Tachykinin NK3-receptor deficiency does not inhibit pulmonary eosinophilia in allergic mice

Kung, Ted T.; Crawley, Yvette; Jones, Howard; Luo, Bin; Gilchrest, Helen; Greenfeder, Scott; Anthes, John C.; Lira, Sérgio A.; Wiekowski, Maria; Cook, Donald N.

doi:10.1016/j.phrs.2004.07.002

Cited by 50 publications

(33 citation statements)

References 18 publications

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“…On the other hand, despite of this apparent functional association between GnRH and NKB in human, there is a report showing that TAC3R knowkout mice are healthy and fertile [31].…”

Section: Discussionmentioning

confidence: 99%

Role of Neurokinin B and Dynorphin A in pituitary gonadotroph and somatolactotroph cell lines

et al. 2012

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“…On the other hand, despite of this apparent functional association between GnRH and NKB in human, there is a report showing that TAC3R knowkout mice are healthy and fertile [31].…”

Section: Discussionmentioning

confidence: 99%

Role of Neurokinin B and Dynorphin A in pituitary gonadotroph and somatolactotroph cell lines

et al. 2012

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“…On the basis of these data, it is tempting to consider that kisspeptin and NKB play similar roles in relaying feedback from sex steroids to GnRH production. However, other observations seem to indicate important differences in their actions, such as the different ability to stimulate GnRH release in different species (kisspeptin can stimulate this release in almost all species, but NKB cannot), or the different phenotypes that have been observed in KO mice models of kisspeptin or NKB resistance, which are associated with a classic ICH phenotype 67 or grossly normal fertility, 68 respectively. NKB has a wider pattern of central nervous system expression than KISS1, 69 which suggests that the arcuate may not be the sole, or even the most important, site at which NKB exerts its influence on reproductive function.…”

Section: Tacr3 and Tac3mentioning

confidence: 99%

New understandings of the genetic basis of isolated idiopathic central hypogonadism

Bonomi¹,

Libri²,

Guizzardi³

et al. 2011

Asian J Androl

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Idiopathic hypogonadotropic hypogonadism is a rare disease that is characterized by delayed/absent puberty and/or infertility due to an insufficient stimulation of an otherwise normal pituitary-gonadal axis by gonadotrophin-releasing hormone (GnRH) action. Because reduced or normal luteinizing hormone (LH)/follicle-stimulating hormone (FSH) levels may be observed in the affected patients, the term idiopathic central hypogonadism (ICH) appears to be more appropriate. This disease should be distinguished from central hypogonadism that is combined with other pituitary deficiencies. Isolated ICH has a complex pathogenesis and is fivefold more prevalent in males. ICH frequently appears in a sporadic form, but several familial cases have also been reported. This finding, in conjunction with the description of numerous pathogenetic gene variants and the generation of several knockout models, supports the existence of a strong genetic component. ICH may be associated with several morphogenetic abnormalities, which include osmic defects that, with ICH, constitute the cardinal manifestations of Kallmann syndrome (KS). KS accounts for approximately 40% of the total ICH cases and has been generally considered to be a distinct subgroup. However, the description of several pedigrees, which include relatives who are affected either with isolated osmic defects, KS, or normo-osmic ICH (nICH), justifies the emerging idea that ICH is a complex genetic disease that is characterized by variable expressivity and penetrance. In this context, either multiple gene variants or environmental factors and epigenetic modifications may contribute to the variable disease manifestations. We review the genetic mechanisms that are presently known to be involved in ICH pathogenesis and provide a clinical overview of the 227 cases that have been collected by the collaborating centres of the Italian ICH Network. Asian Journal of Andrology (2012) 14, 49-56; doi:10.1038/aja.2011.68; published online 5 December 201

