Prenatal protein malnutrition decreases neuron numbers in the parahippocampal region but not prefrontal cortex in adult rats.

Prenatal protein malnutrition brain development malnutrition medial entorhinal cortex neuroanatomy‌ parahippocampal region prefrontal cortex stereology

Journal

Nutritional neuroscience
ISSN: 1476-8305
Titre abrégé: Nutr Neurosci
Pays: England
ID NLM: 100892202

Informations de publication

Date de publication:
01 Aug 2024
Historique:
pubmed: 1 8 2024
medline: 1 8 2024
entrez: 1 8 2024
Statut: aheadofprint

Résumé

Prenatal protein malnutrition produces anatomical and functional changes in the developing brain that persist despite immediate postnatal nutritional rehabilitation. Brain networks of prenatally malnourished animals show diminished activation of prefrontal areas and an increased activation of hippocampal regions during an attentional task [1]. While a reduction in cell number has been documented in hippocampal subfield CA1, nothing is known about changes in neuron numbers in the prefrontal or parahippocampal cortices. In the present study, we used unbiased stereology to investigate the effect of prenatal protein malnutrition on the neuron numbers in the medial prefrontal cortex and the cortices of the parahippocampal region that comprise the larger functional network. Results show that prenatal protein malnutrition does not cause changes in the neuronal population in the medial prefrontal cortex of adult rats, indicating that the decrease in functional activation during attentional tasks is not due to a reduction in the number of neurons. Results also show that prenatal protein malnutrition is associated with a reduction in neuron numbers in specific parahippocampal subregions: the medial entorhinal cortex and presubiculum. The affected regions along with CA1 comprise a tightly interconnected circuit, suggesting that prenatal malnutrition confers a vulnerability to specific hippocampal circuits. These findings are consistent with the idea that prenatal protein malnutrition produces a reorganization of structural and functional networks, which may underlie observed alterations in attentional processes and capabilities.

Identifiants

pubmed: 39088448
doi: 10.1080/1028415X.2024.2371256
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-14

Auteurs

A C Amaral (AC)

Department of Anatomy & Neurobiology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.

J P Lister (JP)

Department of Anatomy & Neurobiology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Department of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA, USA.

J W Rueckemann (JW)

Department of Physiology and Biophysics, University of Washington, Seattle, WA, USA.

M W Wojnarowicz (MW)

Department of Pathology & Laboratory Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.

J A McGaughy (JA)

Department of Psychology, University of New Hampshire, Durham, NH, USA.

D J Mokler (DJ)

Department of Biomedical Sciences, University of New England, Biddeford, ME, USA.

J R Galler (JR)

Department of Psychiatry, Harvard Medical School, Boston, MA, USA.
Department of Pediatrics & Division of Gastroenterology and Nutrition, MassGeneral Hospital for Children, Boston, MA, USA.

D L Rosene (DL)

Department of Anatomy & Neurobiology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.

R J Rushmore (RJ)

Department of Anatomy & Neurobiology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Psychiatry Neuroimaging Laboratory, Department of Psychiatry, Brigham and Women's Hospital, Boston, MA, USA.
Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA.

Classifications MeSH