Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 + 1525 word(s) 1525 2021-07-13 11:21:59 |
2 format change + 889 word(s) 2414 2021-07-29 04:18:56 |

Video Upload Options

Do you have a full video?

Confirm

Are you sure to Delete?
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Wojciechowicz, T. Neuropeptide B. Encyclopedia. Available online: https://encyclopedia.pub/entry/12527 (accessed on 23 April 2024).
Wojciechowicz T. Neuropeptide B. Encyclopedia. Available at: https://encyclopedia.pub/entry/12527. Accessed April 23, 2024.
Wojciechowicz, Tatiana. "Neuropeptide B" Encyclopedia, https://encyclopedia.pub/entry/12527 (accessed April 23, 2024).
Wojciechowicz, T. (2021, July 28). Neuropeptide B. In Encyclopedia. https://encyclopedia.pub/entry/12527
Wojciechowicz, Tatiana. "Neuropeptide B." Encyclopedia. Web. 28 July, 2021.
Neuropeptide B
Edit

Neuropeptide B (NPB) is a peptide hormone that was initially described in 2002. In humans, the biological effects of NPB depend on the activation of two G protein-coupled receptors, NPBWR1 (GPR7) and NPBWR2 (GPR8), and, in rodents, NPBWR1. NPB and its receptors are expressed in the central nervous system (CNS) and in peripheral tissues. NPB is also present in the circulation. In the CNS, NPB modulates appetite, reproduction, pain, anxiety, and emotions. In the peripheral tissues, NPB controls secretion of adrenal hormones, pancreatic beta cells, and various functions of adipose tissue. Experimental downregulation of either NPB or NPBWR1 leads to adiposity. 

appetite neuropeptide B NPBWR1 NPRBWR2 metabolism energy homeostasis

1. Introduction

Peptides that regulate appetite play a prominent role in controlling energy homeostasis and whole-body metabolism. Such peptides are found in brain regions that are involved in the modulation of appetite. In addition, such peptides are present in the circulation and in numerous peripheral tissues. There is growing evidence indicating that peptides that control appetite (e.g., kisspeptin, orexins, spexin, adropin, apelin, phoenixin, ghrelin, amylin, and pancreatic peptides) also modulate the endocrine activity of endocrine glands as well as lipid and glucose metabolism [1][2][3][4][5][6]. Moreover, some peptides are involved in regulating the endocannabinoid system and, through it, food intake, e.g., hemopressin, a small peptide derived from the α-chain of hemoglobin, reduces appetite through increased levels of endocannabinoids [7][8]. On the other hand, endogenous cannabinoids can also increase the secretion of feeding-regulated hypothalamic neuropeptides [9]. Thus, peptide hormones and their receptors may be of interest in therapy for obesity and obesity-related diseases such as type 2 diabetes [1]. Almost 20 years after the discovery of neuropeptide B (NPB), there is growing evidence that this peptide modulates food intake, body weight, and lipid and glucose metabolism. In our narrative review, we discuss current findings regarding the role of NPB and its receptors in controlling food intake and energy homeostasis.

