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Published: 4 June 2021
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1

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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2

EL-AGNAF, Omar M. A., G. Brent IRVINE, Geraldine FITZPATRICK, W. Kenneth GLASS, and David J. S. GUTHRIE. "Comparative studies on peptides representing the so-called tachykinin-like region of the Alzheimer Aβ peptide [Aβ(25–35)]." Biochemical Journal 336, no. 2 (December 1, 1998): 419–27. http://dx.doi.org/10.1042/bj3360419.

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In an attempt to answer the question of whether or not the so-called tachykinin-like region of the Alzheimer β-amyloid protein [Aβ(25–35)] can act as a tachykinin, the sequences Aβ(25–35), Aβ(25–35)amide and their norleucine-35 and phenylalanine-31 analogues were synthesized. These peptides were examined with ligand binding studies, electron microscopy, CD and NMR. In all cases some differences were found between the Aβ(25–35) analogue and the corresponding Phe31 peptide. In addition, in ligand displacement studies on tachykinin NK1 receptors, only the Phe31 analogue showed activity comparable to that of genuine tachykinins. We conclude that peptides based on Aβ(25–35) but with a Phe residue at position 31 do display properties typical of a tachykinin, but that peptides with Ile at this position do not.
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3

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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4

Maggi, C. A. "Tachykinins, tachykinin receptors and airways pathophysiology." Pharmacological Research 26 (September 1992): 7. http://dx.doi.org/10.1016/1043-6618(92)90726-r.

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5

Goto, Tetsuya, and Teruo Tanaka. "Tachykinins and tachykinin receptors in bone." Microscopy Research and Technique 58, no. 2 (July 15, 2002): 91–97. http://dx.doi.org/10.1002/jemt.10123.

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6

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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7

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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8

Pérez, Carolina Thörn, Russell H. Hill, and Sten Grillner. "Endogenous Tachykinin Release Contributes to the Locomotor Activity in Lamprey." Journal of Neurophysiology 97, no. 5 (May 2007): 3331–39. http://dx.doi.org/10.1152/jn.01302.2006.

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Tachykinins are present in lamprey spinal cord. The goal of this study was to investigate whether an endogenous release of tachykinins contributes to the activity of the spinal network generating locomotor activity. The locomotor network of the isolated lamprey spinal cord was activated by bath-applied N-methyl-d-aspartate (NMDA) and the efferent activity recorded from the ventral roots. When spantide II, a tachykinin receptor antagonist, was bath-applied after reaching a steady-state burst frequency (>2 h), it significantly lowered the burst rate compared with control pieces from the same animal. In addition, the time to reach the steady-state burst frequency (>2 h) was lengthened in spantide II. These data indicate that an endogenous tachykinin release contributes to the ongoing activity of the locomotor network by modulating the glutamate–glycine neuronal network responsible for the locomotor pattern. We also explored the effects of a 10-min exogenous application of substance P (1 μM), a tachykinin, and showed that its effect on the burst rate depended on the initial NMDA induced burst frequency. At low initial burst rates (∼0.5 Hz), tachykinins caused a marked further slowing to 0.1 Hz, whereas at higher initial burst rates, it instead caused an enhanced burst rate as previously reported, and in addition, a slower modulation (0.1 Hz) of the amplitude of the motor activity. These effects occurred during an initial period of ∼1 h, whereas a modest long-lasting increase of the burst rate remained after >2 h.
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9

Williams, Ronald, Xiaoyan Zou, and 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, no. 2 (February 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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10

Takano, Yukio, Ryo Saito, Akira Nagashima, Shigeyuki Nonaka, and Hiro-o. Kamiya. "TACHYKININ RECEPTOR SUBTYPE: CARDIOVASCULAR ROLES OF TACHYKININS." Japanese Journal of Pharmacology 52 (1990): 38. http://dx.doi.org/10.1016/s0021-5198(19)54985-x.

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11

Pennefather, Jocelyn N., Alessandro Lecci, M. Luz Candenas, Eva Patak, Francisco M. Pinto, and Carlo Alberto Maggi. "Tachykinins and tachykinin receptors: a growing family." Life Sciences 74, no. 12 (February 2004): 1445–63. http://dx.doi.org/10.1016/j.lfs.2003.09.039.

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12

Patak, Eva, M. Luz Candenas, Jocelyn N. Pennefather, Sebastian Ziccone, Alison Lilley, Julio D. Martín, Carlos Flores, Antonio G. Mantecón, Margot E. Story, and Francisco M. Pinto. "Tachykinins and tachykinin receptors in human uterus." British Journal of Pharmacology 139, no. 3 (June 2003): 523–32. http://dx.doi.org/10.1038/sj.bjp.0705279.

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13

Hamel, R., A. W. Ford-Hutchinson, C. Blazejczak, and A. Van Den Brekel. "Tachykinin involvement in cutaneous anaphylaxis in the guinea pig." Canadian Journal of Physiology and Pharmacology 66, no. 11 (November 1, 1988): 1361–67. http://dx.doi.org/10.1139/y88-223.

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Permeability changes in the guinea-pig skin following intradermal (i.d.) injection of tachykinin agonists or antigen were monitored through the extravasation of 99mTc-labelled human serum albumin and blood flow changes through the accumulation of 51Cr-labelled microspheres. A variety of synthetic and natural tachykinins, including substance P and neurokinins A and B, were shown to be potent inducers of permeability changes. Neurokinins A and B, but not substance P, were also shown to be apparent vasoconstrictor agents. Permeability responses in sensitized guinea pigs to i.d. injection of antigen and substance P, but not histamine, were abolished by pretreatment with the tachykinin antagonists [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-substance P and [D-Pro2, D-Trp7,9]-substance P. Interpretation of such results was complicated by the fact that such antagonists may in themselves induce mast cell activation. Depletion of substance P containing neurons by pretreatment of guinea pigs with capsaicin also produced significant inhibition of antigen-induced permeability changes. These results indicate a possible role for tachykinins, such as substance P, in cutaneous anaphylaxis in the guinea pig.
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14

Parker, D., and S. Grillner. "Tachykinin-mediated modulation of sensory neurons, interneurons, and synaptic transmission in the lamprey spinal cord." Journal of Neurophysiology 76, no. 6 (December 1, 1996): 4031–39. http://dx.doi.org/10.1152/jn.1996.76.6.4031.

