Characterisation, localisation and expression of porcine TACR1, TACR2 and TACR3 genes

Jakimiuk, A.; Podlasz, Piotr; Chmielewska-Krzesińska, Małgorzata; Wąsowicz, Krzysztof

doi:10.17221/23/2017-vetmed

Cited by 5 publications

(3 citation statements)

References 72 publications

(65 reference statements)

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“…Distribution of NK3R throughout the POA and hypothalamus was relatively similar to that previously described for other species [22,23,231,233,238,239]. Regarding areas that are important for reproduction, expression was prevalent in the POA and PVN with a smaller population in the RCh.…”

Section: Discussionsupporting

confidence: 81%

“…Although, NK3R mRNA is located throughout the POA and hypothalamus, with expression noted in the PVN, SON, ventromedial hypothalamus and ARC [22,231,233,238,239], NKB is concentrated only within the ARC [231,233,238,240,241]. NKB-containing fibers from ARC KNDy neurons innervate GnRH axon terminals in the stalk-ME [81,242], but as mentioned earlier, GnRH is not directly modulated by NKB.…”

Section: Distributionmentioning

confidence: 81%

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Characterization of KNDy Neuronal Activity in Gilts: Distribution and Effect of A Progestin

Lindo¹

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Puberty is a process that incorporates a large array of both external factors and internal signals. The endocrinology of puberty has been studied in a number of mammalian species and typically depends upon an increase in hypothalamic secretion of gonadotropin releasing hormone (GnRH). Neural inputs regulating GnRH secretion during the pubertal process are not completely understood. In the past decade, attention has focused on the role for a particular set of neurons located in the arcuate nucleus (ARC) of the hypothalamus. They have been named KNDy neurons because they coexpress kisspeptin, neurokinin B (NKB) and dynorphin and have been shown to stimulate (kisspeptin, NKB) or inhibit (dynorphin) GnRH and luteinizing hormone (LH) secretion. While KNDy neurons have been studied extensively in primates, rodents, and sheep, almost nothing is known about this system in porcine, a species of significant agricultural importance. Our studies describe an initial foray into characterizing this system in the porcine hypothalamus. We first determined that, similar to other species, kisspeptin was expressed in the ARC and that NKB and kisspeptin were coexpressed in this region to a very high extent. We then examined the distribution of receptors for NKB (NK3R) and found them to be expressed in the preoptic area (POA) and several areas of the hypothalamus, including the paraventricular nucleus (PVN) and retrochiasmatic area (RCh). However, there was no evidence of NK3R expression in the ARC. The NK3R-positive cells found in the POA did not co-localize with GnRH but expressed close contacts with GnRH neurons. We then used gilts that were ovariectomized (OVX) or OVX and treated with Altrenogest (OVXA), a progestin, to test the hypothesis that Altrenogest would suppress kisspeptin and NKB immunopositive cell numbers in the ARC and NK3R-positive cell numbers throughout the hypothalamus. Surprisingly, kisspeptin containing cell numbers tended to be increased (p = 0.09) in in OVXA gilts (n = 6) compared to their OVX, untreated counterparts (n = 6). In addition, there was no significant change in NKBpositive cell numbers in response to Altrenogest. Subsequent analysis determined a tendency (p = 0.08) for a decrease in the percentage of kisspeptin neurons expressing c-Fos, a marker of neural activation, in OVXA versus OVX gilts. There was no effect of Altrenogest on NK3Rpositive cell numbers in any area. These studies mark one of the first investigations into the KNDy system in swine. Many of the characteristics examined here are similar to that previously reported for other mammalian species, with the notable exception of an absence of NK3R expression within the ARC. Treatment with a progestin did not suppress kisspeptin or NKB expression but did tend to reduce activity of kisspeptin neurons. These results suggest that, similar to other species, KNDy neurons likely play an important role in regulating reproduction in swine. v

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Section: Discussionsupporting

confidence: 81%

Section: Distributionmentioning

confidence: 81%

Characterization of KNDy Neuronal Activity in Gilts: Distribution and Effect of A Progestin

Lindo¹

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“…This disorder is caused by missense loss-of-function mutations in Tac3 and Tacr3, the genes encoding neurokinin B (TAC3) and its NK3R receptor (TACR3), respectively [16][17][18]. TACR3 is a G protein-coupled receptor widely distributed in the brain, particularly in the hypothalamus, pituitary gland, and hippocampus, and it is known to modulate gonadotropin release through its action on Kisspeptin-1 neurons [19,20]. Downregulation of TACR3 was observed in the lateral habenula of mice showing anxiety-like behaviors, whereas TACR3 overexpression in the same area significantly reversed such anxiety-like behaviors [21].…”

