Maternal behavior during the postpartum period is mediated by various neural mechanisms. While dopamine D2 receptor activation is known to affect maternal behavior in early postpartum, its role in the late postpartum period remains unclear. This study explores the neural mechanisms governing maternal behavior across the early and late postpartum periods by activating D2 receptors in different maternal brain regions: the ventral tegmental area (VTA), nucleus accumbens (NAc), and medial prefrontal cortex (mPFC). In the early (postpartum day [PPD] 4-5) and late (PPD 13-14) postpartum period, a dopamine D2 receptor agonist was microinjected into these regions in lactating rats. Home cage maternal behavior and pup vs. adult male preference were assessed at 10 and 60 min post-injection. In the VTA, D2 receptor activation reduced pup retrieval and increased latency in the early postpartum, with no significant effects in the late postpartum or on pup preference. In the NAc, D2 receptor activation increased retrieval latency and reduced pup crouching, licking, and pup preference in the late postpartum, with no significant effects in the early postpartum. In the mPFC, D2 receptor activation reduced maternal behavior in both periods but increased pup and male exploration during the early postpartum. These findings suggest region- and time-specific roles of D2 receptors in maternal regulation. In the VTA and NAc, D2 activation appears to impair maternal behavior by modulating maternal motivation, particularly in a stage-dependent manner. In the mPFC, D2 receptors may regulate maternal behavior through both motivational and executive control mechanisms depending on postpartum timing.
Differential Effects of Central Dopamine D2 Receptor Activation on the Dynamic Changes of Maternal Behavior Throughout the Postpartum Period.
Yue Teng,Ning Ma,Junqi Wang,Xinxiu Xiong,Rong Zhao,Yu Yang,Ming Li,Jun Gao
Published 2025 in Neuropharmacology
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- Publication year
2025
- Venue
Neuropharmacology
- Publication date
2025-08-14
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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