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1. Tachykinin-like immunoreactivity is found in the dorsal roots, dorsal horn, and dorsal column of the lamprey. The effect of tachykinins on sensory processing was examined by recording intracellularly from primary sensory dorsal cells and second-order spinobulbar giant interneurons. Modulation of synaptic transmission was examined by making paired recordings from dorsal cells and giant interneurons, or by eliciting compound depolarizations in the giant interneurons by stimulating the dorsal root or dorsal column. 2. Bath application of tachykinins depolarized the dorsal cells. This effect was mimicked by stimulation of the dorsal root, suggesting that dorsal root afferents may be a source of endogenous tachykinin input to the spinal cord. The depolarization was reduced by removal of sodium or calcium from the Ringer, or when potassium conductances were blocked, and was not associated with a measurable change in input resistance. Dorsal root stimulation also caused a depolarization in the dorsal cells, and this effect and that of bath-applied substance P, was blocked by the tachykinin antagonist spantide. 3. The tachykinin substance P could reduce inward and outward rectification in the dorsal cells, the effect on outward rectification only being seen when potassium conductances were blocked by tetraethylammonium (TEA). 4. Substance P increased the excitability of the dorsal cells and giant interneurons, shown by the increased spiking in response to depolarizing current pulses. The increased excitability was blocked by the tachykinin antagonist spantide. 5. Substance P modulated the dorsal cell action potential, by increasing the spike duration and reducing the amplitude of the afterhyperpolarization. The spike amplitude was not consistently affected. 6. Stimulation of the dorsal column resulted in either depolarizing or hyperpolarizing potentials in the giant interneurons. The amplitude of the depolarization was increased by substance P, whereas the amplitude of the hyperpolarization was reduced. These effects occurred independently of a measurable change in postsynaptic input resistance, suggesting that the modulation occurred presynaptically. Paired recordings from dorsal cells and giant interneurons failed to reveal an effect of substance P on dorsal cell-evoked excitatory postsynaptic potentials (EPSPs), suggesting that the potentiation of the dorsal column-evoked depolarization was due to an effect on other axons in the dorsal column. Dorsal root-evoked potentials could also be increased in the presence of substance P, although this effect was less consistent than the effect on dorsal column stimulation. 7. These results suggest that tachykinins modulate sensory input to the lamprey spinal cord by increasing the excitability of primary afferents and second-order giant interneurons, and also by modulating synaptic transmission. Tachykinins may result in potentiation of local spinal reflexes and also modulation of descending reticulospinal inputs to the spinal locomotor network as a result of potentiation of spinobulbar inputs.
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15

Souquet, J. C., J. R. Grider, K. N. Bitar, and G. M. Makhlouf. "Receptors for mammalian tachykinins on isolated intestinal smooth muscle cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 249, no. 4 (October 1, 1985): G533—G538. http://dx.doi.org/10.1152/ajpgi.1985.249.4.g533.

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The existence of receptors for three mammalian tachykinins, substance P (SP), substance K (SK), and neuromedin K (NK), was examined in smooth muscle cells, isolated separately from the longitudinal and circular muscle layers of guinea pig ileum. Tachykinin receptors capable of mediating contraction were present in muscle cells from both layers. The receptors were selectively blocked by the tachykinin antagonist [D-Pro2, D-Trp7,9]substance P but not by muscarinic, gastrin/cholecystokinin, or opiate antagonists (0.3 nM atropine, 1 mM proglumide, and 0.3 nM naloxone, respectively). The rank order of potency of tachykinins in causing contraction, NK greater than SP greater than SK, was similar in both muscle cell types. The results obtained in isolated muscle cells were closely paralleled by results obtained in intact muscle strips; the main difference was the greater sensitivity of isolated cells to tachykinin agonists (250-fold) and antagonist (210-fold). The inhibitory dissociation constant (Ki) of [D-Pro2, D-Trp7,9]substance P estimated from the displacement of dose-response curves (muscle cells) or from Schild plots (muscle strips) differed minimally or not at all, when either SP or SK was used as agonist, consistent with interaction of the two peptides with the same receptor subtype. The notion of a single receptor subtype in ileal muscle cells of the guinea pig was further supported by the occurrence of complete cross-desensitization between SP and SK in muscle strips.
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16

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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17

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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18

Almeida, T. A., J. Rojo, P. M. Nieto, F. M. Pinto, M. Hernandez, J. D. Martín, and M. L. Candenas. "Tachykinins and Tachykinin Receptors: Structure and Activity Relationships." Current Medicinal Chemistry 11, no. 15 (August 1, 2004): 2045–81. http://dx.doi.org/10.2174/0929867043364748.

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19

Rogers, Duncan F. "Neurokinin receptors subserving airways secretion." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 932–39. http://dx.doi.org/10.1139/y95-129.

