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Bed nuclei of the stria terminalis modulate memory consolidation via glucocorticoid-dependent and -independent circuits
Journal article   Open access   Peer reviewed

Bed nuclei of the stria terminalis modulate memory consolidation via glucocorticoid-dependent and -independent circuits

Ryan T Lingg, Shane B Johnson, Eric B Emmons, Rachel M Anderson, Sara A Romig-Martin, Nandakumar S Narayanan, James L McGaugh, Ryan T LaLumiere and Jason J Radley
Proceedings of the National Academy of Sciences - PNAS, Vol.117(14), pp.8104-8114
04/07/2020
DOI: 10.1073/pnas.1915501117
PMCID: PMC7148582
PMID: 32193346
url
https://doi.org/10.1073/pnas.1915501117View
Published (Version of record) Open Access

Abstract

There is extensive evidence that glucocorticoid hormones enhance memory consolidation, helping to ensure that emotionally significant events are well remembered. Prior findings suggest that the anteroventral region of bed nuclei of the stria terminalis (avBST) regulates glucocorticoid release, suggesting the potential for avBST activity to influence memory consolidation following an emotionally arousing learning event. To investigate this issue, male Sprague-Dawley rats underwent inhibitory avoidance training and repeated measurement of stress hormones, immediately followed by optogenetic manipulations of either the avBST or its projections to downstream regions, and 48 h later were tested for retention. The results indicate that avBST inhibition augmented posttraining pituitary-adrenal output and enhanced the memory for inhibitory avoidance training. Pretreatment with a glucocorticoid synthesis inhibitor blocked the memory enhancement as well as the potentiated corticosterone response, indicating the dependence of the memory enhancement on glucocorticoid release during the immediate posttraining period. In contrast, posttraining avBST stimulation decreased retention yet had no effect on stress hormonal output. Subsequent experiments revealed that inhibition of avBST input to the paraventricular hypothalamus enhanced stress hormonal output and subsequent retention, whereas stimulation did not affect either. Conversely, stimulation-but not inhibition-of avBST input to the ventrolateral periaqueductal gray impaired consolidation, whereas neither manipulation affected glucocorticoid secretion. These findings indicate that divergent pathways from the avBST are responsible for the mnemonic effects of avBST inhibition versus stimulation and do so via glucocorticoid-dependent and -independent mechanisms, respectively.
contextual fear HPA axis inhibitory avoidance paraventricular nucleus of the hypothalamus ventrolateral periaqueductal gray

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