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Articles

Abnormal maternal behavior in mice lacking phospholipase Cβ1

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Pages 291-299 | Received 25 Aug 2022, Accepted 23 Oct 2022, Published online: 07 Nov 2022
 

ABSTRACT

Motherhood goes through preparation, onset and maintenance phases until the natural weaning. A variety of changes in hormonal/neurohormonal systems and brain circuits are involved in the maternal behavior. Hormones, neuropeptides, and neurotransmitters involved in maternal behavior act via G-protein-coupled receptors, many of which in turn activate plasma membrane enzymes including phospholipase C (PLC) β isoforms. In this study, we examined the effect of PLCβ1 knockout (KO) on maternal behavior. There was little difference between PLCβ1-KO and wild-type (WT) dams in the relative time spent in maternal behavior during the period between 24 h prepartum and 12 h postpartum (−24 h ∼ PPH 12). After PPH 18, however, PLCβ1-KO dams neglected their pups so that they all died in 2–3 days. In the pup retrieval test, latency was not different during the period within PPH 12, but after PPH 18, PLCβ1-KO dams could not finish pup retrieval in a given time. During both periods, FosB expression in the nucleus accumbens (NAcc) of PLCβ1-KO dams was significantly lower than WT, but not different in the medial preoptic area (mPOA). Given that mPOA activity is required for initiation of maternal behavior, and that NAcc is known to be involved in maternal motivation and maintenance of maternal behavior, our results suggest that PLCβ1 signaling is essential for transition from the onset to maintenance phase of maternal behavior.

Acknowledgements

H.-Y.K conceptualized the study and designed the experiments. H.K set up and performed experiments. J.J conducted a part of the pup retrieval test experiments for PLCβ1+/- mice. J.J and H.K did data analysis. H.-Y.K wrote the manuscript. All authors discussed the manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by the KIST Institutional Program (Project No. 2E31512).