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Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester

Alcohol exposure (AE) during the prenatal period could result in fetal alcohol spectrum disorders (FASDs), one of many deficits of which is impaired executive functioning (EF). EF relies on the coordination of activity between the medial prefrontal cortex (mPFC) and hippocampus (HPC) by the thalamic...

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Autores principales: Smith, Ian F., Gursky, Zachary H., Klintsova, Anna Y.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9493097/
https://www.ncbi.nlm.nih.gov/pubmed/36160686
http://dx.doi.org/10.3389/fnbeh.2022.993601
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author Smith, Ian F.
Gursky, Zachary H.
Klintsova, Anna Y.
author_facet Smith, Ian F.
Gursky, Zachary H.
Klintsova, Anna Y.
author_sort Smith, Ian F.
collection PubMed
description Alcohol exposure (AE) during the prenatal period could result in fetal alcohol spectrum disorders (FASDs), one of many deficits of which is impaired executive functioning (EF). EF relies on the coordination of activity between the medial prefrontal cortex (mPFC) and hippocampus (HPC) by the thalamic nucleus reuniens (Re), a structure that has been shown to be damaged following high-dose AE in a rodent model of third trimester exposure. Notably, mPFC neurons do not project directly to HPC, but rather communicate with it via a disynaptic pathway where the first cortical axons synapse on neurons in Re, which in turn send axons to make contacts with hippocampal cells. This experiment investigated the effect of binge AE (5.25 g/kg/day, two doses 2 h apart) during postnatal days 4–9 on the length of medial prefrontal axonal projections within Re in Long Evans rat. AE reduced the cumulative length of mPFC-originating axon terminals in Re in female rats, with male rats exhibiting shorter cumulative lengths when compared to female procedural control animals. Additionally, Re volume was decreased in AE animals, a finding that reproduced previously reported data. This experiment helps us better understand how early life AE affects prefrontal-thalamic-hippocampal connectivity that could underlie subsequent EF deficits.
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spelling pubmed-94930972022-09-23 Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester Smith, Ian F. Gursky, Zachary H. Klintsova, Anna Y. Front Behav Neurosci Neuroscience Alcohol exposure (AE) during the prenatal period could result in fetal alcohol spectrum disorders (FASDs), one of many deficits of which is impaired executive functioning (EF). EF relies on the coordination of activity between the medial prefrontal cortex (mPFC) and hippocampus (HPC) by the thalamic nucleus reuniens (Re), a structure that has been shown to be damaged following high-dose AE in a rodent model of third trimester exposure. Notably, mPFC neurons do not project directly to HPC, but rather communicate with it via a disynaptic pathway where the first cortical axons synapse on neurons in Re, which in turn send axons to make contacts with hippocampal cells. This experiment investigated the effect of binge AE (5.25 g/kg/day, two doses 2 h apart) during postnatal days 4–9 on the length of medial prefrontal axonal projections within Re in Long Evans rat. AE reduced the cumulative length of mPFC-originating axon terminals in Re in female rats, with male rats exhibiting shorter cumulative lengths when compared to female procedural control animals. Additionally, Re volume was decreased in AE animals, a finding that reproduced previously reported data. This experiment helps us better understand how early life AE affects prefrontal-thalamic-hippocampal connectivity that could underlie subsequent EF deficits. Frontiers Media S.A. 2022-09-08 /pmc/articles/PMC9493097/ /pubmed/36160686 http://dx.doi.org/10.3389/fnbeh.2022.993601 Text en Copyright © 2022 Smith, Gursky and Klintsova. 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 Neuroscience
Smith, Ian F.
Gursky, Zachary H.
Klintsova, Anna Y.
Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester
title Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester
title_full Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester
title_fullStr Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester
title_full_unstemmed Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester
title_short Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester
title_sort representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9493097/
https://www.ncbi.nlm.nih.gov/pubmed/36160686
http://dx.doi.org/10.3389/fnbeh.2022.993601
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