<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Silveira-Rosa T</submitter><funding>ICVS Scientific Microscopy Platform</funding><funding>Fundação para a Ciência e a Tecnologia</funding><funding>Fundação Bial</funding><funding>"la Caixa" Foundation</funding><funding>European Research Council</funding><funding>“la Caixa” Foundation</funding><funding>Nature Research Award for Driving Global Impact</funding><pagination>e13165</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8828259</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>55(2)</volume><pubmed_abstract>&lt;h4>Objectives&lt;/h4>The action of stress hormones, mainly glucocorticoids, starts and coordinates the systemic response to stressful events. The HPA axis activity is predicated on information processing and modulation by upstream centres, such as the hippocampus where adult-born neurons (hABN) have been reported to be an important component in the processing and integration of new information. Still, it remains unclear whether and how hABN regulates HPA axis activity and CORT production, particularly when considering sex differences.&lt;h4>Materials and methods&lt;/h4>Using both sexes of a transgenic rat model of cytogenesis ablation (GFAP-Tk rat model), we examined the endocrinological and behavioural effects of disrupting the generation of new astrocytes and neurons within the hippocampal denta</pubmed_abstract><journal>Cell proliferation</journal><pubmed_title>Suppression of adult cytogenesis in the rat brain leads to sex-differentiated disruption of the HPA axis activity.</pubmed_title><pmcid>PMC8828259</pmcid><funding_grant_id>UIDP/50026/2020</funding_grant_id><funding_grant_id>PPBI-POCI-01-0145-FEDER-022122</funding_grant_id><funding_grant_id>UIDB/50026/2020</funding_grant_id><funding_grant_id>2019 Brain Sciences</funding_grant_id><funding_grant_id>101003187</funding_grant_id><funding_grant_id>2020.02855.CEECIND</funding_grant_id><funding_grant_id>LCF/PR/HR20/52400020</funding_grant_id><funding_grant_id>427/14</funding_grant_id><pubmed_authors>Machado-Santos AR</pubmed_authors><pubmed_authors>Sousa N</pubmed_authors><pubmed_authors>Silva JM</pubmed_authors><pubmed_authors>Bessa JM</pubmed_authors><pubmed_authors>Correia JS</pubmed_authors><pubmed_authors>Rodrigues AJ</pubmed_authors><pubmed_authors>Mateus-Pinheiro A</pubmed_authors><pubmed_authors>Alves ND</pubmed_authors><pubmed_authors>Martins-Macedo J</pubmed_authors><pubmed_authors>Loureiro-Campos E</pubmed_authors><pubmed_authors>Silva M</pubmed_authors><pubmed_authors>Araujo B</pubmed_authors><pubmed_authors>Silveira-Rosa T</pubmed_authors><pubmed_authors>Sotiropoulos I</pubmed_authors><pubmed_authors>Patricio P</pubmed_authors><pubmed_authors>Pinto L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Suppression of adult cytogenesis in the rat brain leads to sex-differentiated disruption of the HPA axis activity.</name><description>&lt;h4>Objectives&lt;/h4>The action of stress hormones, mainly glucocorticoids, starts and coordinates the systemic response to stressful events. The HPA axis activity is predicated on information processing and modulation by upstream centres, such as the hippocampus where adult-born neurons (hABN) have been reported to be an important component in the processing and integration of new information. Still, it remains unclear whether and how hABN regulates HPA axis activity and CORT production, particularly when considering sex differences.&lt;h4>Materials and methods&lt;/h4>Using both sexes of a transgenic rat model of cytogenesis ablation (GFAP-Tk rat model), we examined the endocrinological and behavioural effects of disrupting the generation of new astrocytes and neurons within the hippocampal denta</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2025-04-04T12:43:35.191Z</modification><creation>2025-04-04T12:43:35.191Z</creation></dates><accession>S-EPMC8828259</accession><cross_references><pubmed>34970787</pubmed><doi>10.1111/cpr.13165</doi></cross_references></HashMap>