Corticosterone enhances N-methyl-d-aspartate receptor signaling to promote isolated ventral tegmental area activity in a reconstituted mesolimbic dopamine pathway
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- 作者：Jennifer N. Berrya ; c ; jnberry@purdue.edu" class="auth_mail" title="E-mail the corresponding author ; Meredith A. Saundersa ; c ; Lynda J. Sharrett-Fielda ; c ; Anna R. Reynoldsa ; c ; Michael T. Bardoa ; James R. Paulyb ; c ; Mark A. Prendergasta ; c
- 关键词：ACTH ; adrenocorticotropic hormone ; ANOVA ; analysis of variance ; APV ; DL-2-amino-7-phosphonovaleric acid ; Ca2+ ; calcium ; CORT ; corticosterone ; CRH ; corticotrophin releasing hormone ; DMSO ; dimethyl sulfoxide ; FITC ; fluorescein isothiocynate ; GR ; glucocorticoid receptor ; HPA ; hypothalamus&ndash ; pituitary&ndash ; adrenal ; MEM ; minimum essential medium ; MR ; mineralocorticoid receptor ; NA ; ccnucleus accumbens ; NeuN ; neuronal nuclear protein ; NMDA ; N-methyl-d-aspartate ; PBS ; phosphate-buffered saline ; PI
- 刊名：Brain Research Bulletin
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：120
- 期：Complete
- 页码：159-165
- 全文大小：1448 K
文摘
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Midbrain and striatal cultures functionally reintegrate synaptic contacts ex vivo.
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Corticosterone causes glutamate receptor-dependent cell loss in midbrain neurons.
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Ventral striatum is insensitive to effects of either corticosterone or an excitotoxin.