Are biological actions of neurokinin A in the adult brain mediated by a cross-talk between the NK1 and NK2 receptors?

Tauer, Ulrike; Zhao, Yi; Hunt, Stephen P.; Čulman, Juraj

doi:10.1016/j.neuropharm.2012.06.041

Cited by 6 publications

(5 citation statements)

References 35 publications

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“…Although we do not have a precise explanation for why the hyperalgesic action of HK-1 presumably at the NK1 receptors is not observed when SP and NKA are also missing from the system, some hypothesis can be made: a) HK-1 exerts its hyperalgesic effect in the nociceptive pathway through the NK1 tachykinin receptor, but it is counteracted by NKA acting at NK2 receptors in the central nervous system [53], b) HK-1 and SP act at the same receptors (NK1), but they might have different binding sites, affinities and intinsinc efficacies, as well as distinct activation mechanisms and signalling pathways. When both are removed from the system, the inhibition observed in case of the HK-1 absence, might be counteracted via intracellular molecular mechanisms.…”

Section: Discussionmentioning

confidence: 93%

Role of Tachykinin 1 and 4 Gene-Derived Neuropeptides and the Neurokinin 1 Receptor in Adjuvant-Induced Chronic Arthritis of the Mouse

et al. 2013

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ObjectiveSubstance P, encoded by the Tac1 gene, is involved in neurogenic inflammation and hyperalgesia via neurokinin 1 (NK1) receptor activation. Its non-neuronal counterpart, hemokinin-1, which is derived from the Tac4 gene, is also a potent NK1 agonist. Although hemokinin-1 has been described as a tachykinin of distinct origin and function compared to SP, its role in inflammatory and pain processes has not yet been elucidated in such detail. In this study, we analysed the involvement of tachykinins derived from the Tac1 and Tac4 genes, as well as the NK1 receptor in chronic arthritis of the mouse.MethodsComplete Freund’s Adjuvant was injected intraplantarly and into the tail of Tac1−/−, Tac4−/−, Tacr1−/− (NK1 receptor deficient) and Tac1−/−/Tac4−/− mice. Paw volume was measured by plethysmometry and mechanosensitivity using dynamic plantar aesthesiometry over a time period of 21 days. Semiquantitative histopathological scoring and ELISA measurement of IL-1β concentrations of the tibiotarsal joints were performed.ResultsMechanical hyperalgesia was significantly reduced from day 11 in Tac4−/− and Tacr1−/− animals, while paw swelling was not altered in any strain. Inflammatory histopathological alterations (synovial swelling, leukocyte infiltration, cartilage destruction, bone damage) and IL-1β concentration in the joint homogenates were significantly smaller in Tac4−/− and Tac1−/−/Tac4−/− mice.ConclusionsHemokinin-1, but not substance P increases inflammation and hyperalgesia in the late phase of adjuvant-induced arthritis. While NK1 receptors mediate its antihyperalgesic actions, the involvement of another receptor in histopathological changes and IL-1β production is suggested.

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Section: Discussionmentioning

confidence: 93%

Role of Tachykinin 1 and 4 Gene-Derived Neuropeptides and the Neurokinin 1 Receptor in Adjuvant-Induced Chronic Arthritis of the Mouse

et al. 2013

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“…10,15,[24][25][26][27][28] The doses of the NK1R antagonists (10 nmols per MNA) were based on previous publications. 6,24,25,27,[29][30][31] Coadministration of NK1R antagonist at the sensitization site, incorporated with hapten in MNA or injected i.…”

Section: Skin Codelivery Of Hapten and Nk1r Antagonists Integrated In...mentioning

confidence: 99%

Skin codelivery of contact sensitizers and neurokinin-1 receptor antagonists integrated in microneedle arrays suppresses allergic contact dermatitis

Bandyopadhyay

Morelli²,

Balmert³

et al. 2022

Journal of Allergy and Clinical Immunology

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“…However, to date, this claim remains controversial as studies have shown contradictory results. An extensive study conducted by Tauer et al, [218] using NK-1R −/− mice and selective high affinity non peptide NK-1R, NK-2R and NK-3R receptor antagonists revealed that there is a significant probability that the central actions of NKA could be mediated by a cross talk between NK-1R and NK-2R receptors. This study could be used as a reference point in studying the role of NKA in cardiac remodeling since isolated neonatal cardiomyocytes have been shown to express the gene for NK-1R and NK-3R receptors, though not NK-2R receptor.…”

Section: 0 Additional Neuropeptidesmentioning

confidence: 99%

The role of neuropeptides in adverse myocardial remodeling and heart failure

Widiapradja

Chunduri

Levick

2017

Cell. Mol. Life Sci.

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In addition to traditional neurotransmitters of the sympathetic and parasympathetic nervous systems, the heart also contains numerous neuropeptides. These neuropeptides not only modulate the effects of neurotransmitters, but also have independent effects on cardiac function. While in most cases the physiological actions of these neuropeptides are well defined, their contributions to cardiac pathology are less appreciated. Some neuropeptides are cardioprotective, some promote adverse cardiac remodeling and heart failure, and in the case of others their functions are unclear. Some have both cardioprotective and adverse effects depending on the specific cardiac pathology and progression of that pathology. In this review, we briefly describe the actions of several neuropeptides on normal cardiac physiology, before describing in more detail their role in adverse cardiac remodeling and heart failure. It is our goal to bring more focus toward understanding the contribution of neuropeptides to the pathogenesis of heart failure, and to consider them as potential therapeutic targets.

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Are biological actions of neurokinin A in the adult brain mediated by a cross-talk between the NK1 and NK2 receptors?

Cited by 6 publications

References 35 publications

Role of Tachykinin 1 and 4 Gene-Derived Neuropeptides and the Neurokinin 1 Receptor in Adjuvant-Induced Chronic Arthritis of the Mouse

Role of Tachykinin 1 and 4 Gene-Derived Neuropeptides and the Neurokinin 1 Receptor in Adjuvant-Induced Chronic Arthritis of the Mouse

Skin codelivery of contact sensitizers and neurokinin-1 receptor antagonists integrated in microneedle arrays suppresses allergic contact dermatitis

The role of neuropeptides in adverse myocardial remodeling and heart failure

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