Nair, Amrita ; Vadodaria, Krishna C ; Banerjee, Sunayana B ; Benekareddy, Madhurima ; Dias, Brian G ; Duman, Ronald S ; Vaidya, Vidita A (2007) Stressor-Specific Regulation of Distinct Brain-Derived Neurotrophic Factor (BDNF) Transcripts and Cyclic AMP Response Element-Binding Protein (CREB) Expression in the Postnatal and Adult Rat Hippocampus Neuropsychopharmacology, 32 (7). pp. 1504-1519. ISSN 0893-133X
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Official URL: http://doi.org/10.1038/sj.npp.1301276
Related URL: http://dx.doi.org/10.1038/sj.npp.1301276
Abstract
Stress regulation of brain-derived neurotrophic factor (BDNF) is implicated in the hippocampal damage observed in depression. BDNF has a complex gene structure with four 5' untranslated exons (I-IV) with unique promoters, and a common 3' coding exon (V). To better understand the stress regulation of BDNF, we addressed whether distinct stressors differentially regulate exon-specific BDNF transcripts in the postnatal and adult hippocampus. The early life stress of maternal separation (MS) resulted in a time point-dependent differential upregulation of BDNF transcripts restricted to early postnatal life (P14-BDNF II, P21-BDNF IV, V). In adulthood, distinct stressors regulated BDNF transcripts in a signature manner. Immobilization stress, administered once, decreased all BDNF splice variants but had differing effects on BDNF I/II (increase) and III/IV (decrease) when administered chronically. Although immobilization stress reduced BDNF (V) mRNA, chronic unpredictable stress did not influence total BDNF despite altering specific BDNF transcripts. Furthermore, a prior history of MS altered the signature pattern in which adult-onset stress regulated specific BDNF transcripts. We also examined the expression of cyclic AMP response element-binding protein (CREB), an upstream transcriptional activator of BDNF, and observed a CREB induction in the postnatal hippocampus following MS. As a possible consequence of enhanced CREB and BDNF expression following MS, we examined hippocampal progenitor proliferation and observed a significant increase restricted to early life. These results suggest that alterations in CREB/BDNF may contribute to the generation of individual differences in stress neurocircuitry, providing a substrate for altered vulnerability to depressive disorders.
Item Type: | Article |
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Source: | Copyright of this article belongs to Nature Publishing Group. |
ID Code: | 119068 |
Deposited On: | 08 Jun 2021 03:51 |
Last Modified: | 08 Jun 2021 03:51 |
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