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Littérature scientifique sur le sujet « Tachykinins »

Auteur : Grafiati
Publié le 4 juin 2021
Mis à jour le 9 juin 2025

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Articles de revues sur le sujet "Tachykinins"

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López, B. Díaz, and L. Debeljuk. "Prenatal melatonin and its interaction with tachykinins in the hypothalamic - pituitary - gonadal axis." Reproduction, Fertility and Development 19, no. 3 (2007): 443. http://dx.doi.org/10.1071/rd06140.

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The pineal gland, through its hormone melatonin, influences the function of the hypothalamic–pituitary–gonadal axis. Tachykinins are bioactive peptides whose presence has been demonstrated in the pineal gland, hypothalamus, anterior pituitary gland and the gonads, in addition to other central and peripheral structures. Tachykinins have been demonstrated to influence the function of the hypothalamic–pituitary–gonadal axis, acting as paracrine factors at each of these levels. In the present review, we examine the available evidence supporting a role for melatonin in the regulation of reproductive functions, the possible role of tachykinins in pineal function and the possible interactions between melatonin and tachykinins in the hypothalamic–pituitary–gonadal axis. Evidence is presented showing that melatonin, given to pregnant rats, influences the developmental pattern of tachykinins in the hypothalamus and the anterior pituitary gland of the offspring during postnatal life. In the gonads, the effects of melatonin on the tachykinin developmental pattern were rather modest. In particular, in the present review, we have included a summary of our own work performed in the past few years on the effect of melatonin on tachykinin levels in the hypothalamic–pituitary–gonadal axis.
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Fujii, K., H. Kohrogi, H. Iwagoe, J. Hamamoto, N. Hirata, T. Yamaguchi, O. Kawano, and M. Ando. "Evidence that PGF2 alpha-induced contraction of isolated guinea pig bronchi is mediated in part by release of tachykinins." Journal of Applied Physiology 79, no. 5 (November 1, 1995): 1411–18. http://dx.doi.org/10.1152/jappl.1995.79.5.1411.

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To investigate whether prostaglandin F2 alpha (PGF2 alpha) stimulates the release of tachykinins and whether the tachykinins play a role in the PGF2 alpha-induced bronchial contraction, we examined the contractile response to PGF2 alpha in the presence or absence of a neutral endopeptidase (NEP) inhibitor phosphoramidon in the guinea pig main bronchus in vitro. Because NEP effectively cleaves tachykinins, we hypothesized that the inhibition of NEP would enhance a PGF2 alpha-induced bronchial contraction if PGF2 alpha stimulates the release of tachykinins. Phosphoramidon significantly enhanced the concentration-response curve to PGF2 alpha. And it also significantly enhanced 10(-5) M PGF2 alpha-induced contraction. The enhancement was significantly attenuated in tissues where the tachykinins had been depleted by treatment with capsaicin. Furthermore, the enhancement of contraction was also significantly attenuated in the presence of tachykinin antagonist FK-224 (10(-5) M). Tetrodotoxin, a sodium-channel blocker that blocks nerve conduction, did not affect the enhancement. From these results we conclude that 1) PGF2 alpha causes the release of tachykinin-like substances, 2) these substances play a role in bronchial contraction in tissues where NEP activity is inhibited, and 3) nerve conduction is not necessary for the release of these substances in the guinea pig bronchus.
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Payne, Catherine M., Caroline J. Heggie, David G. Brownstein, James P. Stewart, and John P. Quinn. "Role of Tachykinins in the Host Response to Murine Gammaherpesvirus Infection." Journal of Virology 75, no. 21 (November 1, 2001): 10467–71. http://dx.doi.org/10.1128/jvi.75.21.10467-10471.2001.

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ABSTRACT Tachykinins function not only as neurotransmitters but also as immunological mediators. We used infection of tachykinin-deficient (PPT-A −/−) mice and wild-type controls with murine gammaherpesvirus to assess the role of tachykinins in the host response to a virus infection. Although infection was ultimately controlled in PPT-A −/− mice, there were higher titers of infectious virus in the lungs, accompanied by a more rapid influx of inflammatory cells. Clearance of latently infected cells from the spleen was also delayed. This is the first report of the direct influence of tachykinins in the host response to a virus infection.
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Weinstock, J. V., and A. M. Blum. "Tachykinin production in granulomas of murine schistosomiasis mansoni." Journal of Immunology 142, no. 9 (May 1, 1989): 3256–61. http://dx.doi.org/10.4049/jimmunol.142.9.3256.