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Mucus secretion can be induced in the airways by activation of nerves. The principal mechanism mediating neurogenic mucus secretion is cholinergic. However, a small but significant secretory response remains after adrenoceptor and cholinoceptor blockade. The identity of this nonadrenergic, noncholinergic (NANC) neural mechanism is unclear but includes an orthodromic pathway and a capsaicin-sensitive "sensory-efferent" (or "local effector") pathway. The orthodromic pathway comprises cholinergic nerves (and to a much lesser extent adrenergic nerves) in which neuropeptides, including vasoactive intestinal peptide (VIP) and neuropeptide tyrosine (NPY), are colocalised and coreleased with the classical neurotransmitter. Investigation of the contribution of the orthodromic neural pathway to neurogenic secretion awaits development of selective receptor antagonists for VIP and NPY. The neurotransmitters of the sensory-efferent neural pathway include calcitonin gene related peptide and the tachykinins substance P and neurokinin A. The order of potency of the natural tachykinins and synthetic selective tachykinin receptor agonists indicates that the tachykinin NK1 receptor is ubiquitous for airway secretory processes, including mucus secretion and ion transport. Antagonist studies show that the great proportion of the NANC neural mucus secretory response is mediated via NK1 receptors, with little or no contribution from NK2 receptors. The relevance of the sensory-efferent neural pathway in health is equivocal, but it may have increasing importance in chronic inflammatory bronchial diseases associated with mucus hypersecretion, for example, asthma and chronic bronchitis, in which there is some evidence for the potential for increased sensory-efferent neural activity.Key words: tachykinin, sensory nerves, mucus, mucus secretion, asthma.
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20

Ribeiro, J. M. "Characterization of a vasodilator from the salivary glands of the yellow fever mosquito Aedes aegypti." Journal of Experimental Biology 165, no. 1 (April 1, 1992): 61–71. http://dx.doi.org/10.1242/jeb.165.1.61.

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Salivary gland homogenates and oil-induced saliva of the mosquito Aedes aegypti dilate the rabbit aortic ring and contract the guinea pig ileum. The vasodilatory activity is endothelium-dependent, heat-stable, sensitive to both trypsin and chymotrypsin treatments, and both smooth muscle activities cross-desensitize to the tachykinin peptide substance P. Both bioactivities co-elute when salivary gland homogenates are fractionated by reversed-phase HPLC. Molecular sieving chromatography indicates a relative molecular mass of 1400. A monoclonal antibody specific to the carboxy terminal region of tachykinins reacts with material in the posterior part of the central lobe of paraformaldehyde-fixed salivary glands. The presence of a vasodilatory peptide of the tachykinin family in the salivary glands of A. aegypti is proposed and its role in blood feeding is discussed.
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21

Tepper, J. S., D. L. Costa, S. Fitzgerald, D. L. Doerfler, and P. A. Bromberg. "Role of tachykinins in ozone-induced acute lung injury in guinea pigs." Journal of Applied Physiology 75, no. 3 (September 1, 1993): 1404–11. http://dx.doi.org/10.1152/jappl.1993.75.3.1404.

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To examine the hypothesis that the acute reversible changes caused by ozone (O3) exposure are mediated by tachykinin release, guinea pigs were depleted of tachykinins by use of repeated capsaicin (CAP) injections before O3 exposure in an attempt to prevent O3-induced functional changes. Unexpectedly, CAP pretreatment caused divergent results in the functional responses to O3. Ventilatory measurements obtained from CAP-pretreated O3-exposed (CAP-O3) animals were exacerbated rather than diminished compared with the effects of O3 alone. Similarly, lavage fluid protein accumulation was enhanced in the CAP-O3 group compared with the O3-exposed group. In better agreement with our initial hypothesis, the CAP-O3 group was less responsive than the O3-exposed animals to histamine aerosol challenge. Additionally, Evans blue dye accumulation, a hallmark of tachykinin release, was increased in O3-exposed animals and was partially blocked in the CAP-O3 group. These data suggest that tachykinin-containing sensory fibers are unlikely to mediate the acute effects of O3 exposure on tidal breathing and lavage fluid protein accumulation but may play a role in causing post-O3 airway hyperreactivity and protein extravasation into the trachea.
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22

MacNaughton, W., B. Moore, and S. Vanner. "Cellular pathways mediating tachykinin-evoked secretomotor responses in guinea pig ileum." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 5 (November 1, 1997): G1127—G1134. http://dx.doi.org/10.1152/ajpgi.1997.273.5.g1127.

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This study characterized tachykinin-evoked secretomotor responses in in vitro submucosal and mucosal-submucosal preparations of the guinea pig ileum using combined intracellular and Ussing chamber recording techniques. Superfusion of endogenous tachykinins substance P (SP), neurokinin A (NKA), and neurokinin B depolarized single submucosal neurons and evoked increased short-circuit current ( I sc) responses in Ussing chamber preparations. The NK1-receptor agonist [Sar9,Met(O2)11]SP [50% effective concentration (EC50) = 2 nM] depolarized all submucosal neurons examined. The NK3-receptor agonist senktide (EC50 = 20 nM) depolarized ∼50% of neurons examined, whereas the NK2-receptor agonist [Ala5,β-Ala8]NKA-(4—10) had no effect on membrane potential. [Sar9,Met(O2)11]SP and senktide evoked similar increases in I sc that were tetrodotoxin sensitive (91 and 100%, respectively) and were selectively blocked by the NK1antagonist CP-99,994 and the NK3antagonist SR-142801, respectively. Capsaicin-evoked increases in I sc were significantly inhibited (54%, P < 0.05) by CP-99,994 but not by SR-142801. Neither antagonist inhibited slow excitatory postsynaptic potentials. These findings suggest that tachykinin-evoked secretion in guinea pig ileum is mediated by NK1 and NK3 receptors on submucosal secretomotor neurons and that capsaicin-sensitive nerves release tachykinin(s) that activate the NK1 receptors.
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23

Moore, Kimberly A., Eun Joo Oh, and Daniel Weinreich. "5-HT3 receptors mediate inflammation-induced unmasking of functional tachykinin responses in vitro." Journal of Applied Physiology 92, no. 6 (June 1, 2002): 2529–34. http://dx.doi.org/10.1152/japplphysiol.00974.2001.