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“…Sandoval-Guzman and Rance [45] showed that icv injection of NK3 receptor agonist reduced LH secretion in rats. On the other hand, there are several reports indicating that NKB-NK3 signaling is not involved in GnRH secretion; specifically, Tac3r knockout mice were fertile [46] and peripheral or central administration of NKB had no apparent effect on serum LH levels in mice [57]. In this context, the mechanism generating pulsatile GnRH/LH secretion has not yet been fully elucidated in rodents and may involve species differences.…”

mentioning

confidence: 98%

“…Additionally, Krajewski et al [44] showed that a dense interweaving and close apposition of GnRH and NKB-immunoreactive fiber was observed within the rat median eminence, where GnRH axons expressed NK3 receptor immunoreactivity. Indeed, central injection of senktide, an NK3 receptor agonist, inhibited LH secretion in rats and mice [14,45], although NK3 receptor knockout mice are fertile [46]. The overlapping binding activities of neurokinins on their three types of receptor makes it difficult to understand the role of neurokinins in reproductive functions [27].…”

mentioning

confidence: 99%

Involvement of Neurokinin Receptors in the Control of Pulsatile Luteinizing Hormone Secretion in Rats

et al. 2011

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Abstract. It has recently been shown that neurokinin B, a tachykinin, is associated with GnRH pulse generation in sheep and goats. The aim of the present study was to clarify the role of tachykinin receptors in the control of LH secretion in rats. To this end, we evaluated the effect of CS-003, an antagonist for all three neurokinin receptors (NK1, NK2 and NK3 receptors), on pulsatile LH secretion in both sexes of rats with different routes of administration. Both oral and third ventricular administration of CS-003 suppressed LH secretion in both sexes of gonadectomized animals. Furthermore, intact male rats with oral administration of CS-003 showed decreased serum testosterone levels, which might be due to suppressed LH secretion. None of the three subtype-specific neurokinin receptor antagonists showed a significant effect on LH secretion in ovariectomized rats when each antagonist was singly administered. The present results suggest that neurokinins play a role in the control of pulsatile GnRH/LH secretion via multiple neurokinin receptors in both male and female rats. Key words: Luteinizing hormone, Neurokinin, Rat, Receptor (J. Reprod. Dev. 57: [409][410][411][412][413][414][415] 2011) ulsatile gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) release is indispensable for regulation of gonadal functions, such as folliculogenesis, spermatogenesis and steroidogenesis, in rodents [1], ruminants [2,3] and primates [4]. The mechanism generating GnRH/LH pulses, called the GnRH pulse generator, has been suggested to be localized in the hypothalamus [5]. Recent studies have revealed that kisspeptin neurons located in the hypothalamus play a central role in regulating GnRH release [6,7]. Kisspeptin neurons have two populations in the hypothalamus [8]: One is located in the hypothalamic arcuate nucleus (ARC), and the other is located in the anteroventral periventricular nucleus (AVPV). Of these two populations, the AVPV kisspeptin neurons have been reported to be involved in the regulation of GnRH/LH surge [9,10]. On the other hand, the role of ARC kisspeptin neurons is still unclear, but several lines of evidence suggest that the population is associated with GnRH pulse generation [11].Recent studies have shown an interesting and essential aspect of the ARC kisspeptin neurons. Most kisspeptin neurons have neurokinin B (NKB) and dynorphin (Dyn) in sheep [12], goats [13] and rodents [14], and thus the neurons have been called KNDy neurons [15]. Colocalization of those three neuropeptides in the ARC neurons might be associated with GnRH pulse generation. It has recently been reported that mutations of genes encoding NKB and its receptor are associated with gonadotropin deficiency in humans [16], and central administration of a selective NKB receptor agonist stimulates LH secretion in sheep [17] and monkeys [18]. These reports indicate the significance of NKB/NK3 signaling in GnRH/gonadotropin release in these animal species. In addition to neurokinin B, nor-BNI, a κ-opioid receptor antagonist (KOR), rev...

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Tachykinin NK3-receptor deficiency does not inhibit pulmonary eosinophilia in allergic mice

Cited by 50 publications

References 18 publications

Role of Neurokinin B and Dynorphin A in pituitary gonadotroph and somatolactotroph cell lines

Role of Neurokinin B and Dynorphin A in pituitary gonadotroph and somatolactotroph cell lines

New understandings of the genetic basis of isolated idiopathic central hypogonadism

Involvement of Neurokinin Receptors in the Control of Pulsatile Luteinizing Hormone Secretion in Rats

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