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Abstract Preprotachykinins, the products of one gene, are the precursor molecules of three mammalian tachykinins called substance P (SP), substance K (SK), and neuropeptide K. An additional mammalian tachykinin, neurokinin B, has also been described. SP and possibly other tachykinins may modulate immunologic responses. Granulomas that form around parasite ova in murine schistosomiasis were examined for tachykinins. Tachykinins were extracted from granulomas by boiling or with detergent. Extracts examined by RIA and HPLC contained only immunoreactive SP. Granulomas were dispersed with collagenase and cultured in vitro for up to 4 h. Only immunoreactive SP appeared in the culture medium. SP immunoreactivity localized solely to granuloma eosinophils as demonstrated by a sensitive immunohistochemical technique. An antiserum that recognized SK, neuropeptide K, and neurokinin B, but which possessed low reactivity to SP, also stained these cells. Only prior absorption of each antiserum with the appropriate synthetic neuropeptide would abrogate the immunostaining. This suggested that tachykinins other than SP were present within these cells. However, results of in situ hybridization experiments intimated that eosinophils produced predominantly preprotachykinin mRNAs which encode SP but are devoid of the SK/neuropeptide K sequence. It is concluded that granuloma eosinophils make predominantly SP in deference to other tachykinins, and that tachykinins other than SP are unlikely to be important in the regulation of the early granulomatous response of murine schistosomiasis.
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Culman, Juraj, and Thomas Unger. "Central tachykinins: mediators of defence reaction and stress reactions." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 885–91. http://dx.doi.org/10.1139/y95-122.

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The tachykinins substance P, neurokinin A, and neurokinin B are natural agonists for NK1, NK2, and NK3 receptors, respectively. Evidence from biochemical, neurophysiological, pharmacological, and molecular biology studies indicates that the tachykinin-containing pathways within the brain contribute to central cardiovascular and endocrine regulation and to the control of motor activity. The hypothalamus, which represents a site for the integration of central neuroendocrine and autonomic processes, is rich in tachykinin nerve endings and tachykinin receptors. Stimulation of periventricular or hypothalamic NK1 receptors in conscious rats induces an integrated cardiovascular, behavioural, and endocrine response. The cardiovascular response is associated with increased sympathoadrenal activity and comprises an increase in blood pressure and heart rate, mesenteric and renal vasoconstriction, and hind-limb vasodilatation. The behavioural response consists of increased locomotion and grooming behaviour. This response pattern is consistent with an integrated stress response to nociceptive stimuli and pain in rodents. Several studies have demonstrated rapid changes in substance P levels and its receptors in distinct brain areas following acute stress. These data indicate that substance P and other tachykinins, in addition to serving as nociceptive and pain transmitters in the spinal cord, may act in the brain as neurotransmitters–neuromodulators within the neuronal circuits mediating central stress responses.Key words: tachykinins, substance P, central nervous system, defence reaction, stress.
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Weil, M., A. Itin, and E. Keshet. "A role for mesenchyme-derived tachykinins in tooth and mammary gland morphogenesis." Development 121, no. 8 (August 1, 1995): 2419–28. http://dx.doi.org/10.1242/dev.121.8.2419.

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Tachykinin peptides such as substance P (SP) function as neurotransmitters and neuromodulators in the mammalian central and peripheral nervous systems. Here, we provide evidence that they may also play an important role in the morphogenesis of some nonneural organs where epithelial-mesenchymal interactions are involved. We show the following. (1) mRNA encoding tachykinin precursor proteins is expressed transiently in condensing mesenchyme during the development of mouse tooth germ, mammary gland, limb bud, external auditory meatus and genital tubercle. (2) In developing tooth germ and mammary gland; mRNA encoding the neutral endopeptidase (NEP) that degrades secreted tachykinins is spatially and temporally co-expressed with tachykinin precursor mRNA. (3) SP and the mRNA encoding SP receptors are also expressed in the developing tooth germ. (4) Tooth development in explant cultures is blocked both by tachykinin-precursor-specific antisense oligonucleotide and by an SP receptor antagonist: in both cases the block is relieved by exogenous SP. Together, these findings suggest a surprising new role for tachykinins in tooth and mammary gland morphogenesis, and possibly also in limb, ear and external genitalia morphogenesis.
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Kagstrom, J., M. Axelsson, J. Jensen, A. P. Farrell, and S. Holmgren. "Vasoactivity and immunoreactivity of fish tachykinins in the vascular system of the spiny dogfish." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 3 (March 1, 1996): R585—R593. http://dx.doi.org/10.1152/ajpregu.1996.270.3.r585.

