http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
1 online resource (663 pages, 14 unnumbered pages of plates) : illustrations (some color)
Pain is the number one reason that people seek medical attention but pain is still under- and poorly-treated world-wide. The purpose of this book is to give an up to date picture of what causes pain, how pain becomes chronic and what pharmacological targets might be manipulated to alleviate acute and chronic pain. The book will cover a wide array of topics from gene polymorphisms to voltage-gated ion channels moving from cellular biology to whole animal physiology. Written by future leaders in the pain field Covers a wide range of targets Contains provocative i.
Front Cover; Molecular and Cell Biology of Pain; Copyright; Contents; Contributors; Preface; Chapter 1: An Introduction to Pain Pathways and Pain T̀̀argets;́́ 1. An Introduction to Pain and Pain Pathways; 1.1. Neuropathic pain; 1.2. Inflammatory Pain; 2. Ion Channels, Receptors, and Other T̀̀argets ́́for Persistent Inflammatory or Neuropathic Pain; 2.1. Ion channels; 2.2. Sodium channels; 2.3. Calcium channels; 2.4. K+ channels; 2.5. Receptors; 2.6. Purinergic receptors; 2.7. Toll-like receptors; 2.8. PAR receptors; 2.9. Glutamate receptors; 2.10. AMPA receptors; 2.11. NMDA receptors.
2.12. Metabotropic glutamate receptors2.13. Opioid receptors; 2.14. TRPV receptors; 2.15. Prostaglandin (prostanoid) E2; 2.16. Pronociceptive neurotransmitters; 2.16.1. Nitric oxide; 2.16.2. Nerve growth factor; 3. Summary; Acknowledgments; References; Chapter 2: Peripheral Scaffolding and Signaling Pathways in Inflammatory Pain; 1. Introduction; 2. Inflammatory Mediators; 2.1. Bradykinin receptor; 2.2. Prostaglandin receptor; 2.3. Serotonin receptor; 2.4. Purinergic receptors; 2.5. Receptor tyrosine kinases; 2.6. Neurokinin receptor; 2.7. Glutamate receptors.
2.8. Protease-activated receptors2.9. Calcitonin receptor-like receptor and receptor activity-modifying protein 1; 2.10. Endothelin receptors; 3. Signaling Mechanisms; 4. Scaffolding Structures; 4.1. A-kinase anchoring protein 79/150; 4.2. Ý-Arrestin; 5. Concluding Remarks; References; Chapter 3: Contribution of Mechanosensitive Ion Channels to Somatosensation; 1. The Evolution of Mechanosensing; 2. MSCs in Nociceptors; 3. Difficulties in Identifying Genes Encoding MSCs; 3.1. Piezo2 as a mechanosensitive channel in sensory neurons; 4. Gating Mechanisms of MSCs.
5. Role of MSCs in the Transmission of Noxious Mechanical Inputs6. Sensitization of MSCs Is Necessary for the Induction of Mechanical Allodynia; 7. Potassium-Selective MSCs in Nociceptors; References; Chapter 4: Sensory TRP Channels: The Key Transducers of Nociception and Pain; 1. Introduction; 2. Ion Channels in the TRPV Subfamily; 2.1. Transient receptor potential vanilloid 1; 2.1.1. Expression and distribution in nervous system; 2.1.2. Structure; 2.1.3. Functional properties of the channel; 2.1.4. Modulation of channel expression and function; 2.1.5. Channel desensitization.
2.1.6. Involvement in pain conditions2.1.7. Involvement in other physiological and pathological conditions; 2.1.8. Drug development targeting TRPV1; 2.2. Transient receptor potential vanilloid 2, 3, and 4; 3. Ion Channels in the TRPM Subfamily; 3.1. Transient receptor potential melastatin 3; 3.2. Transient receptor potential melastatin 8; 3.2.1. Expression and distribution in nervous system; 3.2.2. Structure; 3.2.3. Functional properties of the channel; 3.2.4. Modulation of channel expression and function; 3.2.5. Involvement in pain conditions; 3.2.6. Drug development targeting TRPM8.
edited by Theodore J. Price, Greg Dussor.
Includes bibliographical references at the end of each chapters and index.
Waltham, Massachusetts : Academic Press, ©2015
Progress in molecular biology and translational science ; v. 131