2. Discovery, Structure, and Expression of NPB and Its Receptors

By analyzing human genomic sequences in the Celera database, in 2002, Fuji et al. identified a new neuropeptide composed of 23 or 29 amino acids that was uniquely modified with bromine. This peptide was termed neuropeptide B (NPB) [10]. The same study showed that NPB interacts with NPBWR1 (GPR7) and less potently with NPBWR2 (GPR8) [10]. At the same time, NPB as a ligand of NPBWR1 and NPBWR2 was reported by two independent laboratories [11][12]. Both NPBWR1 and NPBWR2 belong to the G protein-coupled receptor superfamily [13]. It is important to note that humans express both types of receptors, while rodents express only NPBWR1 [14]. It should be pointed out that both types of NPB receptors interact with another ligand, termed neuropeptide W [11][15]. The intracellular signaling of NPBWR1 and NPBWR1 encompasses the modulation of cAMP, calcium, phospholipase C, or MAP kinase signaling [10][11][16][17]. The expression of NPB and its receptors in the CNS and various peripheral tissues was reported (Table 1 and Table 2).
Table 1. Localization of NPB in central nervous system and peripheral tissues.
  RT-PCR ISH IHC ICC IF WB NB References
Whole brain F - - F - [18][19]
Telencephalic area (Vs/Vp) - F F - F [18][19]
Magnocellular/gigantocellular portions of
magnocellular preoptic nucleus (PMm/PMg)
- F F - F [18][19][20]
Telencephalon Ch - - - - [21]
Cerebral cortex Rt - - - - [10]
Striatum Rt - - - - [10]
Hippocampus Rt, P M, Rt - - - [10][11][22][23]
Thalamus Rt - - - - [10]
Hypothalamus Rt, Ch - Rt - - [10][21][24]
Midbrain Rt, Ch - - - - [10][21]
Cerebellum Rt, P, Ch - Rt - - [10][21][23][24]
Medulla oblongata Rt - - - - [10]
Spinal cord Rt, P, Ch - F - - [10][19][21][23]
Lateral habenular nucleus (LHb) - M - - - [11]
Paraventricular hypothalamic nucleus (PVN) - M Rt - - [11][24]
Edinger–Westphal nucleus - M, Rt - - - [22][24]
Motor root of trigeminal nerve (m5) - M - - - [11]
Sensory root of trigeminal nerve (s5) - M - - - [11]
Lateral parabrachinal nucleus internal part (LPBI) - M - - - [11]
Mesencephalic trigeminal nucleus (Me5) - M - - - [11]
Subcoeruleus nucleus alpha part (Sub CA) - M - - - [11]
Locus coeruleus (LC) - M, Rt - - - [11][22]
Noradrenergic cell group A5 - M - - - [11]
Interior olive subnucleus B (OIB) - M - - - [11]
Anterior olfactory nucleus - Rt - - - [22]
Piriform cortex - Rt   - - [22]
Supraoptic nucleus (SON) - - Rt - - [24]
Median preoptic nucleus - Rt - - - [22]
Basolateral amygdala - Rt - - - [22]
Medial tuberal nucleus - Rt - - - [22]
Substantia nigra - Rt - - - [22]
Dorsal raphne nucleus - Rt - - - [22]
Pituitary gland Rt, Ch - Rt - - [10][21][24]
Eyeball and optic nerve Rt, F (eye) - - - - [10][18]
Gill F - - - - [18]
Thyroid gland Rt - Rt - - [10][24]
Trachea Rt - - - - [10]
Thymus Rt, P - - - - [10][23]
Tonsil P - - - - [23]
Heart Rt. Ch - Rt Rt - [10][21][25]