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Tachykinin control of gut blood flow (measured by pulsed Doppler technique), dorsal aortic pressure, and heart rate were studied in unrestrained spiny dogfish Squalus acanthias injected with the elasmobranch tachykinins scyliorhinin I and II (SCY I and SCY II), the trout tachykinins substance P (SP), and neurokinin A (NKA). Effects on somatic vasculature were measured by in vitro perfusion of the isolated tail. SCY I and trout SP produced hypotension due to a general vasodilation. This caused a transient increase in mesenteric blood flow and a prolonged increase in celiac blood flow. SCY II caused an initial hypertension induced by a general vasoconstriction, followed eventually by an elevated flow in both gut arteries due to dilation of the vascular beds. Trout NKA evoked a short-lasting increase in celiac blood flow due to a decrease in vascular resistance, a late decrease in mesenteric flow due to vasoconstriction, and no effect on the somatic vasculature. None of the peptides affected heart rate. The study demonstrates a significant vasoactive function of fish tachykinins in the vascular system of an elasmobranch species and, in addition, the occurrence of tachykinin receptor subtypes. Immunohistochemistry revealed a NKA/SCY II-like peptide in nerve fibers innervating many vessels, including the celiac and the mesenteric arteries, the gastrointestinal canal, and the heart.
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Jensen, J., K. R. Olson, and J. M. Conlon. "Primary structures and effects on gastrointestinal motility of tachykinins from the rainbow trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 4 (October 1, 1993): R804—R810. http://dx.doi.org/10.1152/ajpregu.1993.265.4.r804.

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Purification and structural characterization of tachykinins from rainbow trout (Oncorhynchus mykiss) intestine has demonstrated the presence of three different peptides related to the mammalian tachykinins: substance P, neurokinin A, and neuropeptide-gamma. The substance P- and the neurokinin A-related peptides present in the intestine are identical to the tachykinins previously isolated from the trout brain. The neuropeptide-gamma-related peptide (Ser-Ser-Ala-Asn-Pro-Gln-Ile-Thr-Arg-Lys-Arg-His-Lys-Ile-Asn-Ser-Phe- Val-Gly-Leu-Met-NH2), not previously identified in brain tissue, has the sequence of the neurokinin A-related tachykinin at its COOH-terminus. Both trout substance P and neurokinin A stimulated the motility of isolated trout intestinal muscle [pD2(-log of EC50) values 8.5 +/- 0.15 and 7.35 +/- 0.08, respectively] and the vascularly perfused trout stomach (pD2 values 9.63 +/- 0.23 and 8.18 +/- 0.23, respectively). Trout substance P was 14 times more potent than trout neurokinin A in the intestine and 28 times more potent in the stomach. The data suggest that receptors interacting with tachykinins in the trout gastrointestinal tract have a similar selectivity as the mammalian NK-1 receptor.
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Cao, Thong, Norma P. Gerard, and Susan D. Brain. "Use of NK1knockout mice to analyze substance P-induced edema formation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 2 (August 1, 1999): R476—R481. http://dx.doi.org/10.1152/ajpregu.1999.277.2.r476.

