力也降低了血糖，增加了血浆ACTH和皮质酮的水平。长期暴露于情绪应激的大鼠在熟悉的环境中表现出运动活动增加，而在新的环境中表现出探索性活动减少。慢性情绪应激大鼠下丘脑中促肾上腺皮质激素释放因子（CRF）的含量显著增加。原位杂交结果表明，5d情绪应激仅诱导大鼠室旁核小细胞神经元表达CRF mRNA。脑内微透析检测显示，情绪应激可增加室旁核去甲肾上腺素的释放。实验第1天情绪应激5 min所引起的去甲肾上腺素的增加在第7天重复同样的应激时没有改变，表明去甲肾上腺素神经元没有发生脱敏。慢性情绪应激引起的这些变化比电击引起的变化小。本研究中所用的情绪应激引起的大鼠与神经性厌食症患者相似的结果，除了性腺功能减退，这伴随着CRF激活和室旁核去甲肾上腺素释放。

项目成果

堀田眞理: "クリニカルファーマシーのための内科学" 溝口秀昭,狩野庄吾編 医薬ジャーナル社, 563 (1994)

Mari Hotta：“临床药学的内科医学”，沟口英明和鹿野正吾编辑，Iyaku Journal，563（1994）

Tamotsu Shibasaki, Mari Hotta et al.: "beta1-Adrenergic mechanism is involved in stress-induced increase in arousal." Neuroscience letters. 180. 167-170 (1994)

Tamotsu Shibasaki、Mari Hotta 等人：“β1-肾上腺素能机制参与了压力引起的兴奋增加。”

Tamotsu Shibasaki Mari Hotta et al.: "The response pattern of noradrenaline release to repeated stress in the hypothalamic paraventricular nucleus differs according to the form of stress in rats." Brain Research. 670. 169-1 (1995)

Tamotsu Shibasaki Mari Hotta 等人：“下丘脑室旁核中去甲肾上腺素释放对重复应激的反应模式根据大鼠应激的形式而有所不同。”

堀田眞理: "クリニカルファーマシーのための内科学(溝口秀昭,狩野庄吾編)" 医薬ジャーナル社, 563 (1994)

堀田麻里：“临床药学内科（沟口英明和嘉纳正吾编辑）” Iyaku Journalsha，563（1994）

Tamotsu Shibasaki, Mari Hotta et al.: "The response pattern of noradrenalline release to repeated stress in the hypothalamic paraventricular nucleus differs according to the form of stress in rats." Brain Research. 670. 169-172 (1995)

Tamotsu Shibasaki、Mari Hotta 等人：“大鼠下丘脑室旁核中去甲肾上腺素释放对重复应激的反应模式因应激形式而异。”