Intranasal Oxytocin Restores Maternal Behavior and Oxytocin Neuronal Activity in the Supraoptic Nucleus in Rat Dams with Cesarean Delivery.


Journal

Neuroscience
ISSN: 1873-7544
Titre abrégé: Neuroscience
Pays: United States
ID NLM: 7605074

Informations de publication

Date de publication:
01 08 2021
Historique:
received: 21 04 2021
revised: 25 05 2021
accepted: 13 06 2021
pubmed: 25 6 2021
medline: 22 7 2021
entrez: 24 6 2021
Statut: ppublish

Résumé

Oxytocin (OT) is a key factor for maternal behavior. However, neurochemical regulation of OT neurons, the major source of OT, remains incompletely understood. Here we report the effect of intranasally-applied OT (IAO) on OT neuronal activity in the supraoptic nucleus (SON) and on maternal behavior in a rat model of cesarean delivery (CD) at day 4-5 (stage I) and day 8-9 (stage II) following delivery. We found that at stage I, CD dams exhibited significantly longer latency of pup retrieval, lower number of anogenital licks and smaller acinar area of the mammary glands. In the SON, the number of OT neurons expressing phosphorylated extracellular signal-regulated protein kinase 1/2 (pERK 1/2) decreased significantly. IAO reversed the depressive-like maternal behavior and involution-like change in the mammary glands, and restored the number of pERK1/2-positive OT neurons in CD dams. At stage II, CD did not significantly influence the latency of retrieval and pERK1/2 expression in the SON. However, CD still reduced the number of anogenital licks during suckling, which was reversed by IAO. Notably, IAO but not hypodermic OT application in CD dams significantly increased litter's body weight gains. In brain slices, CD but not CD plus IAO significantly depolarized membrane potential and increased spike duration in OT neurons. In vasopressin neurons, CD, but not CD plus IAO, significantly depolarized membrane potential and increased the firing rate. Thus, decreased OT neuronal activity and increased vasopressin neuronal activity impair maternal behavior in CD dams, which can be prevented by IAO .

Identifiants

pubmed: 34166764
pii: S0306-4522(21)00312-2
doi: 10.1016/j.neuroscience.2021.06.020
pii:
doi:

Substances chimiques

Oxytocin 50-56-6

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

235-246

Informations de copyright

Copyright © 2021 IBRO. Published by Elsevier Ltd. All rights reserved.

Auteurs

Tong Li (T)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Shu-Wei Jia (SW)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Dan Hou (D)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Xiaoyu Liu (X)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Dongyang Li (D)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Yang Liu (Y)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Dan Cui (D)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Xiaoran Wang (X)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Chunmei Hou (C)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.

Colin H Brown (CH)

Department of Physiology and Center for Neuroendocrinology, University of Otago, Dunedin, New Zealand.

Yu-Feng Wang (YF)

Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China. Electronic address: yufengwang@ems.hrbmu.edu.cn.

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