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The mechanisms involved in tachykinin-induced neurokinin-1 (NK1) receptor-mediated edema formation have been studied in anesthetized wild-type and NK1knockout mice. Intradermally injected substance P (30–300 pmol), NK1agonists septide (3–30 pmol) and GR-73632 (3–30 pmol), and the mast cell-degranulating agent, compound 48/80 induced dose-dependent edema in wild-type skin, measured by the accumulation of intravenously injected125I-labeled albumin. Septide was 3–10× more potent than substance P. The tachykinins were inactive in knockout mice, but compound 48/80 induced a significantly greater edema ( P < 0.05) than that observed in paired wild-type mice. Capsaicin (which releases endogenous neuropeptides) and exogenous tachykinins induced edema formation, which was reduced by the mast cell amine histamine H1antagonist mepyramine ( P < 0.05). These findings confirm that tachykinins mediate edema formation via the NK1receptor and provide direct evidence that the septide-sensitive binding site is on the NK1receptor. Furthermore, results suggest that edema induced by the tachykinins, although totally dependent on NK1receptor-mediated mechanism, contains a mast cell-dependent component. The evidence is in keeping with an NK1receptor on mast cells.
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Williams, Ronald, Xiaoyan Zou та Gary W. Hoyle. "Tachykinin-1 receptor stimulates proinflammatory gene expression in lung epithelial cells through activation of NF-κB via a Gq-dependent pathway". American Journal of Physiology-Lung Cellular and Molecular Physiology 292, № 2 (лютий 2007): L430—L437. http://dx.doi.org/10.1152/ajplung.00475.2005.

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The respiratory tract is innervated by irritant-responsive sensory nerves, which, on stimulation, release tachykinin neuropeptides in the lung. Tachykinins modulate inflammatory responses to injury by binding to tachykinin (neurokinin) receptors present on various pulmonary cell types. In the present study, the activation of the proinflammatory transcription factor NF-κB in lung epithelial cells was investigated as a mechanism by which tachykinins stimulate inflammatory processes. In A549 human lung epithelial cells transfected with the tachykinin-1 receptor (Tacr1), treatment with the Tacr1 ligand substance P (SP) resulted in NF-κB activation, as judged by transcription of an NF-κB-luciferase reporter gene and production of interleukin-8, a chemokine whose expression is upregulated by NF-κB. SP caused a dose-dependent activation of NF-κB that was inhibited by the selective Tacr1 antagonist RP67580. Tacr1 is a G protein-coupled receptor capable of activating both the Gq and Gs families of G proteins. Expression of inhibitory peptides and constitutively active G protein mutants revealed that Gq signaling was both necessary for Tacr1-induced NF-κB activation and sufficient for NF-κB activation in the absence of any other treatment. Treatment with pharmacological inhibitors to investigate events downstream of Gq revealed that Tacr1-induced NF-κB activation proceeded through an intracellular signaling pathway that was dependent on phospholipase C, calcium, Ras, Raf-1, MEK, Erk, and proteasome function. These results identify intracellular signaling mechanisms that underlie the proinflammatory effects of tachykinins, which previously have been implicated in lung injury and disease.
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Thèses sur le sujet "Tachykinins"

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Bell, Nicola Jane. "Peripheral tachykinins and tachykinin receptors." Thesis, University of Reading, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428305.

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Chambers, J. K. "Molecular forms of tachykinins." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334079.

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Makeham, John M. "Functional neuroanatomy of tachykinins in brainstem autonomic regulation." Connect to full text, 2006. http://hdl.handle.net/2123/1960.

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Thesis (Ph. D.)--University of Sydney, 2007.<br>Title from title screen (viewed 1 November 2007). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Discipline of Physiology, Faculty of Medicine. Degree awarded 2007 ; thesis submitted 2006. Bibliography: leaves 239-284. Also issued in print.
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Patak, Eva Nicole. "Modulation of mammalian uterine contractility by tachykinins." Monash University, Dept. of Pharmacology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9501.

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Reynolds, Paul N. "The role of tachykinins in airway inflammation and bronchial hyper-responsiveness /." Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phr464.pdf.

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Makeham, John Murray. "Functional neuroanatomy of tachykinins in brainstem autonomic regulation." University of Sydney, 1997. http://hdl.handle.net/2123/1960.