Lung Rt, Ch - - -- - [10][21]
Liver Rt, Ch, F - - - - [10][18][21]
Spleen Rt, Ch - - - - [10][21]
Lymph node Rt - - - - [10]
Pancreas Rt, Ch - Rt - - [10][21][24]
Kidney Rt, Ch - - - - [10][21]
Adrenal gland (adrenal medulla, adrenal cortex:
zonae glomerulosa and fasciculata/reticularis)
Rt - Rt - - [10][24][26]
Urinary bladder Rt - - - - [10]
Peritoneum Rt - - - - [10]
Stomach - - - - - [10]
Duodenum, jejunum, ileum, cecum, colon, rectum Rt, P, Ch - - - - [10][21][23]
Intestine F - - - - [18]
Skeletal muscle Rt, Ch - - - - [10][21]
Prostate Rt - - - - [10]
Seminal vesicle Rt - - - - [10]
Testes Rt, P, Ch, F - Rt - - [10][18][21][23][24]
Ovary Rt, P, Ch, F - Rt - - [10][18][21][23][24]
Uterus Rt - - - - [10]
Placenta Rt - - - - [10]
Mammary gland Rt - - - - [10]
Skin Rt, Ch - - - - [10][21]
Femur Rt - - - - [10]
Bone marrow Rt - - - - [10]
Costal cartilage Rt - - - - [10]
White adipose tissue Rt, Ch - - - - [10][21][27]
Brown adipose tissue Rt - - - - [10][28]
Fetus Rt - - - - [10]
Embryo F F - - - [18]
Table 2. Localization of NPBWR1 (R1) and NPBWR2 (R2) in central nervous system and peripheral tissues.
  RT-PCR ISH IHC ICC IF WB Reference
Telencephalon Ch (R1, R2) F (R2) - - [19][21]
Cerebral cortex Rt (R1) - - - [10]
Striatum Rt (R1) - - - [10]
Hippocampus Rt (R1) M - - [10]
Thalamus Rt (R1) F (R2) - - [10][19]
Hypothalamus Rt (R1), Ch (R1, R2) Rt (R1), F (R2) - - [10][19][21][22][24]
Midbrain Rt (R1), Ch (R1, R2) F (R2) - - [10][19][21]
Cerebellum Rt (R1) - - - [10]
Medulla oblongata Rt (R1) - - - [10]
Amygdala - Rt (R1) - - [22]
Suprachiasmatic nucleus - Rt (R1) - - [22]
Ventral tuberomammillary nucleus - Rt (R1) - - [22]
Dorsal endopiriform - Rt (R1) - - [22]
Dorsal tenia tecta - Rt (R1) - - [22]
Bed nucleus - Rt (R1) - - [22]
Red nucleus - Rt (R1) - - [22]
Parastrial nucleus - Rt (R1) - - [22]
Laterodorsal tegmentum - Rt (R1) - - [22]
Superior colliculus - Rt (R1) - - [22]
Locus coeruleus - Rt (R1) - - [22]
Nucleus of solitary tract - Rt (R1) - - [22]
Spinal cord Rt (R1), Ch (R1, R2) F (R2) - - [10][19][21]
Pituitary gland Rt (R1), Ch (R2) F (R2) - Ch (R1, R2) [10][19][21][24]
Eyeball and optic nerve Rt (R1) - - - [10]
Thyroid gland Rt (R1) - - - [10][24]
Trachea Rt (R1) - - - [10]
Thymus Rt (R1) - - - [10]
Lung Rt (R1) - - - [10]
Heart Rt (R1) - Rt (R1) Rt (R1) [25]
Adrenal gland (adrenal medulla, adrenal cortex: zonae glomerulosa and fasciculata/reticularis) Rt (R1) - - - [10][24][26]
Stomach Rt (R1) - - - [10]
Duodenum, jejunum, ileum, cecum, colon, rectum Rt (R1), Ch (R1) - - - [10][21]
Testes Rt (R1), P (R1, R2) - - - [10][23][24]
Ovary Rt (R1), P (R1, R2) - - - [10][23][24]
Uterus Rt (R1) - - - [10]
Placenta Rt (R1) - - - [10]
Mammary gland Rt (R1) - - - [10]
Skin Rt (R1) - - - [10]
Fetus Rt (R1) - - - [10]
Pancreas Ch (R2) - - - [21]
Spleen Ch (R2) - - - [21]
Muscle Ch (R1) - - - [21]
Brown preadipocytes Rt (R1) - - - [28]
White adipocytes Rt (R1) - - - [27]