Section: Introductionmentioning

confidence: 99%

Interplay between hippocampal TACR3 and systemic testosterone in regulating anxiety-associated synaptic plasticity

Wojtas,

Diaz-González,

Stavtseva

et al. 2023

Mol Psychiatry

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Tachykinin receptor 3 (TACR3) is a member of the tachykinin receptor family and falls within the rhodopsin subfamily. As a G protein-coupled receptor, it responds to neurokinin B (NKB), its high-affinity ligand. Dysfunctional TACR3 has been associated with pubertal failure and anxiety, yet the mechanisms underlying this remain unclear. Hence, we have investigated the relationship between TACR3 expression, anxiety, sex hormones, and synaptic plasticity in a rat model, which indicated that severe anxiety is linked to dampened TACR3 expression in the ventral hippocampus. TACR3 expression in female rats fluctuates during the estrous cycle, reflecting sensitivity to sex hormones. Indeed, in males, sexual development is associated with a substantial increase in hippocampal TACR3 expression, coinciding with elevated serum testosterone and a significant reduction in anxiety. TACR3 is predominantly expressed in the cell membrane, including the presynaptic compartment, and its modulation significantly influences synaptic activity. Inhibition of TACR3 activity provokes hyperactivation of CaMKII and enhanced AMPA receptor phosphorylation, associated with an increase in spine density. Using a multielectrode array, stronger cross-correlation of firing was evident among neurons following TACR3 inhibition, indicating enhanced connectivity. Deficient TACR3 activity in rats led to lower serum testosterone levels, as well as increased spine density and impaired long-term potentiation (LTP) in the dentate gyrus. Remarkably, aberrant expression of functional TACR3 in spines results in spine shrinkage and pruning, while expression of defective TACR3 increases spine density, size, and the magnitude of cross-correlation. The firing pattern in response to LTP induction was inadequate in neurons expressing defective TACR3, which could be rectified by treatment with testosterone. In conclusion, our study provides valuable insights into the intricate interplay between TACR3, sex hormones, anxiety, and synaptic plasticity. These findings highlight potential targets for therapeutic interventions to alleviate anxiety in individuals with TACR3 dysfunction and the implications of TACR3 in anxiety-related neural changes provide an avenue for future research in the field.

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The role of neurokinin A and its receptor in the regulation of prolactin secretion by the anterior pituitary of cyclic pigs

Czelejewska

Zmijewska

Dziekoński

et al. 2020

Reprod Domestic Animals

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In pigs, plasma prolactin concentration markedly changes during the oestrous cycle and the regulation of its secretion is very complex. The contribution of neurokinins in this process has not been sufficiently delineated. The aim of the study was to examine the effects of neurokinin A (NKA) on prolactin synthesis and secretion in cyclic gilts. The expression of NKA precursor (Ppta) and receptor (Tacr2) genes as well as NKA and TACR proteins content in the porcine pituitaries (days 2–3, 9–10, 12–13, 15–16 and 19–20 of the cycle) was determined. Furthermore, the in vitro influence of NKA on the expression of prolactin (Prl), dopamine receptor (D2r), TRH receptor (Trhr) genes and prolactin secretion by the porcine pituitary cells (days 9–10, 15–16 and 19–20 of the cycle) was assessed. The expression of Ppta and Tacr2 as well as NKA and TACR proteins in the pituitary tissue has been changing throughout the oestrous cycle. NKA affected in vitro the expression of studied genes and prolactin secretion depending on the stage of the cycle, dose of NKA and/or duration of the cell incubation. Altogether, the study indicates that NKA is engaged in the modulation of prolactin secretion in the pig during the oestrous cycle.

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Characterisation, localisation and expression of porcine TACR1, TACR2 and TACR3 genes

Cited by 5 publications

References 72 publications

Characterization of KNDy Neuronal Activity in Gilts: Distribution and Effect of A Progestin

Characterization of KNDy Neuronal Activity in Gilts: Distribution and Effect of A Progestin

Interplay between hippocampal TACR3 and systemic testosterone in regulating anxiety-associated synaptic plasticity

The role of neurokinin A and its receptor in the regulation of prolactin secretion by the anterior pituitary of cyclic pigs

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