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Doctor of Philosophy (PhD)<br>Little is known about the role that tachykinins, such as substance P and its receptor, the neurokinin-1 receptor, play in the generation of sympathetic nerve activity and the integration within the ventrolateral medulla (VLM) of many vital autonomic reflexes such as the baroreflex, chemoreflex, somato-sympathetic reflex, and the regulation of cerebral blood flow. The studies described in this thesis investigate these autonomic functions and the role of tachykinins through physiological (response to hypercapnoea, chapter 3), anatomical (neurokinin-1 receptor immunohistochemistry, chapter 4) and microinjection (neurokinin-1 receptor activation and blockade, chapters 5 and 6) experiments. In the first series of experiments (chapter 3) the effects of chemoreceptor activation with hyperoxic hypercapnoea (5%, 10% or 15% CO2 in O2) on splanchnic sympathetic nerve activity and sympathetic reflexes such as the baroreflex and somato-sympathetic reflex were examined in anaesthetized rats. Hypercapnoea resulted in sympatho-excitation in all groups and a small increase in arterial blood pressure in the 10 % CO2 group. Phrenic nerve amplitude and phrenic frequency were also increased, with the frequency adapting back to baseline during the CO2 exposure. Hypercapnoea selectively attenuated (5% CO2) or abolished (10% and 15% CO2) the somato-sympathetic reflex while leaving the baroreflex unaffected. This selective inhibition of the somato-sympathetic reflex while leaving the baroreflex unaffected was also seen following neurokinin-1 receptor activation in the rostral ventrolateral medulla (RVLM) (see below). Microinjection of substance P analogues into the RVLM results in a pressor response, however the anatomical basis for this response is unknown. In the second series of experiments (chapter 4), the distribution of the neurokinin-1 receptor in the RVLM was investigated in relation to catecholaminergic (putative sympatho-excitatory “C1”) and bulbospinal neurons. The neurokinin-1 receptor was demonstrated on a small percentage (5.3%) of C1 neurons, and a small percentage (4.7%) of RVLM C1 neurons also receive close appositions from neurokinin-1 receptor immunoreactive terminals. This provides a mechanism for the pressor response seen with RVLM microinjection of substance P analogues. Neurokinin-1 receptor immunoreactivity was also seen a region overlapping the preBötzinger complex (the putative respiratory rhythm generation region), however at this level a large percentage of these neurons are bulbospinal, contradicting previous work suggesting that the neurokinin-1 receptor is an exclusive anatomical marker for the propriobulbar rhythm generating neurons of the preBötzinger complex. The third series of experiments (chapter 5) investigated the effects of neurokinin-1 receptor activation and blockade in the RVLM on splanchnic sympathetic nerve activity, arterial blood pressure, and autonomic reflexes such as the baroreflex, somato-sympathetic reflex, and sympathetic chemoreflex. Activation of RVLM neurokinin-1 receptors resulted in sympatho-excitation, a pressor response, and abolition of phrenic nerve activity, all of which were blocked by RVLM pre-treatment with a neurokinin-1 receptor antagonist. As seen with hypercapnoea, RVLM neurokinin-1 receptor activation significantly attenuated the somato-sympathetic reflex but did not affect the sympathetic baroreflex. Further, blockade of RVLM neurokinin-1 receptors significantly attenuated the sympathetic chemoreflex, suggesting a role for RVLM substance P release in this pathway. The fourth series of experiments (chapter 6) investigated the role of neurokinin-1 receptors in the RVLM, caudal ventrolateral medulla (CVLM), and nucleus tractus solitarius (NTS) on regional cerebral blood flow (rCBF) and tail blood flow (TBF). Activation of RVLM neurokinin-1 receptors increased rCBF associated with a decrease in cerebral vascular resistance (CVR). Activation of CVLM neurokinin-1 receptors decreased rCBF, however no change in CVR was seen. In the NTS, activation of neurokinin-1 receptors resulted in a biphasic response in both arterial blood pressure and rCBF, but no significant change in CVR. These findings suggest that in the RVLM substance P and the neurokinin-1 receptor play a role in the regulation of cerebral blood flow, and that changes in rCBF evoked in the CVLM and NTS are most likely secondary to changes in arterial blood pressure. Substance P and neurokinin-1 receptors in the RVLM, CVLM and NTS do not appear to play a role in the brainstem regulation of tail blood flow. In the final chapter (chapter 7), a model is proposed for the role of tachykinins in the brainstem integration of the sympathetic baroreflex, sympathetic chemoreflex, cerebral vascular tone, and the sympatho-excitation seen following hypercapnoea. A further model for the somato-sympathetic reflex is proposed, providing a mechanism for the selective inhibition of this reflex seen with hypercapnoea (chapter 3) and RVLM neurokinin-1 receptor activation (chapter 5). In summary, the ventral medulla is essential for the generation of basal sympathetic tone and the integration of many vital autonomic reflexes such as the baroreflex, chemoreflex, somato-sympathetic reflex, and the regulation of cerebral blood flow. The tachykinin substance P, and its receptor, the neurokinin-1 receptor, have a role to play in many of these vital autonomic functions. This role is predominantly neuromodulatory.
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Kaiser, William Joseph. "Peripheral tachykinins in platelets, plasma & endocrine tissues." Thesis, University of Reading, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542266.

