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Dopamine downregulation in novel rodent models useful for the study of postpartum depression

Postpartum depression (PPD) is the most common psychiatric disorder following childbirth and is characterized by maternal mood disturbances, impaired maternal responses, and disrupted caregiving- all of which negatively impact offspring development. Since PPD has detrimental consequences for both mo...

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Autores principales: Rincón-Cortés, Millie, Grace, Anthony A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9812956/
https://www.ncbi.nlm.nih.gov/pubmed/36620861
http://dx.doi.org/10.3389/fnbeh.2022.1065558
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author Rincón-Cortés, Millie
Grace, Anthony A.
author_facet Rincón-Cortés, Millie
Grace, Anthony A.
author_sort Rincón-Cortés, Millie
collection PubMed
description Postpartum depression (PPD) is the most common psychiatric disorder following childbirth and is characterized by maternal mood disturbances, impaired maternal responses, and disrupted caregiving- all of which negatively impact offspring development. Since PPD has detrimental consequences for both mother and child, clinical and preclinical research has focused on identifying brain changes associated with this disorder. In humans, PPD is linked to dysregulated mesolimbic dopamine (DA) system function and altered neural responses (i.e., decreased reward-related activity) to infant-related cues, which are considered hallmark features of PPD. In accordance, rodent models employing translational risk factors useful for the study of PPD have demonstrated alterations in mesolimbic DA system structure and function, and these changes are reviewed here. We also present two novel rodent models based on postpartum adversity exposure (i.e., pup removal, scarcity-adversity) which result in PPD-relevant behavioral changes (e.g., disrupted mother-infant interactions, deficits in maternal behavior, depressive-like phenotypes) and attenuated ventral tegmental area (VTA) DA neuron activity consistent with a hypodopaminergic state. Furthermore, we highlight open questions and future directions for these rodent models. In sum, human and rodent studies converge in showing blunted mesolimbic DA function (i.e., DA downregulation) in PPD. We propose that reduced activity of VTA DA neurons, resulting in downregulation of the mesolimbic DA system, interferes with reward-related processes necessary for maternal motivation and responsiveness. Thus, the mesolimbic DA system may constitute a therapeutic target for ameliorating reward-related deficits in PPD.
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spelling pubmed-98129562023-01-06 Dopamine downregulation in novel rodent models useful for the study of postpartum depression Rincón-Cortés, Millie Grace, Anthony A. Front Behav Neurosci Behavioral Neuroscience Postpartum depression (PPD) is the most common psychiatric disorder following childbirth and is characterized by maternal mood disturbances, impaired maternal responses, and disrupted caregiving- all of which negatively impact offspring development. Since PPD has detrimental consequences for both mother and child, clinical and preclinical research has focused on identifying brain changes associated with this disorder. In humans, PPD is linked to dysregulated mesolimbic dopamine (DA) system function and altered neural responses (i.e., decreased reward-related activity) to infant-related cues, which are considered hallmark features of PPD. In accordance, rodent models employing translational risk factors useful for the study of PPD have demonstrated alterations in mesolimbic DA system structure and function, and these changes are reviewed here. We also present two novel rodent models based on postpartum adversity exposure (i.e., pup removal, scarcity-adversity) which result in PPD-relevant behavioral changes (e.g., disrupted mother-infant interactions, deficits in maternal behavior, depressive-like phenotypes) and attenuated ventral tegmental area (VTA) DA neuron activity consistent with a hypodopaminergic state. Furthermore, we highlight open questions and future directions for these rodent models. In sum, human and rodent studies converge in showing blunted mesolimbic DA function (i.e., DA downregulation) in PPD. We propose that reduced activity of VTA DA neurons, resulting in downregulation of the mesolimbic DA system, interferes with reward-related processes necessary for maternal motivation and responsiveness. Thus, the mesolimbic DA system may constitute a therapeutic target for ameliorating reward-related deficits in PPD. Frontiers Media S.A. 2022-12-22 /pmc/articles/PMC9812956/ /pubmed/36620861 http://dx.doi.org/10.3389/fnbeh.2022.1065558 Text en Copyright © 2022 Rincón-Cortés and Grace. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Behavioral Neuroscience
Rincón-Cortés, Millie
Grace, Anthony A.
Dopamine downregulation in novel rodent models useful for the study of postpartum depression
title Dopamine downregulation in novel rodent models useful for the study of postpartum depression
title_full Dopamine downregulation in novel rodent models useful for the study of postpartum depression
title_fullStr Dopamine downregulation in novel rodent models useful for the study of postpartum depression
title_full_unstemmed Dopamine downregulation in novel rodent models useful for the study of postpartum depression
title_short Dopamine downregulation in novel rodent models useful for the study of postpartum depression
title_sort dopamine downregulation in novel rodent models useful for the study of postpartum depression
topic Behavioral Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9812956/
https://www.ncbi.nlm.nih.gov/pubmed/36620861
http://dx.doi.org/10.3389/fnbeh.2022.1065558
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