3. The Role of NPB in Appetite Modulation

The initial study showed that NPB mRNA is expressed in brain regions that are crucially relevant in the regulation of food intake. NPB mRNA was reported in the dorsomedial, paraventricular, and arcuate nuclei [11]. In their pioneer work, Tanaka et al. investigated the effects of NPB administration on food intake in mice. Initially, the authors investigated the effects of NPB administration on appetite during the light phase. However, they did not observe any influence of NPB on appetite control in animals. In contrast, i.c.v. administration of NPB during the dark phase led to stimulated food intake during the first 2 h [11]. In contrast, after 2 more hours, NPB caused appetite suppression. The same study evaluated the effects on appetite of co-administration of NPB and corticotropin-releasing factor (CRF), a well-known suppressor of food intake [18]. Tanaka et al. reported that CRF significantly enhanced the suppression of appetite induced by NPB, suggesting an interaction between CRF and urocortin systems [11]. In summary, this study showed, for the first time, that the effects of NPB on food intake are biphasic.
The anorexigenic activity of the NPB/NPBW1 system was additionally confirmed by Ishii et al., who found that GPR7−/− male mice ate more food than wild-type GPR7 mice [19]. It is worth noting that GPR7−/− mice had reduced NPY mRNA and increased POMC mRNA expression in the hypothalamus. Of note, NPY promotes food intake, while POMC has the opposite effect [20]. Another animal study showed that i.c.v. administration of NPB (during the light phase) in male rats promoted feeding behavior [21]. Stimulation of food intake was detected 30 min after NPB administration and lasted at least 4 h. In contrast, NPB did not affect water intake [21]. It is important to note that, in contrast to NPBW1−/− mice, NPB−/− mice had a normal feeding behavior [22]. Studies addressing the role of NPB in appetite regulation are not restricted to rodents. For instance, it was found that i.p. injection of NPB stimulated mRNA expression of NPY and CCK1 in the hypothalamus of Nile tilapia Oreochromis niloticus [23]. Since NPY stimulates food intake and CCK1 suppresses appetite [24], it is difficult to define the role of NPB in controlling feeding behavior in tilapia, and more studies need to be conducted.
Discussing the contribution of NPB to appetite modulation, it is worth noting that a human study was conducted on circulating NPB in blood in patients with anorexia nervosa (AN). Grzelak et al. reported that patients who suffer from AN are characterized by lower levels of NPB in the circulation compared to healthy controls, suggesting the use of NPB in diagnosing AN [25]. Nevertheless, as pointed out in this work, NPB levels were evaluated in only 30 healthy controls and 46 patients with anorexia [25]; therefore, these results should be interpreted cautiously. The downregulation of circulating NPB levels in patients with anorexia was independently confirmed by a study of 30 healthy controls and 30 patients with AN [26]. Importantly, this study additionally showed that increased NPB levels are not affected by body weight normalization after hospitalization [26]. More studies are needed to elucidate the potential role of NPB in the diagnosis of AN.
In summary, animal studies have shown that i.c.v. administration of NPB during the dark phase biphasically modulates food intake. NPB promotes food intake during the first 2 h, followed by appetite suppression. In contrast, rat studies showed that NPB displays orexigenic effects during the light phase. The role of NPB in controlling feeding behavior is complex; therefore, more studies are needed.

