TY - GEN
T1 - Stress sensitization in schizophrenia
AU - Yuii, Kunio
AU - Suzuki, Michio
AU - Kurachi, Masayoshi
PY - 2007/10
Y1 - 2007/10
N2 - 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).
AB - 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).
KW - Ameloblast stress line
KW - Glutamate
KW - Negative affect
KW - Schizophrenia
KW - Stress sensitization
KW - Volume loss of cortex
UR - http://www.scopus.com/inward/record.url?scp=35548959617&partnerID=8YFLogxK
U2 - 10.1196/annals.1391.013
DO - 10.1196/annals.1391.013
M3 - 会議への寄与
C2 - 17584979
AN - SCOPUS:35548959617
SN - 157331675X
SN - 9781573316750
T3 - Annals of the New York Academy of Sciences
SP - 276
EP - 290
BT - Stress Responses
PB - Blackwell Publishing Inc.
ER -