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Exogenously applied tachykinins produce no measurable electrophysiological responses in the somata of vagal afferent neurons [nodose ganglion neurons (NGNs)] isolated from naive guinea pigs. By contrast, after in vitro antigen challenge of nodose ganglia from guinea pigs immunized with chick ovalbumin, ∼60% (53 of 89) of NGNs were depolarized an average of 13 ± 1.2 mV by substance P (SP; 100 nM; n = 53). Receptor antagonists and enzyme inhibitors were utilized to screen a number of mast cell-derived mediators for their role in the uncovering or “unmasking” of functional tachykinin receptors after antigen challenge. Two chemically distinct 5-hydroxytryptamine-3-receptor antagonists significantly reduced the percentage of NGNs displaying depolarizing SP responses. Treatment with Y-25130 (1 or 10 μM) or tropisetron (1 μM) 15 min before and during antigen challenge reduced the percentage of SP-responsive neurons to ∼20 and ∼15%, respectively. These results suggest that activation of 5-hydroxytryptamine-3 receptors plays an integral role in the unmasking of functional tachykinin receptors after specific antigen challenge of nodose ganglia. The mediator(s) underlying tachykinin-receptor unmasking in the remainder of the NGNs has yet to be characterized. However, it does not appear to be histamine, prostanoids, or peptidoleukotrienes.
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24

Barber, W. D., G. D. Stevenson, and T. F. Burks. "Tachykinins: local gastric effects and brain stem responses." American Journal of Physiology-Gastrointestinal and Liver Physiology 252, no. 3 (March 1, 1987): G365—G373. http://dx.doi.org/10.1152/ajpgi.1987.252.3.g365.

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The gastric motor or mechanical effects of a group of peptides, the tachykinins, were evaluated in anesthetized cats to determine the relationship between local motor events and brain stem neurons that regulate gastric activity. The peptides evaluated were substance P, physalaemin, and eledoisin. The tachykinin-induced gastric changes were dose related and were characterized by initial distention-sustained contraction-late distention phases. At lower doses distention was the dominant effect with a sustained contraction-late distention response appearing as the dose increased. The sustained contraction-late distention phases were frequently accompanied by phasic contractions with a frequency of 2-4/min. Atropine had a significant effect on the sustained contraction phase but no effect on the phasic contractions or distention phases. Bilateral cervical vagotomy had a significant effect on the early distention phase, suggesting a link with brain stem mechanisms. The activity of brain stem units that responded to phasic distention of the stomach reflected the tachykinin-induced changes in gastric distention. Although the gastric effects of these tachykinins shared distinct similarities, certain differences in the time sequence of the distention-contraction interactions suggests the possibility that dissimilar receptor types may be involved in the mechanisms of action. Their mechanisms of action may also involve a direct effect on the effector organ.
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25

Geppetti, Pierangelo, Claude Bertrand, Fabio M. L. Ricciardolo, and Jay A. Nadei. "New aspects on the role of kinins in neurogenic inflammation." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 843–47. http://dx.doi.org/10.1139/y95-115.

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The inflammatory response to injury consists of the activation of several protective mechanisms involving different cellular systems. Among the mechanisms and systems that exert their effects rapidly, peptide transmitters released from peripheral endings of primary sensory neurons (evoking neurogenic inflammation) play a major role in the response to tissue injury. Noxious stimuli may directly activate sensory nerves to release proinflammatory neuropeptides. More recently, evidence has accumulated suggesting that indirect mechanisms leading to sensory neuropeptide release are also activated in relevant models of pathophysiological conditions. Tachykinin NK1 and NK2 receptor antagonists reduced the plasma extravasation in the trachea and nasal mucosa and the bronchoconstriction caused by antigen challenge in sensitized guinea-pigs. Blockade of kinin B2 receptors with the selective antagonist HOE-140 had a similar inhibitory effect. The magnitude of the inhibition observed with the kinin receptor antagonist alone was similar to that caused by a combination a tachykinin and kinin receptor antagonists. This suggests activation of a common final pathway by these two groups of mediators. Pharmacological and biochemical evidence suggests that in the airways of sensitized guinea-pigs, kinins released by the anaphylactic reaction stimulate the release of tachykinins from sensory nerves, thus contributing to their proinflammatory action.Key words: kinins, tachykinins, neurogenic inflammation, antigen challenge, airways, nitric oxide.
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26

Candenas, Luz, Alessandro Lecci, Francisco M. Pinto, Eva Patak, Carlo Alberto Maggi, and Jocelyn N. Pennefather. "Tachykinins and tachykinin receptors: effects in the genitourinary tract." Life Sciences 76, no. 8 (January 2005): 835–62. http://dx.doi.org/10.1016/j.lfs.2004.10.004.

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27

Mukda, S., B. Chetsawang, P. Govitrapong, P. T. Schmidt, A. Hay-Schmidt, and M. Møller. "Tachykinins and tachykinin-receptors in the rat pineal gland." European Journal of Neuroscience 21, no. 10 (May 2005): 2743–51. http://dx.doi.org/10.1111/j.1460-9568.2005.04088.x.

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28

Maggi, Carlo Alberto, Riccardo Patacchini, Paolo Rovero, and Antonio Giachetti. "Tachykinin receptors and tachykinin receptor antagonists." Journal of Autonomic Pharmacology 13, no. 1 (February 1993): 23–93. http://dx.doi.org/10.1111/j.1474-8673.1993.tb00396.x.

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29

Noveral, J. P., and M. M. Grunstein. "Tachykinin regulation of airway smooth muscle cell proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 3 (September 1, 1995): L339—L343. http://dx.doi.org/10.1152/ajplung.1995.269.3.l339.