4. The Role of NPB in Brain

Beside its role in feeding behavior, in the CNS, NPB modulates locomotion and analgesia [11]. An i.c.v. injection of NPB in rats significantly increased locomotion in an open-field test in both the bright and dark phases. On the other hand, Hirashima et al. demonstrated that i.c.v. injection of NPB in mice reduced locomotor activity during the dark period, but not during the light phase. The activity of mice was measured using an infrared activity monitor [27]. In experiments using Npb−/− mice, no significant differences in activity levels were found compared to littermate controls [22].
In the CNS, NPB impacts analgesia. Tanaka et al. reported that i.c.v. injection of NPB in rats reduced licking duration in the formalin test, which indicates an analgesic role of the peptide against chemically induced pain [11]. These effects could be conferred via NPB and NPBWR1, which are found in the periaqueductal gray matter and amygdala, areas that are also known to express opioid receptors [28]. It is worth mentioning that NPBWR1 binds non-selective opioid ligands such as β-endorphin [13]. The analgesic effect of NPB was also observed after intrathecal injection in the formalin test, and mechanical allodynia was inducible by carrageenan injection [29]. However, NPB had no effect on the level of thermal hyperalgesia induced by paw carrageenan injection in rats [29] and NPB−/− mice [22].
The pain response is tightly connected to anxiety [30]. The role of NPB in regulating anxiety has been investigated using the cued and contextual fear test and elevated plus maze test. NPBWR1−/− mice had similar behavior in the contextual fear test compared to wild-type mice [31]. However, unlike wild-type mice, NPBWR1−/− mice showed behavioral changes in social interactions [31]. The role of NPB in the context of social behavior was evaluated by Watanabe et al. [32]. They showed that genetic changes in NPWR1 (single-nucleotide polymorphism at nucleotide 404 resulted in an amino acid change, Y135F) modulated emotional responses to facial expression. The 404AT subjects were less submissive to angry faces than 404AA subjects.
There is evidence that NPB is involved in sleep/wakefulness [27]. An i.c.v. injection of NPB in mice during the dark period decreased time in the waking state and increased time in slow-wave sleep, whereas no change in paradoxical sleep time was observed. Moreover, NPBWR1+/− and NPBWR1−/− mice did not present any abnormalities compared with wild-type mice, indicating a modulatory role of NPB and NPBWR1 in the sleep/wakefulness pattern [27].
In summary, NPB plays a role in the regulation of locomotion and decreases locomotor activity during the dark phase. Moreover, during the dark period, NPB decreases the waking state time. It also plays an analgesic role in chemically induced pain and decreases social anxiety.

