Role of Tachykinins in the Gastrointestinal Tract

Holzer, Peter

doi:10.1007/978-3-642-18891-6_16

Cited by 3 publications

(2 citation statements)

References 310 publications

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“…It is well established that intestinal inflammation, such as IBD, may be associated to neuronal plasticity of tachykinergic innervation (Holzer, 2004). In our study, the percentages of MP and SMP SP-IR neurons did not change in the INF-dogs as well as the density of SP-IR nerve fibers in the CML and LML.…”

Section: Sp-immunoreactivity Of Neurons and Nerve Fiberscontrasting

confidence: 43%

Substance P and the neurokinin-1 receptor expression in dog ileum with and without inflammation

Polidoro

Giancola

Fracassi

et al. 2017

Research in Veterinary Science

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Section: Sp-immunoreactivity Of Neurons and Nerve Fiberscontrasting

confidence: 43%

Substance P and the neurokinin-1 receptor expression in dog ileum with and without inflammation

Polidoro

Giancola

Fracassi

et al. 2017

Research in Veterinary Science

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“…Most spinal afferents supplying the viscera of rodents contain the tachykinins substance P and neurokinin A, and tachykinin NK 1 , NK 2 and NK 3 receptors are expressed at many levels of the gut–brain axis. While a large number of preclinical studies attest to a role of tachykinin receptors in visceral hyperalgesia [48], clinical trials of NK 1 and NK 3 receptor antagonists failed to reveal any benefit in IBS and oesophageal hypersensitivity [49]. Results obtained with NK 2 receptor antagonists or compounds targeting more than one tachykinin receptor in visceral pain syndromes have not yet been disclosed.…”

Section: Drug Targets On Visceral Sensory Neuronsmentioning

confidence: 99%

Pharmacology of Inflammatory Pain: Local Alteration in Receptors and Mediators

Holzer

Holzer‐Petsche

2009

Dig Dis

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Background: Inflammation is commonly associated with hyperalgesia. Ideally, this change should abate once inflammation is resolved, but this is not necessarily the case because phenotypic changes in the tissue can persist, as appears to be the case in post-infectious irritable bowel syndrome. Basically, all primary afferent neurons supplying the gut can be sensitized in response to pro-inflammatory mediators, and the mechanisms whereby hypersensitivity is initiated and maintained are, thus, of prime therapeutic interest. Experimental and Clinical Findings: There is a multitude of molecular nocisensors that can be responsible for the hypersensitivity of afferent neurons. These entities include: (i) receptors and sensors at the peripheral terminals of afferent neurons that are relevant to stimulus transduction, (ii) ion channels that govern the excitability and conduction properties of afferent neurons, and (iii) transmitters and transmitter receptors that mediate communication between primary afferents and second-order neurons in the spinal cord and brainstem. Persistent increases in the sensory gain may result from changes in the expression of transmitters, receptors or ion channels; changes in the subunit composition and biophysical properties of receptors and ion channels; or changes in the structure, connectivity and survival of afferent neurons. Particular therapeutic potential is attributed to targets that are selectively expressed by afferent neurons and whose number and function are altered in abdominal hypersensitivity. Conclusion: Emerging targets of therapeutic relevance include distinct members of the transient receptor potential (TRP) channel family (TRPV1, TRPV4, TRPA1), acid-sensing ion channels, protease-activated receptors, corticotropin-releasing factor receptors and sensory neuron-specific sodium channels.

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Tachykinins

Holzer¹

2013

Handbook of Biologically Active Peptides

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Role of Tachykinins in the Gastrointestinal Tract

Cited by 3 publications

References 310 publications

Substance P and the neurokinin-1 receptor expression in dog ileum with and without inflammation

Substance P and the neurokinin-1 receptor expression in dog ileum with and without inflammation

Pharmacology of Inflammatory Pain: Local Alteration in Receptors and Mediators

Tachykinins

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