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Substance P : from pain to cancer /

Substance P: From Pain to Cancer, a volume in the Molecular Mediators in Health and Disease: How Cells Communicate series, provides a complete discussion of substance P biology, its role in normal physiology and a variety of diseases. The volume provides an introduction to substance P and its pharma...

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Bibliographic Details
Other Authors: Vink, Robert, 1958- (Editor)
Format: Electronic eBook
Language:English
Published: London, United Kingdom : Academic Press, [2025]
Series:Molecular Mediators in Health and Disease: How Cells Communicate
Subjects:
Substance P > Physiological effect.
Substance P > Effets physiologiques.
Substance P > Physiological effect
Online Access:ScienceDirect
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Table of Contents:
  • Intro
  • Substance P: From Pain to Cancer
  • Copyright
  • Contents
  • Contributors
  • Preface
  • Series preface
  • Chapter 1: The synthesis, release, and binding of substance P
  • 1. Introduction
  • 2. Substance P synthesis
  • 3. Substance P release
  • 4. Substance P binds to neurokinin receptors
  • 5. Substance P binding activates a variety of signaling pathways
  • 6. Regulation of substance P/NK-1 receptor activity
  • 7. Conclusion
  • References
  • Chapter 2: Distribution of substance P receptors in mammals
  • 1. Introduction
  • 2. NK1R
  • 2.1. Biochemical and phylogenetic characteristics of NK1R
  • 2.2. Tissue distribution of NK1R in mammals
  • 2.2.1. NK1R in the nociceptive and neurogenic inflammation system
  • 2.2.2. NK1R in the brain
  • 2.2.3. NK1R in the gastrointestinal tract
  • 2.2.4. NK1R in the cardiovascular system
  • 2.2.5. NK1R in the respiratory system
  • 2.2.6. NK1R in skin
  • 2.2.7. NK1R in immune cells
  • 2.2.8. NK1R in reproductive organs
  • 3. MRGPRX2 (MRGX2)
  • 3.1. Biochemical and phylogenetic characteristics of MRGPRX2 (MRGX2)
  • 3.2. Tissue-distribution of MRGPRX2 in human and MrgprB2 in mice
  • 4. Conclusion and perspectives
  • References
  • Chapter 3: Substance P in nonmammalian biology: Evolutionarily conserved tachykinin signaling
  • 1. Introduction
  • 2. Tachykinins and their receptors in mammals
  • 3. Tachykinins and their receptors in deuterostome invertebrates and protochordates
  • 4. Tachykinins and their receptors in nonmammalian vertebrates
  • 4.1. TK signaling in cephalochordates and agnate chordates
  • 4.2. TK signaling in elasmobranchs (sharks)
  • 4.3. TK signaling in teleost fish
  • 4.4. Tachykinin signaling in amphibians
  • 4.4.1. Frog and toad tachykinins and receptors
  • 4.4.2. Frog skin tachykinins
  • 5. Tachykinins and their receptors in protostome invertebrates.
  • 5.1. Identification of invertebrate tachykinin precursors and receptors
  • 5.2. Distribution and functions of tachykinins in invertebrates
  • 5.2.1. Early studies of distribution and functional diversity of tachykinins in invertebrates
  • 5.2.2. Distribution and functions of TKs in insects
  • 5.2.3. TK signaling in crustaceans
  • 5.2.4. Mollusks
  • 5.2.5. Nematode worms
  • 5.3. Functional roles of TK signaling in Drosophila
  • 5.4. Invertebrate gland tachykinins as secreted toxins or vasodilatory factors
  • 5.5. A case of novel ligands for an insect TK receptor and a case of promiscuity
  • 5.6. Natalisins, a sister group of tachykinins in arthropods
  • 6. Conserved roles of tachykinin signaling in the animal kingdom
  • 7. Notes on the evolution of tachykinin signaling
  • 8. Conclusions and perspectives
  • 9. Summary
  • Acknowledgments
  • References
  • Chapter 4: Methodological foundations of substance P detection
  • 1. Introduction
  • 2. SP measurement: Handling of blood sample
  • 3. SP measurements from tissues
  • 3.1. Sample obtaining
  • 3.2. Sample preparation
  • 3.3. Solid-phase extraction (SPE)
  • 4. Detection by radioimmunoassay (RIA) and enzyme immunoassay (EIA)
  • 5. Effects of protease inhibitor cocktail in EIA
  • 6. Differentiation of neuronal and nonneuronal SP levels
  • 7. Immunohistochemical detection
  • 8. Measurement of SP in tears
  • 9. SP levels in other body secretions
  • 10. Conclusion
  • References
  • Chapter 5: Substance P receptor antagonists
  • 1. Introduction
  • 2. Ligands of the neurokinin-1 receptor
  • 2.1. Neurokinin-1 receptor is the high-affinity receptor for substance P
  • 2.2. The design and synthesis of peptide and nonpeptide neurokinin-1 receptor antagonists
  • 2.3. The neurokinin-1 receptor antagonists binding sites
  • 3. Current medical use of neurokinin-1 receptor antagonists.
  • 3.1. Neurokinin-1 receptor antagonists as antiemetics
  • 3.2. Studies in other pathologies
  • 3.3. Features of neurokinin-1 receptor antagonists worth considering for broader clinical use
  • 4. Concluding remarks
  • References
  • Chapter 6: Substance P in the cardiovascular system
  • 1. Introduction
  • 2. Substance P in the heart
  • 2.1. Localization of SP in the heart
  • 2.2. SP receptors
  • 2.3. Function of SP in the heart
  • 2.3.1. Effect throughout intracardiac nervous system
  • 2.3.2. Effect of SP on coronary circulation