References

  1. Greenwood, H.C.; Bloom, S.R.; Murphy, K.G. Peptides and their potential role in the treatment of diabetes and obesity. Rev. Diabet. Stud. RDS 2011, 8, 355–368.
  2. Timper, K.; Bruning, J.C. Hypothalamic circuits regulating appetite and energy homeostasis: Pathways to obesity. Dis. Models Mech. 2017, 10, 679–689.
  3. Murphy, K.G.; Bloom, S.R. Gut hormones and the regulation of energy homeostasis. Nature 2006, 444, 854–859.
  4. Kołodziejski, P.A.; Pruszyńska-Oszmałek, E.; Wojciechowicz, T.; Sassek, M.; Leciejewska, N.; Jasaszwili, M.; Billert, M.; Małek, E.; Szczepankiewicz, D.; Misiewicz-Mielnik, M. The Role of Peptide Hormones Discovered in the 21st Century in the Regulation of Adipose Tissue Functions. Genes 2021, 12, 756.
  5. Dudek, M.; Ziarniak, K.; Sliwowska, J.H. Kisspeptin and Metabolism: The Brain and Beyond. Front. Endocrinol. 2018, 9, 145.
  6. Skrzypski, M.; Billert, M.; Nowak, K.W.; Strowski, M.Z. The role of orexin in controlling the activity of the adipo-pancreatic axis. J. Endocrinol. 2018, 238, R95–R108.
  7. Macedonio, G.; Stefanucci, A.; Maccallini, C.; Mirzaie, S.; Novellino, E.; Mollica, A. Hemopressin Peptides as Modulators of the Endocannabinoid System and their Potential Applications as Therapeutic Tools. Protein Pept. Lett. 2016, 23, 1045–1051.
  8. Stefanucci, A.; Macedonio, G.; Dvoracsko, S.; Tomboly, C.; Mollica, A. Novel Fubinaca/Rimonabant hybrids as endocannabinoid system modulators. Amino Acids 2018, 50, 1595–1605.
  9. Dimmito, M.P.; Stefanucci, A.; Pieretti, S.; Minosi, P.; Dvoracsko, S.; Tomboly, C.; Zengin, G.; Mollica, A. Discovery of Orexant and Anorexant Agents with Indazole Scaffold Endowed with Peripheral Antiedema Activity. Biomolecules 2019, 9, 492.
  10. Fujii, R.; Yoshida, H.; Fukusumi, S.; Habata, Y.; Hosoya, M.; Kawamata, Y.; Yano, T.; Hinuma, S.; Kitada, C.; Asami, T.; et al. Identification of a neuropeptide modified with bromine as an endogenous ligand for GPR7. J. Biol. Chem. 2002, 277, 34010–34016.
  11. Tanaka, H.; Yoshida, T.; Miyamoto, N.; Motoike, T.; Kurosu, H.; Shibata, K.; Yamanaka, A.; Williams, S.C.; Richardson, J.A.; Tsujino, N.; et al. Characterization of a family of endogenous neuropeptide ligands for the G protein-coupled receptors GPR7 and GPR8. Proc. Natl. Acad. Sci. USA 2003, 100, 6251–6256.
  12. Brezillon, S.; Lannoy, V.; Franssen, J.D.; Le Poul, E.; Dupriez, V.; Lucchetti, J.; Detheux, M.; Parmentier, M. Identification of natural ligands for the orphan G protein-coupled receptors GPR7 and GPR8. J. Biol. Chem. 2003, 278, 776–783.
  13. O’Dowd, B.F.; Scheideler, M.A.; Nguyen, T.; Cheng, R.; Rasmussen, J.S.; Marchese, A.; Zastawny, R.; Heng, H.H.; Tsui, L.C.; Shi, X.; et al. The cloning and chromosomal mapping of two novel human opioid-somatostatin-like receptor genes, GPR7 and GPR8, expressed in discrete areas of the brain. Genomics 1995, 28, 84–91.
  14. Lee, D.K.; Nguyen, T.; Porter, C.A.; Cheng, R.; George, S.R.; O’Dowd, B.F. Two related G protein-coupled receptors: The distribution of GPR7 in rat brain and the absence of GPR8 in rodents. Brain Res. Mol. Brain Res. 1999, 71, 96–103.
  15. Shimomura, Y.; Harada, M.; Goto, M.; Sugo, T.; Matsumoto, Y.; Abe, M.; Watanabe, T.; Asami, T.; Kitada, C.; Mori, M.; et al. Identification of neuropeptide W as the endogenous ligand for orphan G-protein-coupled receptors GPR7 and GPR8. J. Biol. Chem. 2002, 277, 35826–35832.
  16. Mazzocchi, G.; Rebuffat, P.; Ziolkowska, A.; Rossi, G.P.; Malendowicz, L.K.; Nussdorfer, G.G. G protein receptors 7 and 8 are expressed in human adrenocortical cells, and their endogenous ligands neuropeptides B and w enhance cortisol secretion by activating adenylate cyclase- and phospholipase C-dependent signaling cascades. J. Clin. Endocrinol. Metab. 2005, 90, 3466–3471.