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Jones, Sarah. "Peripheral tachykinins and the NK1 receptor regulate platelet function." Thesis, University of Reading, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493813.

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Tachykinins are a family of neuropeptides characterised by the conserved C-terminal motif FXGLM-NH2, where X represents a hydrophobic amino acid. Substance P (SP) a member of the tachykinin family has recently been shown to stimulate platelet aggregation and a SP-like immunoreactivity has been demonstrated in platelets and shown to be released upon platelet activation, suggesting that SP may act as a secondary platelet agonist. In recent years a gene encoding new members of the tachykinin family has been identified named TTAC4, which unlike the classical tachykinins is predominantly expressed in the periphery, with high expression in the megakaryocytic cell line HEL. The predicted products of the human TAC4 gene, endokinins A and B share high homology with SP and display similar binding characteristics as SP for the neurokinin-1 (NKl) receptor, which is present on the platelet surface. The high sequence homology between endokinins A and B and SP renders them indistinguishable using SP-imunoassays raising the possibility that platelets may be a source of endokinins. The purpose of this study was to assess the roles of peripheral tachykinins in regulating platelet function.
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Landis, Geoffrey Carrothers. "Synthesis and biological activities of tachykinin and opioid-related compounds, synthesis of unusual amino acids, and the investigations into the smooth muscle pharmacology of tachykinins." Diss., The University of Arizona, 1989. http://hdl.handle.net/10150/184656.

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Eight cyclic analogues of Substance P were made in order to investigate the conformation of the C-terminal end of the peptide. These analogues were designed to test three literature models describing the active conformation of substance P. Although the potencies of the analogues were low (in the micromolar range), our results support Cotrait's and Hospital's model (1986). Several substance P antagonists were synthesized. These compounds did not demonstrate agonistic activity nor anatagonistic activity. The tryptophan side chain is contributing to the antagonistic activity of these analogues, and not just the chirality of the α-carbon. Highly potent and selective photoaffinity ligands of H-Tyr-D-Pen-Gly-Phe-D-Pen-OH (DPDPE) and D-Phe-Cys-Tyr-D-Trp-Lys-Thr-Pen-Thr-NH₂ (CTP) were synthesized. These compounds will be useful in the isolation of δ and μ opioid receptors. Several new amino acids designed and synthesized to contain both the natural amino acid side chain and a thiol group which can be used to make disulfide constraints. The racemic amino acids made were as follows: (1) 2-amino-4-methyl-2- [(p-methylbenzyl)thiomethyl] pentanoic acid; (2) 2-amino-2- [(p-methylbenzyl)thiomethyl] -3-phenylpropanoic acid; (3) 2-amino-e- [(p-methylbenzyl)thio] pentanoic acid; and (4) 2-amino-3- [(p-methylbenzyl)-thio] -3-phenyl-pentanoic acid. These amino acids will be useful in the conformational restriction of peptides. To investigate the δ-opioid receptor conformation proposed for DPDPE by Hruby et al. (1988) and the μ-opioid receptor conformation proposed for Tyr-c [Abu₂,Gly,Phe,Leu] by Mierke et al. (1988), constrained phenylalanine amino acids were incorporated into H-Try-D-Pen-Gly-Phe-D-Pen-OH (DPDPE) in the four position. Our results indicate that these models are correct. And in an investigation into the physical-chemical properties of the delta opioid receptor, our results suggest that the δ receptor topochemical site for the Phe⁴ residue contains a partial positive charge on its surface and has specific steric requirements.
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Schamber, Kristopher Cody. "Tachykinin NK3R protein levels in the PVN of rats following an osmotic challenge." Laramie, Wyo. : University of Wyoming, 2007. http://proquest.umi.com/pqdweb?did=1407489691&sid=1&Fmt=2&clientId=18949&RQT=309&VName=PQD.

