Allostatic gene regulation of inhibitory synaptic factors in the rat ventral hippocampus in a juvenile/adult stress model of psychopathology.
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| Title: | Allostatic gene regulation of inhibitory synaptic factors in the rat ventral hippocampus in a juvenile/adult stress model of psychopathology. |
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| Authors: | Albrecht, Anne (AUTHOR), Segal, Menahem (AUTHOR), Stork, Oliver (AUTHOR), Sandi, Carmen (AUTHOR) |
| Source: | European Journal of Neuroscience. May2022, Vol. 55 Issue 9/10, p2142-2153. 12p. 1 Chart, 4 Graphs. |
| Subjects: | Neural transmission, Glutamate decarboxylase, Genetic regulation, RNA regulation, Gene expression, Glutamine synthetase, Glucocorticoid receptors, Immobilization stress |
| Abstract: | Early life stress is an important vulnerability factor for the development of anxiety disorders, depression and late‐onset cognitive decline. Recently, we demonstrated that juvenile stress (JS) lastingly enhanced long‐term potentiation via reduction of steady‐state glutamine synthetase mRNA expression and the associated dysregulation of the astrocytic glutamate‐glutamine cycle in the rat ventral CA1. We now investigated the regulation of steady‐state mRNA expression of neuronal gene products that determine GABAergic and glutamatergic neurotransmission in layers of the ventral and dorsal CA1 after JS. We further studied their interaction with stress in young adult age (AS) to address their putative role in psychopathology development. Strikingly, mRNA levels of the glutamic acid decarboxylase (GAD) isoforms GAD65 and of the GABA‐A receptor α2 (Gabra2) were increased after single JS or AS, but not after combined JS/AS stress experience. In fact, JS/AS resulted in layer‐specific reduction of Gabra2 and also of Gabra1 mRNA levels in the ventral CA1. Furthermore, GAD65 and Gabra2 mRNAs were correlated with glutamatergic AMPA and NMDA receptor subunit mRNAs after single JS and AS, but not after combined JS/AS. Together, these data indicate a loss of allostatic regulation of steady‐state mRNA levels of key GABAergic components that may result in a dysregulation of excitation/ inhibition balance in the ventral CA1 upon dual stress exposure. Finally, individual differences in local glucocorticoid receptor mRNA expression may contribute to this regulation. [ABSTRACT FROM AUTHOR] |
| Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
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| Header | DbId: pbh DbLabel: Psychology and Behavioral Sciences Collection An: 157124858 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: Allostatic gene regulation of inhibitory synaptic factors in the rat ventral hippocampus in a juvenile/adult stress model of psychopathology. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Albrecht%2C+Anne%22">Albrecht, Anne</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Segal%2C+Menahem%22">Segal, Menahem</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Stork%2C+Oliver%22">Stork, Oliver</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Sandi%2C+Carmen%22">Sandi, Carmen</searchLink> (AUTHOR) – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. May2022, Vol. 55 Issue 9/10, p2142-2153. 12p. 1 Chart, 4 Graphs. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22Neural+transmission%22">Neural transmission</searchLink><br /><searchLink fieldCode="DE" term="%22Glutamate+decarboxylase%22">Glutamate decarboxylase</searchLink><br /><searchLink fieldCode="DE" term="%22Genetic+regulation%22">Genetic regulation</searchLink><br /><searchLink fieldCode="DE" term="%22RNA+regulation%22">RNA regulation</searchLink><br /><searchLink fieldCode="DE" term="%22Gene+expression%22">Gene expression</searchLink><br /><searchLink fieldCode="DE" term="%22Glutamine+synthetase%22">Glutamine synthetase</searchLink><br /><searchLink fieldCode="DE" term="%22Glucocorticoid+receptors%22">Glucocorticoid receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Immobilization+stress%22">Immobilization stress</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Early life stress is an important vulnerability factor for the development of anxiety disorders, depression and late‐onset cognitive decline. Recently, we demonstrated that juvenile stress (JS) lastingly enhanced long‐term potentiation via reduction of steady‐state glutamine synthetase mRNA expression and the associated dysregulation of the astrocytic glutamate‐glutamine cycle in the rat ventral CA1. We now investigated the regulation of steady‐state mRNA expression of neuronal gene products that determine GABAergic and glutamatergic neurotransmission in layers of the ventral and dorsal CA1 after JS. We further studied their interaction with stress in young adult age (AS) to address their putative role in psychopathology development. Strikingly, mRNA levels of the glutamic acid decarboxylase (GAD) isoforms GAD65 and of the GABA‐A receptor α2 (Gabra2) were increased after single JS or AS, but not after combined JS/AS stress experience. In fact, JS/AS resulted in layer‐specific reduction of Gabra2 and also of Gabra1 mRNA levels in the ventral CA1. Furthermore, GAD65 and Gabra2 mRNAs were correlated with glutamatergic AMPA and NMDA receptor subunit mRNAs after single JS and AS, but not after combined JS/AS. Together, these data indicate a loss of allostatic regulation of steady‐state mRNA levels of key GABAergic components that may result in a dysregulation of excitation/ inhibition balance in the ventral CA1 upon dual stress exposure. Finally, individual differences in local glucocorticoid receptor mRNA expression may contribute to this regulation. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1111/ejn.15091 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 12 StartPage: 2142 Subjects: – SubjectFull: Neural transmission Type: general – SubjectFull: Glutamate decarboxylase Type: general – SubjectFull: Genetic regulation Type: general – SubjectFull: RNA regulation Type: general – SubjectFull: Gene expression Type: general – SubjectFull: Glutamine synthetase Type: general – SubjectFull: Glucocorticoid receptors Type: general – SubjectFull: Immobilization stress Type: general Titles: – TitleFull: Allostatic gene regulation of inhibitory synaptic factors in the rat ventral hippocampus in a juvenile/adult stress model of psychopathology. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Albrecht, Anne – PersonEntity: Name: NameFull: Segal, Menahem – PersonEntity: Name: NameFull: Stork, Oliver – PersonEntity: Name: NameFull: Sandi, Carmen IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 05 Text: May2022 Type: published Y: 2022 Identifiers: – Type: issn-print Value: 0953816X Numbering: – Type: volume Value: 55 – Type: issue Value: 9/10 Titles: – TitleFull: European Journal of Neuroscience Type: main |
| ResultId | 1 |