وبلاگ بلیان

تنظیم انتقال و تبدیل درد توسط نیتریک اکسید

Regulation of Nociceptive Transduction and Transmission by Nitric Oxide

معرفی کتاب «تنظیم انتقال و تبدیل درد توسط نیتریک اکسید» (با عنوان لاتین Regulation of Nociceptive Transduction and Transmission by Nitric Oxide) نوشتهٔ Alexis Bavencoffe; Shao-Rui Chen; Hui-Lin Pan، منتشرشده توسط نشر Academic Press در سال 2014. این کتاب در فرمت pdf، زبان انگلیسی ارائه شده است.

The potential involvement of nitric oxide (NO), a diffusible gaseous signaling messenger, in nociceptive transduction and transmission has been extensively investigated. However, there is no consistent and convincing evidence supporting the pronociceptive action of NO at the physiological concentration, and the discrepancies are possibly due to the nonspecificity of nitric oxide synthase inhibitors and different concentrations of NO donors used in various studies. At the spinal cord level, NO predominantly reduces synaptic transmission by inhibiting the activity of NMDA receptors and glutamate release from primary afferent terminals through S-nitrosylation of voltage-activated calcium channels. NO also promotes synaptic glycine release from inhibitory interneurons through the cyclic guanosine monophosphate/protein kinase G signaling pathway. Thus, NO probably functions as a negative feedback regulator to reduce nociceptive transmission in the spinal dorsal horn during painful conditions. Content: Front Cover Nitric Oxide Copyright Former Editors Contents Contributors Preface Chapter One: Regulation of Nociceptive Transduction and Transmission by Nitric Oxide 1. Introduction 2. Role of NO in Nociceptive Transduction at the Periphery 3. Diverse Effects of NO on Ion Channels Expressed on Primary Sensory Neurons 3.1. Acid-sensing ion channels 3.2. Transient receptor potential channels 3.2.1. TRPV1 3.2.2. TRPA1 3.2.3. TRPV3 and TRPV4 3.3. KATP channels 4. Role of NO in Regulating Nociceptive Transmission at the Spinal Cord Level. 5. NO Reduces Excitatory, But Potentiates Inhibitory, Synaptic Transmission in Spinal Cords5.1. Glutamatergic input from primary afferent nerves 5.2. Voltage-activated calcium channels in sensory neurons 5.3. Synaptic NMDA receptors 5.4. Synaptic release of glycine 6. Conclusions and Future Directions Acknowledgments References Chapter Two: microRNA and Human Inducible Nitric Oxide Synthase 1. Introduction 2. Regulation of Human iNOS Gene 2.1. Transcriptional 2.2. Posttranscriptional 3. miRNAs Regulation 3.1. miR-939 3.2. other miRNAs 4. Conclusion References. Chapter Three: Heart Mitochondrial Nitric Oxide Synthase: A Strategic Enzyme in the Regulation of Cellular Bioenergetics1. Introduction 2. Heart Mitochondrial NO Production 2.1. Heart mtNOS activity 2.2. Heart mtNOS identity 3. Regulation of Heart mtNOS 3.1. Effect of substrates and cofactors 3.2. Effect of mitochondrial metabolic state and membrane potential 4. Effects of NO on Heart Mitochondrial Function 4.1. Nitric oxide consumption reactions in mitochondria 4.2. Regulation of mitochondrial function by NO 4.3. Mitochondrial NOS functional activity. 5. Physiopathological Regulation of Heart mtNOS5.1. Heart chronic hypoxia 5.2. Heart acute hypoxia and ischemia-reperfusion 6. Conclusions and Future Directions Acknowledgments References Chapter Four: Nitric Oxide Regulation of Adult Neurogenesis 1. Introduction 2. Adult Neurogenesis 3. Expression of NOS in Neurogenic Regions 4. Pharmacological Studies of NO on Adult Neurogenesis In Vivo 5. NOS Knockout Animals and Adult Neurogenesis 6. Neuropeptide Y and NO 7. The Dual Role of NO in Adult Neurogenesis 8. Concentration-Dependent Effects of NO 9. Conclusions References. Chapter Five: Nitric Oxide in the Nervous System: Biochemical, Developmental, and Neurobiological Aspects1. Introduction 1.1. Brief history and biochemistry of NOS 1.2. NO classical actions 1.3. Interesting partners in the CNS: Focusing on NMDA receptors 2. NO Signaling Pathways 2.1. PKG modulation by NO 2.2. AKT modulation by NO 2.3. ERK1/2 modulation by NO 2.4. Src modulation by NO 2.5. CREB modulation by NO 3. NO and Neuronal Viability 4. NO and Neurotransmitters Release 4.1. Glutamate release 4.2. GABA release 4.3. DA release 4.4. 5-Hydroxytryptamine release.

First published in 1943, Vitamins and Hormones is the longest-running serial published by Academic Press.

The Series provides up-to-date information on vitamin and hormone research spanning data from molecular biology to the clinic. A volume can focus on a single molecule or on a disease that is related to vitamins or hormones. A hormone is interpreted broadly so that related substances, such as transmitters, cytokines, growth factors and others can be reviewed.

This volume focuses on nitric oxide.



Key features:

  • Expertise of the contributors
  • Coverage of a vast array of subjects
  • In depth current information at the molecular to the clinical levels
  • Three-dimensional structures in color
  • Elaborate signaling pathways
First published in 1943, Vitamins and Hormones is the longest-running serial published by Academic Press. The Series provides up-to-date information on vitamin and hormone research spanning data from molecular biology to the clinic. A volume can focus on a single molecule or on a disease that is related to vitamins or hormones. A hormone is interpreted broadly so that related substances, such as transmitters, cytokines, growth factors and others can be reviewed. This volume focuses on nitric oxide. Key features: Expertise of the contributors Coverage of a vast array of subjects In depth current information at the molecular to the clinical levels Three-dimensional structures in color Elaborate signaling pathways
دانلود کتاب تنظیم انتقال و تبدیل درد توسط نیتریک اکسید