The Serotonin Receptors From Molecular Pharmacology to Human Therapeutics /
The recent cloning and identification of a large number of serotonin (5-HT) receptors-a major family of therapeutic targets-holds out the possibility of developing novel, subtype-selective 5-HT receptor agonists and antagonists for use as psychiatric, cardiovascular, and neurological medications. In...
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Format: | Electronic eBook |
Language: | English |
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Totowa, NJ :
Humana Press,
2006.
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Series: | The Receptors
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Online Access: | Full Text via HEAL-Link |
Table of Contents:
- Molecular Biology and Genomic Organization of G Protein-Coupled Serotonin Receptors
- Structure and Function Reveal Insights in the Pharmacology of 5-HT Receptor Subtypes
- Polymorphic and Posttranscriptional Modifications of 5-HT Receptor Structure
- Strategies for the Development of Selective Serotonergic Agents
- 5-HT Receptor Signal Transduction Pathways
- Agonist-Directed Trafficking of 5-HT Receptor-Mediated Signal Transduction
- Identification of 5-HT2 and 5-HT4 Receptor-Interacting Proteins
- 5-HT Receptor-Associated Proteins (FRAPs)
- Cellular and Subcellular Localization of Serotonin Receptors in the Central Nervous System
- Chemical Neuroanatomy of 5-HT Receptor Subtypes in the Mammalian Brain
- Modulation of the Neuronal Activity and Neurotransmitter Release by 5-HT1A and 5-HT1B/1D Receptors
- Electrophysiology of 5-HT2A Receptors and Relevance for Hallucinogen and Atypical Antipsychotic Drug Actions
- The Emergence of 5-HT2B Receptors as Targets to Avoid in Designing and Refining Pharmaceuticals
- The 5-HT3 Receptor
- 5-HT3 and 5-HT4 Receptors as Targets for Drug Discovery for Dementia
- Electrophysiological Properties of G?s-Coupled 5-HT Receptors (5-HT4, 5-HT6, 5-HT7)
- 5-HT6 Receptors as Targets for the Treatment of Cognitive Deficits in Schizophrenia
- 5-HT7 Receptors as Favorable Pharmacological Targets for Drug Discovery
- Serotonin System Gene Knockouts
- Effects of Serotonin-Related Gene Deletion on Measures of Anxiety, Depression, and Neurotransmission.