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The tachykinins, substance P (SP) and neurokinins A (NKA) and B (NKB), have been identified in the respiratory tract and implicated in mediating neurogenic inflammation of the airways. To the extent that these neuropeptides may be involved in the pathogenesis of asthma, a condition associated with hyperplasia of airway smooth muscle (ASM), we examined the mitogenic effects and mechanisms of action of tachykinins in cultured rabbit ASM cells. SP was found to elicit dose-dependent (10(-14) to 10(-4) M) stimulation of ASM cell proliferation, with a mean (+/- SE) maximal increase in cell number of 169 +/- 6.1% of control. In contrast, NKA and NKB had little and no effect on ASM cell growth, respectively. Because SP is nonselective in its binding to the tachykinin receptors, to identify the specific NK receptor subtype(s) mediating the promitogenic action of SP, in separate studies we found that 1) the NK1-receptor-specific agonist, [beta-Ala4, Sar9, Met(O2)11]SP-(4-11) induced stimulation of ASM cell growth similar in magnitude to that elicited by SP; 2) in contrast, neither the NK1- nor NK2-receptor-specific agonists, [beta-Ala8]NKA-(4-10) and [MePhe7]NKB, respectively, had any effect on ASM cell growth; and 3) the promitogenic action of SP was inhibited by the NK1-receptor antagonist, GR-82,334. Moreover, in extended experiments, we found that the phospholipase C and phospholipase A2 inhibitors, neomycin and quinacrine, respectively, each inhibited SP-induced ASM cell proliferation by approximately 45%. Collectively, these observations provide new evidence that the tachykinin SP induces ASM cell proliferation, and that this action is mediated by transmembrane signaling coupled to selective activation of the NK1 receptor.
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30

Wang, Y., T. Badgery-Parker, S. Lovas, N. Chartrel, H. Vaudry, E. Burcher, and J. M. Conlon. "Primary structure and receptor-binding properties of a neurokinin A-related peptide from frog gut." Biochemical Journal 287, no. 3 (November 1, 1992): 827–32. http://dx.doi.org/10.1042/bj2870827.

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A tachykinin peptide was isolated from an extract of the intestine of the European green frog, Rana ridibunda, and its primary structure was established as: His-Lys-Leu-Asp-Ser-Phe-Ile-Gly-Leu-Met.CONH2. This sequence was confirmed by chemical synthesis and shows two amino acid substitutions (leucine for threonine at position 3 and isoleucine for valine at position 7) compared with neurokinin A. Binding parameters for synthetic [Leu3, Ile7]neurokinin A and mammalian tachykinins were compared using receptor-selective radioligands and crude membranes from tissues enriched in the NK1, NK2 and NK3 receptors. [Leu3, Ile7]Neurokinin A was approx. 3-fold less potent than substance P in inhibiting the binding of 125I-labelled [Sar9, Met(O2)11]substance P (labelled with Bolton-Hunter reagent) to rat submandibular gland (NK1 receptor), 8-fold less potent than neurokinin A in inhibiting the binding of [2-[125I]iodohistidine1]neurokinin A to rat stomach fundus (NK2 receptor) and 6-fold less potent than neurokinin B in inhibiting the binding of 125I-Bolton-Hunter-labelled scyliorhinin II to rat brain (NK3 receptor). Thus the frog neurokinin A-related peptide shows moderate affinity but lack of selectivity for all three tachykinin-binding sites in rat tissues. This non-selectivity is similar to that displayed by the molluscan tachykinin, eledoisin, which also contains an isoleucine residue in the corresponding position in the molecule.
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31

Lee, H. K., C. W. Shuttleworth, and K. M. Sanders. "Tachykinins activate nonselective cation currents in canine colonic myocytes." American Journal of Physiology-Cell Physiology 269, no. 6 (December 1, 1995): C1394—C1401. http://dx.doi.org/10.1152/ajpcell.1995.269.6.c1394.

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The mechanism of tachykinin-induced excitation was studied in isolated colonic muscle cells and intact muscle strips. In whole cell voltage-clamp studies performed at 33 degrees C, neurokinin A (NKA) and substance P (SP) reduced L-type Ca2+ current. NKA and SP activated a cationic current that reversed near 0 mV. This current (INKA or ISP, respectively) had properties similar to the acetylcholine (ACh)-activated nonselective cation conductance (IACh), activated by muscarinic stimulation in other gastrointestinal smooth muscle cells. INKA and ISP were decreased when external Na+ was reduced. In contrast to IACh, INKA and ISP were not facilitated by increases in internal Ca2+, but little or no current was activated by these peptides when extracellular Ca2+ was low. INKA (10(-7) M) and ISP (10(-5) M) were blocked by Cd2+ (5 x 10(-4) M), quinine (10(-3) M), and the tachykinin-receptor antagonist [D-Pro2,D-Trp7,9]SP (10(-5) M). Current clamp recordings and intracellular recordings of intact tissues showed that NKA and SP depolarized the cell membrane, which is consistent with the activation of a nonselective cation conductance. These data suggest that a primary mechanism of the tachykinins is to activate a nonselective cation conductance that leads to depolarization. The increase in Ca2+ entry due to tachykinin stimulation appears to be secondary to the activation of the nonselective cation conductance.
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32

Thörn Pérez, Carolina, Russell H. Hill, Abdeljabbar El Manira, and Sten Grillner. "Endocannabinoids Mediate Tachykinin-Induced Effects in the Lamprey Locomotor Network." Journal of Neurophysiology 102, no. 3 (September 2009): 1358–65. http://dx.doi.org/10.1152/jn.00294.2009.

