Abstract：
:1. The effect of chronic antidepressant administration on CRE-, SP1- and GRE-binding activity was studied in rat hippocampus and frontal cortex. 2. Fluoxetine and desipramine (3 and 10 mg/kg/day respectively) were given to rats for 21 consecutive days. The animals were killed 3 hr after the last injection and nuclear extracts were prepared to perform the DNA-protein reaction with consensus CRE, SP1 and GRE oligonucleotides. 3. Gel-shift assays showed that CRE-binding activity was increased in both frontal cortex and hippocampus by chronic fluoxetine treatment. Desipramine, however, only enhanced this activity in the frontal cortex. 4. Chronic fluoxetine decreased SP1-binding activity in the two selected brain regions. Again, desipramine only produced a significant reduction in the frontal cortex. 5. GRE-binding in the hippocampus was only enhanced by desipramine. Since chronic desipramine, and not fluoxetine, is able to increase hippocampal glucocorticoid receptor (GR) expression, interactions of GR with CREB and SP1 may determine the lack of effect of desipramine on binding activity of the two latter transcription factors in this brain region. 6. Overall, the results show a differential and region-specific effect of chronic, and not acute, antidepressant treatment on the DNA-binding activities studied and are consonant with the possible role of changes in gene expression in the mechanism of antidepressant action.
journal_name
Prog Neuropsychopharmacol Biol Psychiatryauthors
Frechilla D,Otano A,Del Río Jdoi
10.1016/s0278-5846(98)00040-2subject
Has Abstractpub_date
1998-07-01 00:00:00pages
787-802issue
5eissn
0278-5846issn
1878-4216pii
S0278584698000402journal_volume
22pub_type
杂志文章abstract：:Metformin is widely used to treat type II diabetes and other metabolic syndromes. In addition, it has been shown to increase neurogenesis, spatial memory formation and reduce the risk of Parkinson's disease. On this basis, the aim of the present study was the investigation of the protective potential of metformin in t...
journal_title：Progress in neuro-psychopharmacology & biological psychiatry
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
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doi：10.1016/j.pnpbp.2014.02.001
更新日期：2014-06-03 00:00:00
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
pub_type： 临床试验,杂志文章
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
pub_type： 杂志文章,评审
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
pub_type： 杂志文章
doi：10.1016/j.pnpbp.2004.06.008
更新日期：2004-11-01 00:00:00
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
pub_type： 杂志文章
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更新日期：2009-08-31 00:00:00
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
pub_type： 临床试验,杂志文章
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更新日期：2008-04-01 00:00:00
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journal_title：Progress in neuro-psychopharmacology & biological psychiatry
pub_type： 杂志文章
doi：10.1016/j.pnpbp.2007.09.019
更新日期：2008-02-15 00:00:00
