Stress sensitization in schizophrenia

Kunio Yuii*, Michio Suzuki, Masayoshi Kurachi

*この論文の責任著者

研究成果: 書籍の章/レポート/会議録会議への寄与査読

43 被引用数 (Scopus)

抄録

It is well known that environmental factors, such as early life events, perinatal damage, and urbanicity, which interact with multiple genes, induces persistent sensitization to stress possibly through an imbalance in interactions between dopaminergic and glutamatergic systems. This stress sensitization may be critical in the development or relapse of schizophrenia. The neural correlates of a negative mood might be impaired, resulting in stress sensitization and difficulties in social adjustment (Dr. Habel). Urbanicity is associated with later schizophrenia. Metabolic stress induces stress sensitization via dysregulation of dopaminergic and/or noradrenergic systems in activated HVA and cortical response (Dr. Marcelis). The glutamatergic regulation activates HPA axis in stress response (Dr. Zelena). Ameloblast activity in human molar's enamel slowed by exposure to stress, and the segment of enamel rods is smaller, making a particular dark line. Stress sensitization may be induced at the age of 10.5 to 11.5 years resulting from severe emotional stress at the age of 10.5 to 11.5 years (Dr. Yui). It has been reported that volume reductions in the amygdala, hippocampus, superior temporal gyrus, and anterior parietal cortex common to both patient groups may represent the vulnerability to schizophrenia, while volume loss of the prefrontal cortex, posterior parietal cortex, cingulate, insula, and fusiform cortex preferentially observed in schizophrenia may be critical for overt manifestation of psychosis (Dr. Suzuki).

本文言語英語
ホスト出版物のタイトルStress Responses
出版社Blackwell Publishing Inc.
ページ276-290
ページ数15
ISBN(印刷版)157331675X, 9781573316750
DOI
出版ステータス出版済み - 2007/10

出版物シリーズ

名前Annals of the New York Academy of Sciences
1113
ISSN(印刷版)0077-8923
ISSN(電子版)1749-6632

ASJC Scopus 主題領域

  • 神経科学一般
  • 生化学、遺伝学、分子生物学一般
  • 科学史および科学哲学

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