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The spinal network underlying locomotion in lamprey is composed of excitatory and inhibitory interneurons mediating fast ionotropic action. In addition, several modulator systems are activated as locomotion is initiated, including the tachykinin system and the metabotropic glutamate receptor 1 (mGluR1), the latter operating partially via the endocannabinoid system. The effects of mGluR1 agonists and tachykinins resemble each other. Like mGluR1 agonists, the tachykinin substance P accelerates the burst rate and reduces the crossed inhibition in an activity-dependent fashion. The present study therefore explores whether tachykinins also use the endocannabinoid system to modulate the locomotor frequency. By monitoring fictive locomotion, we were able to compare the facilitatory effects exerted by applying substance P (1 μM, 20 min), on the burst frequency before and during application of the endocannabinoid CB1 receptor antagonist AM251 (2–5 μM). By using two different lamprey species, we showed that the response to substance P on the burst frequency is significantly reduced during the application of AM251. To examine whether endocannabinoids are involved in the substance P–mediated modulation of reciprocal inhibition, the commissural axons were stimulated, while recording intracellularly from motoneurons. We compare the effect of substance P on the amplitude of the contralateral compound glycinergic inhibitory postsynaptic potential (IPSP) in control and in the presence of AM251. The blockade of CB1 receptors reduced the substance P–mediated decrease in the amplitude by 29%. The present findings suggest that the effects of substance P on the increase in the locomotor burst frequency and depression of IPSPs are mediated partially via release of endocannabinoids acting through CB1 receptors.
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33

Merighi, A., J. M. Polak, G. Fumagalli, and D. T. Theodosis. "Ultrastructural localization of neuropeptides and GABA in rat dorsal horn: a comparison of different immunogold labeling techniques." Journal of Histochemistry & Cytochemistry 37, no. 4 (April 1989): 529–40. http://dx.doi.org/10.1177/37.4.2564404.

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Several immunogold techniques were used to determine the ultrastructural localization of calcitonin gene-related peptide (CGRP), tachykinin, somatostatin, and gamma-amino-butyric acid (GABA) immunoreactivity in the dorsal horn of rat spinal cord. The immunocytochemical reactions were carried out directly on ultrathin sections from non-osmicated frozen tissue, non-osmicated low temperature-embedded (Lowicryl K4M) tissue, and osmicated epoxy-embedded material. Preservation of ultrastructural morphology and immuno-labeling efficiency were compared. Morphology of subcellular organelles was relatively good in ultra-thin frozen sections, which showed the highest immunoreactivity. However, only very small samples of tissue could be examined. Although there was relatively good immunolabeling in the Lowicryl K4M-embedded tissue, the ultrastructure of the neuropil, and particularly that of synapses, was poorly maintained. In contrast, the osmicated epoxy-embedded material offered optimal morphological preservation together with accurate subcellular localization of all antigens under study. The latter approach thus enabled clear visualization of CGRP, tachykinin, and somatostatin immunoreactivity restricted to large dense-cored vesicles (90-150 nm diameter) in many axonal and synaptic profiles in the superficial layers of the dorsal horn. CGRP- and tachykinin-positive profiles were also present in the tract of Lissauer. GABA immunoreactivity was present mainly in axons and terminals, and less frequently in somatic and dendritic profiles. In terminals, which often formed symmetrical synapses on immunonegative dendritic profiles, it was associated with small (30-60 nm diameter) clear vesicles and mitochondria. Double immunolabeling was possible on all preparations, but the osmicated, epoxy-embedded material clearly showed co-localization of peptides, especially of CGRP and tachykinins, within the same dense-cored vesicles in axonal fibers and/or terminals. On the other hand, peptide and GABA immunoreactivity were consistently seen in different nerve profiles. In a few cases, GABAnergic terminals were seen to synapse on tachykinin-positive fibers.
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34

Couture, Réjean, Pierre Picard, Philippe Poulat, and Alexandre Prat. "Characterization of the tachykinin receptors involved in spinal and supraspinal cardiovascular regulation." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 892–902. http://dx.doi.org/10.1139/y95-123.

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The pharmacological characterization of the tachykinin receptors involved in spinal and supraspinal cardiovascular regulation is reviewed in this report. In conscious rats, substance P (SP), neurokinin A (NKA), neurokinin B (NKB), neuropeptide K (NPK), and neuropeptide γ (NPγ) were injected either intrathecally (i.t.) or intracerebroventricularly (i.c.v.), and their effects were assessed on mean arterial blood pressure (MAP) and heart rate (HR). Moreover, selective antagonists for NK1 ((±)-CP-96345 and RP-67580), NK2 (SR-48968), and NK3 (R-486) receptors were tested against the agonists. I.t. tachykinins elicited dose-dependent increases in MAP and HR (NPK > NPγ > SP > NKA > NKB). The cardiovascular response to i.t. SP, NPK, and NPγ was significantly attenuated by the prior i.t. administration of (±)-CP-96345 and RP-67580 but not by SR-48968 and R-486. By the i.c.v. route, tachykinins also elicited pressor and tachycardiac responses dose dependently (NPK > NPγ > SP > NKA > NKB). Senktide and [MePhe7]NKB, two NK3-selective agonists, were slightly more potent than NKB on both parameters. Whereas the cardiovascular response to NPK was largely blocked by (±)-CP-96345 and RP-67580, that to SP was reduced by 40–50%. This treatment had no effect on the cardiovascular response to NKA and [MePhe7]NKB. Conversely, SR-48968 reduced by 40–50% the NKA-induced cardiovascular changes without affecting the central mediated effects of NPK, SP, and [MePhe7]NKB. However, when coadministered, RP-67580 and SR-48968 abolished the effects to SP and NKA while leaving untouched those induced by [MePhe7]NKB. Finally, the central effects mediated by [MePhe7]NKB, senktide, and NKB were blocked by R-486. These findings suggest that the i.t. action of tachykinins on the rat cardiovascular system is mediated by a NK1 receptor in the spinal cord, while NK1, NK2, and NK3 receptors are likely involved in the supraspinal (hypothalamus) effects of these neuropeptides. It is also concluded that NPK is a pure and powerful NK1 agonist, in contrast to SP and NKA, which are not selective for NK1 or NK2 receptors, respectively.Key words: tachykinins, spinal cord, central cardiovascular control, tachykinin receptor antagonists.
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35

Inoue, K., K. Nakazawa, K. Inoue, and K. Fujimori. "Nonselective cation channels coupled with tachykinin receptors in rat sensory neurons." Journal of Neurophysiology 73, no. 2 (February 1, 1995): 736–42. http://dx.doi.org/10.1152/jn.1995.73.2.736.