  17. Billert, M.; Sassek, M.; Wojciechowicz, T.; Jasaszwili, M.; Strowski, M.Z.; Nowak, K.W.; Skrzypski, M. Neuropeptide B stimulates insulin secretion and expression but not proliferation in rat insulinproducing INS1E cells. Mol. Med. Rep. 2019, 20, 2030–2038.
  18. Nakayama, N.; Suzuki, H.; Li, J.B.; Atsuchi, K.; Tsai, M.; Amitani, H.; Asakawa, A.; Inui, A. The role of CRF family peptides in the regulation of food intake and anxiety-like behavior. Biomol. Concepts 2011, 2, 275–280.
  19. Ishii, M.; Fei, H.; Friedman, J.M. Targeted disruption of GPR7, the endogenous receptor for neuropeptides B and W, leads to metabolic defects and adult-onset obesity. Proc. Natl. Acad. Sci. USA 2003, 100, 10540–10545.
  20. Sohn, J.W. Network of hypothalamic neurons that control appetite. BMB Rep. 2015, 48, 229–233.
  21. Samson, W.K.; Baker, J.R.; Samson, C.K.; Samson, H.W.; Taylor, M.M. Central neuropeptide B administration activates stress hormone secretion and stimulates feeding in male rats. J. Neuroendocrinol. 2004, 16, 842–849.
  22. Kelly, M.A.; Beuckmann, C.T.; Williams, S.C.; Sinton, C.M.; Motoike, T.; Richardson, J.A.; Hammer, R.E.; Garry, M.G.; Yanagisawa, M. Neuropeptide B-deficient mice demonstrate hyperalgesia in response to inflammatory pain. Proc. Natl. Acad. Sci. USA 2005, 102, 9942–9947.
  23. Yang, L.; Sun, C.; Li, W. Neuropeptide B in Nile tilapia Oreochromis niloticus: Molecular cloning and its effects on the regulation of food intake and mRNA expression of growth hormone and prolactin. Gen. Comp. Endocrinol. 2014, 200, 27–34.
  24. Perry, B.; Wang, Y. Appetite regulation and weight control: The role of gut hormones. Nutr. Diabetes 2012, 2, e26.
  25. Grzelak, T.; Tyszkiewicz-Nwafor, M.; Dutkiewicz, A.; Mikulska, A.A.; Dmitrzak-Weglarz, M.; Slopien, A.; Czyzewska, K.; Paszynska, E. Neuropeptide B and Vaspin as New Biomarkers in Anorexia Nervosa. BioMed Res. Int. 2018, 2018, 9727509.
  26. Grzelak, T.; Tyszkiewicz-Nwafor, M.; Dutkiewicz, A.; Mikulska, A.A.; Dmitrzak-Weglarz, M.; Slopien, A.; Czyzewska, K.; Paszynska, E. Vaspin (but not neuropeptide B or neuropeptide W) as a possible predictor of body weight normalization in anorexia nervosa. Arch. Med. Sci. AMS 2021, 17, 376–381.
  27. Hirashima, N.; Tsunematsu, T.; Ichiki, K.; Tanaka, H.; Kilduff, T.S.; Yamanaka, A. Neuropeptide B induces slow wave sleep in mice. Sleep 2011, 34, 31–37.
  28. Lau, B.K.; Winters, B.L.; Vaughan, C.W. Opioid presynaptic disinhibition of the midbrain periaqueductal grey descending analgesic pathway. Br. J. Pharmacol. 2020, 177, 2320–2332.
  29. Yamamoto, T.; Saito, O.; Shono, K.; Tanabe, S. Anti-hyperalgesic effects of intrathecally administered neuropeptide W-23, and neuropeptide B, in tests of inflammatory pain in rats. Brain Res. 2005, 1045, 97–106.
  30. Cimpean, A.; David, D. The mechanisms of pain tolerance and pain-related anxiety in acute pain. Health Psychol. Open 2019, 6, 2055102919865161.
  31. Nagata-Kuroiwa, R.; Furutani, N.; Hara, J.; Hondo, M.; Ishii, M.; Abe, T.; Mieda, M.; Tsujino, N.; Motoike, T.; Yanagawa, Y.; et al. Critical role of neuropeptides B/W receptor 1 signaling in social behavior and fear memory. PLoS ONE 2011, 6, e16972.
  32. Watanabe, N.; Wada, M.; Irukayama-Tomobe, Y.; Ogata, Y.; Tsujino, N.; Suzuki, M.; Furutani, N.; Sakurai, T.; Yamamoto, M. A single nucleotide polymorphism of the neuropeptide B/W receptor-1 gene influences the evaluation of facial expressions. PLoS ONE 2012, 7, e35390.
More
Information
Subjects: Cell Biology
Contributor MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
View Times: 451
Revisions: 2 times (View History)
Update Date: 29 Jul 2021
1000/1000