Diversity and Functions of GABA Receptors: A Tribute to Hanns Möhler, Part B
- 1st Edition, Volume 73 - January 22, 2015
- Latest edition
- Editor: Uwe Rudolph
- Language: English
- Hardback ISBN:9 7 8 - 0 - 1 2 - 8 0 2 6 5 8 - 8
- eBook ISBN:9 7 8 - 0 - 1 2 - 8 0 2 6 9 1 - 5
Diversity and Functions of GABA Receptors: A Tribute to Hanns Möhler, Part B, a new volume of Advances in Pharmacology, presents the diversity and functions of GABA Receptors.… Read more
Diversity and Functions of GABA Receptors: A Tribute to Hanns Möhler, Part B
, a new volume of Advances in Pharmacology, presents the diversity and functions of GABA Receptors. The volume looks at research performed in the past 20 years, which has revealed specific physiological and pharmacological functions of individual GABAA receptor subtypes, providing novel opportunities for drug development.- Contributions from the best authors in the field
- An essential resource for pharmacologists, immunologists, and biochemists
Pharmacologists and Neuroscientists
- Preface: A Tribute to Professor Hanns Möhler
- Chapter One: Reflections on More Than 30 Years Association with Hanns
- Abstract
- 1 Introduction
- 2 Conclusion
- Conflict of Interest
- Chapter Two: Significance of GABAA Receptor Heterogeneity: Clues from Developing Neurons
- Abstract
- 1 Introduction
- 2 Conclusion
- Conflict of Interest
- Acknowledgments
- Chapter Three: Regulation of Cell Surface GABAB Receptors: Contribution to Synaptic Plasticity in Neurological Diseases
- Abstract
- 1 Introduction
- 2 Phosphorylation of GABAB Receptors
- 3 Degradation of GABAB Receptors
- 4 Contribution of Altered Cell Surface GABAB Receptor Expression to Neurological Diseases
- 5 Potential Therapeutic Implications
- 6 Conclusion
- Conflict of Interest
- Chapter Four: Restoring the Spinal Pain Gate: GABAA Receptors as Targets for Novel Analgesics
- Abstract
- 1 Introduction
- 2 Synaptic Disinhibition in Pathological Pain
- 3 Spinal GABAAR Subtypes Mediating Antihyperalgesia: Evidence from Genetically Engineered Mice
- 4 Mechanisms of Spinal Benzodiazepine-Mediated Antihyperalgesia
- 5 Antihyperalgesic Action of Benzodiazepines with Improved Subtype Specificity: Preclinical Studies
- 6 Clinical Studies on Antihyperalgesia by Benzodiazepines
- 7 Open Questions
- 8 Conclusion
- Conflict of Interest Statement
- Acknowledgment
- Chapter Five: GABAergic Control of Depression-Related Brain States
- Abstract
- 1 Introduction
- 2 The GABAergic Deficit Hypothesis of MDD
- 3 GABAergic Transmission and Heritability of MDD
- 4 GABAergic Transmission in Relation to the Monoamine Deficiency Hypothesis of MDD
- 5 GABAergic Transmission in Relation to Stress-Based Etiologies of MDD
- 6 GABAergic Transmission in Relation to the Neurotrophic Deficit Hypothesis of MDD
- 7 GABAergic Transmission in Relation to Glutamatergic Etiologies of MDD
- 8 Conclusion
- Conflict of Interest
- Acknowledgments
- Chapter Six: Mechanisms of Fast Desensitization of GABAB Receptor-Gated Currents
- Abstract
- 1 Introduction
- 2 Homologous Desensitization Operating at the Receptor
- 3 Homologous Desensitization Operating at the α and βγ Subunits of the G Protein
- 4 Slow and Fast Mechanisms of Desensitization Influence Each Other
- 5 Conclusion
- Conflict of Interest
- Acknowledgments
- Chapter Seven: Allosteric Ligands and Their Binding Sites Define γ-Aminobutyric Acid (GABA) Type A Receptor Subtypes
- Abstract
- 1 Introduction
- 2 Conclusion
- Conflict of Interest
- Acknowledgments
- Chapter Eight: Diversity in GABAergic Signaling
- Abstract
- 1 Introduction
- 2 Factors Shaping the Neuronal Transmembrane Chloride Gradient
- 3 Experimental Techniques to Study Chloride Homeostasis and E-GABAA
- 4 Variability of GABAergic Signaling
- 5 Conclusion
- Conflict of Interest
- Chapter Nine: The Diversity of GABAA Receptor Subunit Distribution in the Normal and Huntington's Disease Human Brain
- Abstract
- 1 Introduction
- 2 Neuropathology of the Basal Ganglia in Huntington's Disease
- 3 Cellular and Neurochemical Changes
- Conflict of Interest
- Acknowledgments
- Index
- Edition: 1
- Latest edition
- Volume: 73
- Published: January 22, 2015
- Language: English
UR
Uwe Rudolph
Dr. Rudolph is Director of the Laboratory of Genetic Neuropharmacoloy at McLean Hospital and Professor of Psychiatry at Harvard Medical School. He studied medicine and completed a research thesis on G proteins at the Freie Universitat Berlin, Germany. After postdoctoral training at Baylor College of Medicine in Houston, Texas, where he developed a mouse model of inflammatory bowel disease and colon cancer, he moved to the Institute of Pharmacology and Toxicology of the University of Zurich to work on GABAA receptors. There, he developed different lines of knock-in mice in which diazepam-sensitive GABAA receptor subtypes were rendered insensitive to diazepam by a histidine to arginine point mutation. Studying these mice enables researchers to uncover unique functional roles of GABAA receptor subtypes. In 2005, he joined McLean Hospital in Belmont, MA, and Harvard Medical School, where his research group is elucidating the functions of GABAA receptor subtypes in defined neuronal populations.
Affiliations and expertise
Genetic Neuropharmacology Laboratory, McLean Hospital, Belmont, MA, USARead Diversity and Functions of GABA Receptors: A Tribute to Hanns Möhler, Part B on ScienceDirect