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1. Effects of substance P (SP) and other tachykinins on membrane currents were investigated using whole cell voltage clamp in cultured sensory neurons isolated from rat dorsal root ganglia. 2. SP (100 nM) evoked an inward current in two-thirds of the cells at negative potentials. In most of the cells that generated the inward current in response to SP, capsaicin also activated an inward current. The SP-evoked inward current was not observed in cells loaded with 2 mM guanosine 5'-O-(2-thiodiphosphate) (GDP beta S). 3. Neurokinin A (NKA) or neurokinin B (NKB) also activated an inward current. At 100 nM of each agonist, the order was NKB > NKA > SP with respect to activated current amplitude. 4. The tachykinin-activated current was reversed around +10 mV with a standard extracellular solution containing 140 mM NaCl. The reversal potential became more negative when extracellular NaCl was reduced by substituting with sucrose. The inward current was also activated in cells bathed in an extracellular solution containing Cs+, tetraethylammonium (TEA) or N-methyl-D-glucamine (NMDG) as a major cation instead of Na+. The order of permeability, determined from the reversal potential of the current, was Cs+ not equal to Na+ > TEA > NMDG. The amplitude of the inward current activated by NKB was increased when extracellular Na+ was replaced with Cs+, TEA or NMDG. 5. Permeability of Ca2+ was tested using an extracellular solution containing Ca2+ as the only cation (111.8 mM Ca2+ outside). Under this condition, NKB evoked an inward current that reversed around +30 mV. 6. The results suggest that SP and other tachykinins activate nonselective cation channels, which are also permeable to Ca2+, through receptors which are more responsive to NKB than to SP or NKA. The channel activation may serve as a mechanism underlying tachykinin-mediated excitatory neurotransmission in sensory neurons.
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36

Leon, Silvia, and Víctor M. Navarro. "Novel Biology of Tachykinins in Gonadotropin-Releasing Hormone Secretion." Seminars in Reproductive Medicine 37, no. 03 (May 2019): 109–18. http://dx.doi.org/10.1055/s-0039-3400252.

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AbstractThe tachykinin family of peptides, composed of the neurokinins A and B (NKA, NKB) and substance P are involved in the central control of gonadotropin-releasing hormone (GnRH) release through a variety of neuronal circuitries that mediate the activation of Kiss1 neurons and the synchronization of their activity within the arcuate nucleus. The major outcome of this role is the precise regulation of the pulsatile pattern of GnRH release. In addition, tachykinins are involved in the maturation of the reproductive axis by determining the optimal timing of puberty onset, as well as in the timing of the preovulatory luteinizing hormone surge in females. Therefore, the action of tachykinins in reproduction appears to extend to all the critical aspects required for the successful attainment and maintenance of fertility. In this review, we summarize the latest advances in our understanding of the biology of tachykinins in the control of GnRH release, addressing the existing controversies, open questions, and future perspectives.
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37

Pinto, Francisco M., Teresa A. Almeida, Mariano Hernandez, Philippe Devillier, Charles Advenier, and M. Luz Candenas. "mRNA expression of tachykinins and tachykinin receptors in different human tissues." European Journal of Pharmacology 494, no. 2-3 (June 2004): 233–39. http://dx.doi.org/10.1016/j.ejphar.2004.05.016.

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38

Lavielle, S., G. Chassaing, O. Ploux, D. Loeuillet, J. Besseyre, S. Julien, A. Marquet, et al. "Analysis of tachykinin binding site interactions using constrained analogues of tachykinins." Biochemical Pharmacology 37, no. 1 (January 1988): 41–49. http://dx.doi.org/10.1016/0006-2952(88)90753-8.

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39

Stroff, T., S. Plate, J. S. Ebrahim, K. H. Ehrlich, M. Respondek, and B. M. Peskar. "Tachykinin-induced increase in gastric mucosal resistance: role of primary afferent neurons, CGRP, and NO." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 6 (December 1, 1996): G1017—G1027. http://dx.doi.org/10.1152/ajpgi.1996.271.6.g1017.

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The tachykinins [Ala5,beta-Ala8]neurokinin A-(4-10) -[Ala5,beta-Ala8]NKA-(4-10) inverted question mark and NKA-(4-10) dose dependently protected against ethanol-induced gastric mucosal damage in rats (half-maximal inhibitory dose, 46 and 48 nmol/kg, respectively). These effects were abolished by primary afferent nerve denervation, calcitonin gene-related peptide (CGRP) immunoneutralization, the CGRP receptor antagonist human (h) hCGRP-(8-37), and inhibition of nitric oxide (NO) biosynthesis by NG-nitro-L-arginine methyl ester. Tachykinin-induced protection occurred despite marked depression of gastric mucosal blood flow and was not associated with increased acid secretion. NK2-receptor blockade antagonized the protective effects of [Ala5,beta-Ala8]NKA-(4-10) and NKA-(4-10), whereas NK1-receptor blockade was ineffective. Blockade of NK2 but not NK1 receptors prevented by 65% the protection evoked by topical capsaicin without affecting capsaicin-induced hyperemia. We conclude that the increase in gastric mucosal resistance evoked by tachykinins is NK2 receptor-mediated and involves primary afferent neurons, CGRP, and NO. Gastric mucosal hyperemia and increased acid secretion do not participate in the effect. Tachykinins activating NK2 receptors contribute to the increase in gastric mucosal resistance but not the increment in mucosal blood flow after primary afferent nerve stimulation by capsaicin.
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40

Satake, Honoo, Michio Ogasawara, Tsuyoshi Kawada, Katsuyoshi Masuda, Masato Aoyama, Hiroyuki Minakata, Takuto Chiba, Hitoe Metoki, Yutaka Satou, and Nori Satoh. "Tachykinin and Tachykinin Receptor of an Ascidian,Ciona intestinalis." Journal of Biological Chemistry 279, no. 51 (October 12, 2004): 53798–805. http://dx.doi.org/10.1074/jbc.m408161200.