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Livres sur le sujet "Tachykinins"

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Holzer, Peter, ed. Tachykinins. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18891-6.

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R, Andrews P. L., and Holzer, Peter, Mag. rer. nat. Dr. phil., eds. Tachykinins. Berlin: Springer, 2004.

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institutet, Karolinska, ed. Brain tachykinins and their interaction with dopaminergic transmission. [s.l.]: [s.n.], 1987.

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L, Henry J., International Union of Physiological Sciences. Congress, and IUPS Satellite Symposium "Substance P and Neurokinins - Montreal '86" (1986 : McGill University), eds. Substance P and neurokinins: Proceedings of "substance P and neurokinins--Montreal '86" : a satellite symposium of the XXX International Congress of the International Union of Physiological Sciences. New York: Springer-Verlag, 1987.

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5

Martling, Claes-Roland. Sensory nerves containing tachykinins and CGRP in the lower air ways: Functional implications for bronchoconstriction, vasodilation and protein extravasation. Oxford [Oxfordshire]: Published for the Scandinavian Physiological Society by Blackwell Scientific Publications, 1987.

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Lantz, Ingrid. Angiotensin-converting enzyme and its interaction with various tachykinins and opioid peptides. Uppsala: Univ., 1992.

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Lundquist, C. Tomas. Localization and chemical properties of peptides related to galanin and tachykinins in the blowfly nervous system. Stockholm: Dept. of Zoology, Stockholm University, 1993.

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Buck, Stephen H., ed. The Tachykinin Receptors. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4612-0301-8.

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H, Buck Stephen, ed. The Tachykinin receptors. Totowa, N.J: Humana Press, 1994.

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Rolka, Krzysztof. Chemiczna synteza miniproteinowych inhibitorów enzymów proteolitycznych oraz zmiany strukturalne tachykinin a aktywność biologiczna. Gdańsk: Uniwersytet Gdański, 1991.

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Chapitres de livres sur le sujet "Tachykinins"

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Turiault, Marc, Caroline Cohen, Guy Griebel, David E. Nichols, Britta Hahn, Gary Remington, Ronald F. Mucha, et al. "Tachykinins." In Encyclopedia of Psychopharmacology, 1301–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_210.

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Turiault, Marc, Caroline Cohen, and Guy Griebel. "Tachykinins." In Encyclopedia of Psychopharmacology, 1695–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_210.

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Tuluc, Florin. "Tachykinins." In Encyclopedia of Cancer, 1–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7200-3.

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Holzer, Peter. "Tachykinins." In Drug Development, 113–46. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-202-9_5.

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Tuluc, Florin. "Tachykinins." In Encyclopedia of Cancer, 4437–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_7200.

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Turiault, Marc, Caroline Cohen, and Guy Griebel. "Tachykinins." In Encyclopedia of Psychopharmacology, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27772-6_210-2.

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Conlon, J. M., C. F. Deacon, M. Thorndyke, L. Thim, and S. Falkmer. "Phylogeny of the Tachykinins." In Substance P and Neurokinins, 15–17. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4612-4672-5_6.

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Manzini, Stefano, Cristina Goso, and Arpad Szallasi. "Sensory Nerves and Tachykinins." In Neuropeptides in Respiratory Medicine, 173–96. Taylor & Francis Group, 6000 Broken Sound Parkway NW, Suite 300, Boca Raton, FL 33487-2742: CRC Press, 2017. http://dx.doi.org/10.4324/9780203745915-9.

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Conlon, J. M. "The Tachykinin Peptide Family, with Particular Emphasis on Mammalian Tachykinins and Tachykinin Receptor Agonists." In Handbook of Experimental Pharmacology, 25–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18891-6_2.

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Helke, Cinda J., and Hiroyuki Ichikawa. "Tachykinins, Tachykinin Receptors, and the Central Control of the Cardiovascular System." In Central Neural Mechanisms in Cardiovascular Regulation, 248–65. Boston, MA: Birkhäuser Boston, 1992. http://dx.doi.org/10.1007/978-1-4684-9184-5_9.

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Actes de conférences sur le sujet "Tachykinins"

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Zaidi, Sarah, George Gallos, and Charles Emala. "Tachykinin Receptors Modulate Human Airway Smooth Muscle Proliferation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2146.

