NPBWR1 and NPBWR2: Implications in Energy Homeostasis, Pain, and Emotion

Sakurai, Takeshi

doi:10.3389/fendo.2013.00023

Cited by 39 publications

(33 citation statements)

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“…Neuropeptide B (NPB) and neuropeptide W (NPW) are endogenous neuropeptide ligands for NPBWR1 and NPBWR2, which are members of the G protein-coupled receptor (GPCR) family, originally termed GPR7 and GPR8, respectively (Tanaka et al, 2003;Sakurai, 2013). Whereas humans and other primates express both NPBWR1 and NPBWR2, a functional NPBWR2 ortholog has not been demonstrated in rodents.…”

Section: Introductionmentioning

confidence: 99%

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Transient expression of neuropeptide W in postnatal mouse hypothalamus – A putative regulator of energy homeostasis

et al. 2015

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Neuropeptide B and W (NPB and NPW) are cognate peptide ligands for NPBWR1 (GPR7), a G protein-coupled receptor. In rodents, they have been implicated in the regulation of energy homeostasis, neuroendocrine/autonomic responses, and social interactions. Although localization of these peptides and their receptors in adult rodent brain has been well documented, their expression in mouse brain during development is unknown. Here we demonstrate the transient expression of NPW mRNA in the dorsomedial hypothalamus (DMH) of postnatal mouse brain and its co-localization with neuropeptide Y (NPY) mRNA. Neurons expressing both NPW and NPY mRNAs begin to emerge in the DMH at about postnatal day 0 (P-0) through P-3. Their expression is highest around P-14, declines after P-21, and by P-28 only a faint expression of NPW and NPY mRNA remains. In P-18 brains, we detected NPW neurons in the region spanning the subincertal nucleus (SubI), the lateral hypothalamic (LH) perifornical (PF) areas, and the DMH, where the highest expression of NPW mRNA was observed. The majority of these postnatal hypothalamic NPW neurons co-express NPY mRNA. A cross of NPW-iCre knock-in mice with a Cre-dependent tdTomato reporter line revealed that more than half of the reporter-positive neurons in the adult DMH, which mature from the transiently NPW-expressing neurons, are sensitive to peripherally administrated leptin. These data suggest that the DMH neurons that transiently co-express NPW and NPY in the peri-weaning period might play a role in regulating energy homeostasis during postnatal development.

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Section: Introductionmentioning

confidence: 99%

“…NPB and NPW are encoded by two separate genes and together with NPBWR1 (and NPBWR2 in primates) constitute a neuropeptide-receptor system (Tanaka et al, 2003;Sakurai, 2013). NPB is a 29-amino acid peptide with a unique brominated N-terminal tryptophan; the physiological function of this bromination remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Transient expression of neuropeptide W in postnatal mouse hypothalamus – A putative regulator of energy homeostasis

et al. 2015

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“…We and other groups have isolated neuropeptide B (NPB) and neuropeptide W (NPW) as cognate endogenous ligands for NPBWR1 and NPBWR2 (23)(24)(25)(26). NPB and NPW are encoded by two separate genes and together with NPBWR1 (and NPBWR2 in primates) constitute a neuropeptide receptor system (27). NPB consists of 29…”

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confidence: 99%

Mesolimbic neuropeptide W coordinates stress responses under novel environments

Motoike

Long

Tanaka

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Neuropeptide B (NPB) and neuropeptide W (NPW) are endogenous neuropeptide ligands for the G protein-coupled receptors NPBWR1 and NPBWR2. Here we report that the majority of NPW neurons in the mesolimbic region possess tyrosine hydroxylase immunoreactivity, indicating that a small subset of dopaminergic neurons coexpress NPW. These NPW-containing neurons densely and exclusively innervate two limbic system nuclei in adult mouse brain: the lateral bed nucleus of the stria terminalis and the lateral part of the central amygdala nucleus (CeAL). In the CeAL of wild-type mice, restraint stress resulted in an inhibition of cellular activity, but this stressinduced inhibition was attenuated in the CeAL neurons of NPW −/− mice. Moreover, the response of NPW −/− mice to either formalininduced pain stimuli or a live rat (i.e., a potential predator) was abnormal only when they were placed in a novel environment: The mice failed to show the normal species-specific self-protective and aversive reactions. In contrast, the behavior of NPW −/− mice in a habituated environment was indistinguishable from that of wildtype mice. These results indicate that the NPW/NPBWR1 system could play a critical role in the gating of stressful stimuli during exposure to novel environments.L imbic structures, including the amygdala and bed nucleus of the stria terminalis (BST), where different modalities of environmental stimuli can converge and interact, are critical for the response to stress (1). The basolateral amygdala (BLA) receives sensory information from the thalamus and cortex and transfers that information to the central amygdala (CeA), an output center for the amygdaloid complex. Subsequently, the CeA relays this information through axonal projections to nuclei in diverse areas, such as the hypothalamus, brainstem, and pons (2, 3). These circuits are essential for mediating fear and anxiety, especially for fear conditioning using auditory or visual conditioned stimuli (4, 5). Indeed, in a recent report, optogenetic manipulation of the BLA-CeA pathway was found to modulate the expression of anxiety in the mouse (6).The lateral BST (BSTL) and CeA (CeAL) are two major components of the central extended amygdala, a continuum of telencephalic structures of the forebrain (7,8). Both the BSTL and CeAL contain numerous GABAergic as well as peptidergic neurons, such as those producing enkephalin, corticotropin-releasing factor, and somatostatin (9-13); these GABAergic neurons form dense local inhibitory circuits within these nuclei. The GABAergic microcircuit in the CeAL is thought to play pivotal roles in mediating fear and anxiety, as recently dissected at the cellular level by studies that combined optogenetics and electrophysiology (14-17). A subpopulation of GABAergic neurons in the CeAL, which is inhibited by a conditioned stimulus (CS), is differentiated by the expression PKCδ (14). These PKCδ + GABAergic neurons were shown to provide feed-forward disinhibition on output neurons in the medial CeA (CeAM), resulting in a conditioned freezi...

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“…Another study demonstrated that NPW23 influences the PVN neurons that synthesize oxytocin, vasopressin, and thyrotropinreleasing hormone (Price et al, 2009). These findings suggest that NPW neurons in the PVN are involved in neuroendocrine and autonomic regulation (Sakurai, 2013). In addition, dense NPW-ir fibers were observed in the pig PVN, ARC, VMH, DMH, SON, and LH.…”

Section: Discussionmentioning

confidence: 95%