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41

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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42

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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43

Liu, Lu, Irit Markus, Robert J. Vandenberg, Brett A. Neilan, Michael Murray, and Elizabeth Burcher. "Molecular identification and characterization of three isoforms of tachykinin NK1-like receptors in the cane toad Bufo marinus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 3 (September 2004): R575—R585. http://dx.doi.org/10.1152/ajpregu.00051.2004.

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The tachykinin peptide bufokinin, isolated from the cane toad intestine, is important in intestinal and cardiovascular regulation in the toad. In this study, three tachykinin NK1-like receptor isoforms, bNK1-A, bNK1-B, and bNK1-C, encoding proteins of 309, 390, and 371 amino acids, respectively, were cloned from the toad brain and intestine. These isoforms differ only at the intracellular COOH terminus. The bNK1-A and bNK1-B isoforms are similar to the truncated and full-length forms of the mammalian NK1 receptor, whereas bNK1-C is unique and does not correspond to any previously described receptor. RT-PCR studies demonstrated that three isoform transcripts are widely distributed in the toad with high expression in gut, spinal cord, brain, lung, and skeletal muscle. When expressed in COS-7 cells, bufokinin showed similar high affinity (IC50 0.6–0.8 nM) in competing for 125I-labeled Bolton-Hunter bufokinin binding at all receptors, but the binding affinities of substance P (SP) and neurokinin A (NKA) were very different at each isoform. When expressed in Xenopus oocytes, the truncated isoform, bNK1-A, was inactive, whereas bNK1-B and bNK1-C produced changes in chloride current when stimulated by tachykinins (minimum concentrations: bufokinin, 0.1 nM; SP, 1 nM; and NKA, 10 nM). A marked desensitization of the response was seen to subsequent applications of tachykinins, as experienced by the mammalian NK1 receptor. In summary, our study describing three isoforms of NK1-like receptor from the toad suggests that the alternative splicing of NK1 receptor is a physiologically conserved mechanism and raises a fundamental question as to the physiological role of each isoform.
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Piedimonte, G., J. I. Hoffman, W. K. Husseini, R. M. Snider, M. C. Desai, and J. A. Nadel. "NK1 receptors mediate neurogenic inflammatory increase in blood flow in rat airways." Journal of Applied Physiology 74, no. 5 (May 1, 1993): 2462–68. http://dx.doi.org/10.1152/jappl.1993.74.5.2462.

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We studied the effect of neurogenic inflammation on airway blood flow in anesthetized F-344 rats. Three successive determinations of blood flow were made by injecting radionuclide-labeled microspheres suspended in 70% dextrose into the left ventricle. A selective agonist of the tachykinin receptor neurokinin 1 (NK1) increased airway blood flow, but NK2- and NK3-selective agonists were without effect. The natural agonist of NK1 receptors, substance P (1 micrograms/kg), increased airway blood flow, an effect that was abolished by the selective NK1 receptor antagonist CP-99,994 [(+)-(2S,3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine] but not by the (2R,3R)-enantiomer CP-100,263. Capsaicin (25 micrograms/kg), a drug that releases tachykinins and calcitonin gene-related peptide from sensory nerves, increased airway blood flow, and again this effect was abolished by CP-99,994. We also studied the effect of a selective inhibitor (captopril, 2.5 mg/kg) of the tachykinin-degrading enzyme kininase II [or angiotensin-converting enzyme (ACE)] on substance P-induced airway vasodilation. Captopril potentiated and prolonged the vasodilator effect of substance P. We conclude that neurogenic vasodilation in rat airways is due to the release of substance P, acts via NK1 receptors, and may be modulated by ACE.
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45

Conlon, J. Michael. "The tachykinin receptors." FEBS Letters 356, no. 2-3 (December 19, 1994): 374. http://dx.doi.org/10.1016/s0014-5793(94)80082-0.

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46

Morton, Ian K. M. "The tachykinin receptors." Trends in Pharmacological Sciences 16, no. 1 (January 1995): 31. http://dx.doi.org/10.1016/s0165-6147(00)88970-1.

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47

Nakanishi, S. "Mammalian Tachykinin Receptors." Annual Review of Neuroscience 14, no. 1 (March 1991): 123–36. http://dx.doi.org/10.1146/annurev.ne.14.030191.001011.

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48

TAKANO, YUKIO, AKIRA NAGASHIMA, TETSUYA HAGIO, YASUHISA NAKAYAMA, and HIRO-O. KAMIYA. "Tachykinin Receptor Subtype." Annals of the New York Academy of Sciences 632, no. 1 Substance P a (September 1991): 476–78. http://dx.doi.org/10.1111/j.1749-6632.1991.tb33162.x.

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49

Hagan, R. M., S. J. Ireland, I. J. M. Beresford, P. J. Birch, P. J. Elliott, A. B. McElroy, and P. Ward. "Tachykinin receptor antagonists." Neuropeptides 22, no. 1 (May 1992): 27–28. http://dx.doi.org/10.1016/0143-4179(92)90408-o.

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50

Quirion, Rémi. "Multiple tachykinin receptors." Trends in Neurosciences 8 (January 1985): 183–85. http://dx.doi.org/10.1016/0166-2236(85)90073-6.

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