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Agaeva, G. A. "Computational study of the conformational flexibility of the amphibian tachykinin neuropeptides." In 2012 6th International Conference on Application of Information and Communication Technologies (AICT). IEEE, 2012. http://dx.doi.org/10.1109/icaict.2012.6398530.

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Misu, Ryosuke, Taro Noguchi, Hiroaki Ohno, Shinya Oishi, and Nobutaka Fujii. "Structure-Activity Relationship Study of Tachykinin Peptides for the Development of Novel NK3 Receptor Agonists." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.060.

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Mohbeddin, Abeer, Nawar Haj Ahmed, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Innate Immunity on Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0224.

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Apart from its traditional role in disease control, recent body of evidence has implicated a role of the immune system in regulating metabolic homeostasis. Owing to the importance of this “immune-metabolic alignment” in dictating a state of health or disease, a proper mechanistic understanding of this alignment is crucial in opening up for promising therapeutic approaches against a broad range of chronic, metabolic, and inflammatory disorders like obesity, diabetes, and inflammatory bowel syndrome. In this project, we addressed the role of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) innate immune pathway in regulating different metabolic parameters using the Drosophila melanogaster (DM) fruit fly model organism. Mutant JAK/STAT pathway flies with a systemic knockdown of either Domeless (Dome) [domeG0282], the receptor that activates JAK/STAT signaling, or the signal-transducer and activator of transcription protein at 92E (Stat92E) [stat92EEY10528], were used. The results of the study revealed that blocking JAK/STAT signaling alters the metabolic profile of mutant flies. Both domeG0282 and stat92EEY10528 mutants had an increase in body weight, lipid deprivation from their fat body (lipid storage organ in flies), irregular accumulation of lipid droplets in the gut, systemic elevation of glucose and triglyceride levels, and differential down-regulation in the relative gene expression of different peptide hormones (Tachykinin, Allatostatin C, and Diuretic hormone 31) known to regulate metabolic homeostasis in flies. Because the JAK/STAT pathway is evolutionary conserved between invertebrates and vertebrates, our potential findings in the fruit fly serves as a platform for further immune-metabolic translational studies in more complex mammalian systems including humans.
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Al-Asmar, Jawaher, Sara Rashwan, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Bacterial Infection on Host Survival and Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0186.

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Enterobacteriaceae, a large family of facultative anaerobic bacteria, encloses a broad spectrum of bacterial species including Escherichia coli, Salmonella enterica, and Shigella sonnei, that produce enterotoxins and cause gastrointestinal tract diseases. While much is known about the regulation and function of enterotoxins within the intestine of the host; the lack of cheap, practical, and genetically tractable model organisms has restricted the investigation of others facets of this host-pathogen interaction. Our group, among others, has employed Drosophila melanogaster, as a model organism to shed more light on some aspects of host-pathogen interplays. In this project, we addressed the effect of Escherichia coli, Salmonella enterica, and Shigella sonnei infection on altering the metabolic homeostasis of the host. Drosophila melanogaster flies were orally infected with Escherichia coli, Salmonella enterica, or Shigella sonnei, a method that mimics the natural route used by enteric pathogens to gain access to the gastrointestinal tract in humans. The results of our study revealed that both Escherichia coli and Shigella sonnei pathogens were capable of colonizing the host gut, resulting in a reduction in the life span of the infected host. Escherichia coli and Shigella sonnei infected flies also exhibited altered metabolic profiles including lipid droplets deprivation from their fat body (normal lipid storage organ in flies), irregular accumulation of lipid droplets in their gut, and significant elevation of systemic glucose and triglyceride levels. These metabolic alterations could be mechanistically attributed to the differential down-regulation in the expression of metabolic peptide hormones (Allatostatin A, Diuretic hormone 31, and Tachykinin) detected in the gut of Escherichia coli and Shigella sonnei infected flies. Salmonella enterica; however, was unable to colonize the gut of the host; and therefore, Salmonella enterica infected flies exhibited a relatively normal metabolic status as that of non infected flies. Gaining a proper mechanistic understanding of infection-induced metabolic alterations helps in modulating the pathogenesis of gastrointestinal tract diseases in a host and opens up for promising therapeutic approaches for infection induced metabolic disorders
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