Juvenile antioxidant treatment prevents adult deficits in a developmental model of schizophrenia.
Juvenile antioxidant treatment prevents adult deficits in a developmental model of schizophrenia.
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DOI:
10.1016/j.neuron.2014.07.028
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发表时间:
2014-09-03
期刊:
影响因子:
16.2
通讯作者:
O'Donnell P
中科院分区:
文献类型:
--
作者:
Cabungcal JH;Counotte DS;Lewis E;Tejeda HA;Piantadosi P;Pollock C;Calhoon GG;Sullivan E;Presgraves E;Kil J;Hong LE;Cuenod M;Do KQ;O'Donnell P
Abnormal development can lead to deficits in adult brain function, a trajectory likely underlying adolescent-onset psychiatric conditions such as schizophrenia. Developmental manipulations yielding adult deficits in rodents provide an opportunity to explore mechanisms involved in a delayed emergence of anomalies driven by developmental alterations. Here we assessed whether oxidative stress during presymptomatic stages causes adult anomalies in rats with a neonatal ventral hippocampal lesion, a developmental rodent model useful for schizophrenia research. Juvenile and adolescent treatment with the antioxidant N-acetyl cysteine prevented the reduction of prefrontal parvalbumin interneuron activity observed in this model, as well as electrophysiological and behavioral deficits relevant to schizophrenia. Adolescent treatment with the glutathione peroxidase mimic ebselen also reversed behavioral deficits in this animal model. These findings suggest that presymptomatic oxidative stress yields abnormal adult brain function in a developmentally compromised brain, and highlight redox modulation as a potential target for early intervention.
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影响因子:
15.9
作者:
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通讯作者:
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影响因子:
3.3
作者:
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DOI:
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2011-01-01
期刊:
ANIMAL MODELS OF SCHIZOPHRENIA AND RELATED DISORDERS
影响因子:
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DOI:
10.1111/j.1463-1326.2010.01266.x
发表时间:
2010-10
期刊:
Diabetes, obesity & metabolism
影响因子:
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作者:
Jones DP;Go YM
通讯作者:
Go YM