  • 2.3.3. Direct effect of SP on cardiomyocytes and fibroblasts
  • 3. Substance P in the vascular system
  • 3.1. Localization of members of the SP signaling system in the vessels
  • 3.2. Effects of SP on the vessels of the bloodstream
  • 4. Effect of SP on the control of cardiovascular system functions
  • 5. Conclusion
  • References
  • Chapter 7: Substance P in lower urinary tract function and dysfunction
  • 1. Introduction
  • 1.1. Overview
  • 1.2. Neural circuits in control of urinary continence and micturition
  • 2. Effects of capsaicin on substance P in micturition
  • 3. Bladder function in neonates and preprotachykinin A gene deletion
  • 3.1. Bladder function in neonates
  • 3.2. Preprotachykinin A gene deletion
  • 4. Components of the urinary system that control lower urinary tract function
  • 4.1. Bladder
  • 4.2. Urethra
  • 4.3. Ganglionic neurons
  • 4.4. Spinal cord
  • 4.5. Supraspinal regions
  • 5. Effects of systemic administration of NK1 antagonist in animals
  • 6. Pathophysiological changes in the lower urinary tract
  • 6.1. Animal models of lower urinary tract dysfunction
  • 6.1.1. Chemically induced cystitis
  • 6.1.2. Bladder outlet obstruction
  • 6.1.3. Hyperreflexia after spinal cord injury
  • 6.2. Lower urinary tract dysfunction in humans
  • 6.2.1. Interstitial cystitis
  • 6.2.2. Bladder outflow obstruction.
  • 6.2.3. Detrusor overactivity
  • 6.2.4. Genitourinary prolapse
  • 7. Clinical trials
  • 7.1. Serlopitant
  • 7.2. Aprepitant
  • 7.3. Cizolirtine
  • 8. Concluding remarks
  • References
  • Chapter 8: Role of the substance P in learning and memory
  • 1. Introduction
  • 2. Nonassociative learning-Habituation and sensitization
  • 3. Simple associative learning-Classical conditioning
  • 4. Simple associative learning-Operant conditioning
  • 5. Memory for innate behavioral sequences
  • 6. Memory for learned behavioral sequences
  • 7. Summary and conclusion
  • References
  • Chapter 9: Substance P in nausea and vomiting
  • 1. Introduction
  • 1.1. Nausea and vomiting in health, disease and therapy
  • 1.1.1. Definitions and terminology
  • 1.1.2. Nausea and vomiting in biological and clinical contexts
  • 1.1.3. The need for drugs to block nausea and vomiting
  • 1.2. A brief overview of nausea and vomiting physiology and pharmacology
  • 1.2.1. Induction of vomiting
  • Abdominal vagal afferents
  • Area postrema
  • Vestibular system
  • Descending cerebral pathways
  • 1.2.2. Induction of nausea
  • 2. Links between substance P, nausea and vomiting
  • 2.1. Induction of vomiting by exogenous SP and related tachykinins in preclinical models
  • 2.1.1. Systemic administration
  • 2.1.2. Central nervous system administration
  • 2.1.3. SP secreting tumors and tachykinin administration in humans
  • 2.2. Actions of tachykinins on the digestive tract potentially contributing to the induction of nausea and vomiting and a ...
  • 2.2.1. Exogenous tachykinins
  • 2.2.2. Effects of receptor antagonists on GI functions
  • 2.2.3. Effects of receptor antagonists on GI functions associated with nausea and vomiting
  • Upper GI vagal functions
  • Gastric ICCs
  • 2.3. Presence of SP and NK1 receptors in neural pathways implicated in nausea and vomiting
  • 2.3.1. Abdominal vagal afferents.
  • 2.3.2. Brainstem
  • Area postrema
  • Nucleus tractus solitarius
  • Ventrolateral brainstem
  • 2.3.3. Mid-brain and cerebral structures
  • 2.3.4. Digestive tract
  • 2.4. Release of SP by emetic stimuli in humans and animals
  • 3. Vomit-blocking effects of NK1 receptor antagonists and studies with antagonists at other tachykinin receptors
  • 3.1. Preclinical studies of NK1RAs in species with a vomiting reflex
  • 3.2. Are NK2 and NK3 receptors involved in vomiting?
  • 3.3. Some challenges of species differences in studying the antivomiting effects of NK1RAs
  • 3.3.1. Species and receptor selectivity
  • 3.3.2. Anomalies
  • 3.3.3. Studies in the least shrew (Cryptotis parva)
  • 4. Clinical efficacy of NK1 receptor antagonists
  • 4.1. Spectrum of efficacy
  • 4.1.1. Chemotherapy-induced nausea and vomiting
  • 4.1.2. Postoperative nausea and vomiting
  • 4.1.3. Gastroparesis
  • 4.1.4. Other clinical indications
  • 4.1.5. Motion sickness
  • 5. Site(s) of action
  • 6. Concluding comments
  • Acknowledgments
  • References
  • Chapter 10: Substance P in the central control of respiration
  • 1. Introduction
  • 2. Substance P in the control of breathing
  • 3. Localization of substance P and neurokinin receptors
  • 4. Cellular actions within central respiratory sites
  • 5. Physiological role(s) of substance P in the control of breathing
  • 6. Chemosensitivity
  • 7. The broader role of neuromodulation in the orchestration of behavioral functions
  • References
  • Chapter 11: Substance P in bone metabolism
  • 1. Introduction
  • 1.1. Bone structure
  • 1.2. Bone metabolism
  • 2. Substance P and bone cells
  • 2.1. Substance P and osteoclasts
  • 2.2. Substance P and osteoblasts
  • 2.3. Substance P and osteocytes
  • 3. Substance P and bone metabolism
  • 3.1. Health
  • 3.2. Trauma
  • 3.3. Disease-Osteoporosis
  • 4. Conclusion
  • References.

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