Abstract
Neurotensin (NT) is a neuropeptide identical in mice and humans that is produced and released in many CNS regions associated with maternal behavior. NT has been linked to aspects of maternal care and previous studies have indirectly suggested that endogenous NT signaling is altered in the postpartum period. In the present study, we directly examine whether NT and its receptors exhibit altered gene expression in maternal relative to virgin outbred mice using real time quantitative PCR (qPCR) across multiple brain regions. We also examine NT protein levels using anti-NT antibodies and immunohistochemistry in specific brain regions. In the medial preoptic area (MPOA), which is critical for maternal behaviors, mRNA of NT and NT receptor 3 (Sort1) were significantly up-regulated in postpartum mice compared to virgins. NT mRNA was also elevated in postpartum females in the bed nucleus of the stria terminalis dorsal. However, in the lateral septum, NT mRNA was down-regulated in postpartum females. In the paraventricular nucleus of the hypothalamus (PVN), Ntsr1 expression was down-regulated in postpartum females. Neurotensin receptor 2 (Ntsr2) expression was not altered in any brain region tested. In terms of protein expression, NT immunohistochemistry results indicated that NT labeling was elevated in the postpartum brain in the MPOA, lateral hypothalamus, and two subregions of PVN. Together, these findings indicate that endogenous changes occur in NT and its receptors across multiple brain regions, and these likely support the emergence of some maternal behaviors.
Highlights
In mammals, the transition from a virgin to a postpartum state is accompanied by a suite of physiological, sensory, and behavioral changes
In the medial preoptic area (MPOA), NT mRNA was up-regulated in lactating mice compared to virgins (p = 0.023), as was sortilin 1 (Sort1) (p = 0.002) (Fig. 1A)
No difference in expression was found in the MPOA for Neurotensin receptor 2 (Ntsr2) (Table 1)
Summary
The transition from a virgin to a postpartum state is accompanied by a suite of physiological, sensory, and behavioral changes. Progesterone, estradiol, and prolactin release in late pregnancy and early postpartum, as well as sensory input from pups, have been shown to help facilitate the onset of maternal behaviors in rodents, such as pup retrieval, pup licking and grooming, nursing, and offspring protection [1,2]. Hormonal changes and sensory input from offspring modulate the CNS in part by altering expression of critical maternal behavior genes. Recent studies have indicated that modulation of signaling of the neuropeptide, neurotensin (NT), may contribute to the maternal state. Intracerebroventricular (icv) injections of NT suppress offspring protection, while antagonizing neurotensin receptor 1 (Ntsr1) elevates defense [13]. NT could have a complex action with it supporting some maternal behaviors in certain brain regions (e.g., MPOA) and suppressing other behaviors, such as offspring protection, in different regions
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