Elements of molecular neurobiology.

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Bibliographic Details
Author / Creator:Smith, C. U. M. (Christopher Upham Murray)
Edition:3rd ed.
Imprint:Chichester, West Sussex ; Hoboken, NJ : Wiley, c2002.
Description:xvi, 613 p. ; 26 cm.
Language:English
Subject:
Format: Print Book
URL for this record:http://pi.lib.uchicago.edu/1001/cat/bib/4776613
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ISBN:0470843535 (case)
0471560383 (paper)
Table of Contents:
  • Preface
  • Preface to the First Edition
  • Preface to the Second Edition
  • 1. Introductory Orientation
  • 1.1. Outline of Nervous Systems
  • 1.2. Vertebrate Nervous Systems
  • 1.3. Cells of the Nervous Systems
  • 1.3.1. Neurons
  • 1.3.2. Glia
  • 1.4. Organisation of Synapses
  • 1.5. Organisation of Neurons in the Brain
  • 2. The Conformation of Informational Macromolecules
  • 2.1. Proteins
  • 2.1.1. Primary Structure
  • 2.1.2. Secondary Structure
  • 2.1.3. Tertiary Structure
  • 2.1.4. Quaternary Structure
  • 2.1.5. Molecular Chaperones
  • 2.2. Nucleic Acids
  • 2.2.1. DNA
  • 2.2.2. RNA
  • 2.3. Conclusion
  • 3. Information Processing in Cells
  • 3.1. The Genetic Code
  • 3.2. Replication
  • 3.3. 'DNA Makes RNA and RNA Makes Protein'
  • 3.3.1. Transcription
  • 3.3.2. Post-transcriptional Processing
  • 3.3.3. Translation
  • Box 3.1. Antisense and triplex oligonucleotides
  • 3.4. Control of the Expression of Genetic Information
  • 3.4.1. Genomic Control
  • 3.4.2. Transcriptional Control
  • Box 3.2. Oncogenes, protooncogenes and IEGs
  • 3.4.3. Post-transcriptional Control
  • 3.4.4. Translational Control
  • 3.4.5. Post-translational Control
  • 3.5. Conclusion
  • 4. Molecular Evolution
  • 4.1. Mutation
  • 4.1.1. Point Mutations
  • 4.1.2. Proof-reading and Repair Mechanisms
  • 4.1.3. Chromosomal Mutations
  • 4.2. Protein Evolution
  • 4.2.1. Evolutionary Development of Protein Molecules and Phylogenetic Relationships
  • 4.2.2. Evolutionary Relationships of Different Proteins
  • 4.2.3. Evolution by Differential Post-transcriptional and Post-translational Processing: the Opioids and Other Neuroactive Peptides
  • 4.3. Conclusion
  • 5. Manipulating Biomolecules
  • 5.1. Restriction Endonucleases
  • 5.2. Separation of Restriction Fragments
  • 5.3. Restriction Maps
  • 5.4. Recombination
  • 5.5. Cloning
  • 5.5.1. Plasmids
  • 5.5.2. Phage
  • 5.5.3. Cosmids
  • 5.5.4. Bacterial Artificial Chromosomes (BACs)
  • 5.5.5. Yeast Artifical Chromosomes (YACs)
  • 5.6. Isolating Bacteria Containing Recombinant Plasmids or Phage
  • 5.7. The 'Shotgun' Construction of 'Genomic' Gene Libraries
  • 5.8. A Technique for Finding a Gene in the Library
  • 5.9. Construction of a 'cDNA' Gene Library
  • 5.10. Fishing for Genes in a cDNA Library
  • 5.11. Positional Cloning
  • 5.12. The Polymerase Chain Reaction (PCR)
  • 5.13. Sequence Analysis of DNA
  • 5.14. Prokaryotic Expression Vectors for Eukaryotic DNA
  • 5.15. Xenopus Oocyte as an Expression Vector for Membrane Proteins
  • 5.16. Site-directed Mutagenesis
  • 5.17. Gene Targeting and Knockout Genetics
  • 5.18. Targeted Gene Expression
  • 5.19. Hybridisation Histochemistry
  • 5.20. DNA Chips
  • 5.21. Conclusion
  • 6. Genomics
  • 6.1. Some History
  • 6.2. Methodology
  • 6.3. Salient Features of the Human Genome
  • 6.4. The Genes of Neuropathology
  • 6.5. Single Nucleotide Polymorphisms (SNPs)
  • 6.6. Other Genomes
  • 6.7. Conclusion
  • 7. Biomembranes
  • 7.1. Lipids
  • 7.1.1. Phospholipids
  • 7.1.2. Glycolipids
  • 7.1.3. Cholesterol
  • 7.2. Membrane Order and Fluidity
  • 7.3. Membrane Asymmetry
  • 7.4. Proteins
  • 7.5. Mobility of Membrane Proteins
  • 7.6. Synthesis of Biomembranes
  • 7.7. Myelin and Myelination
  • 7.8. The Submembranous Cytoskeleton
  • 7.9. Junctions Between Cells
  • 7.9.1. Tight Junctions
  • 7.9.2. Gap Junctions
  • 7.10. Gap Junctions and Neuropathology
  • 7.10.1. Deafness
  • 7.10.2. Cataract
  • 7.10.3. Charcot-Marie-Tooth (Type 2) Disease
  • 7.10.4. Spreading Hyperexcitability (Epilepsy) and Hypoexcitability (Spreading Depression)
  • 7.11. Conclusion and Forward Look
  • 8. G-protein-coupled Receptors
  • 8.1. Messengers and Receptors
  • 8.2. The 7TM Serpentine Receptors
  • 8.3. G-proteins
  • Box 8.1. The GTPase superfamily
  • 8.4. G-protein Collision-coupling Systems
  • 8.5. Effectors and Second Messengers
  • 8.5.1. Adenylyl Cyclases
  • 8.5.2. PIP[subscript 2]-phospholipase (Phospholipase C-[beta])
  • 8.6. Synaptic Significance of 'Collision-coupling' Systems
  • 8.7. Networks of G-protein Signalling Systems
  • 8.8. The Adrenergic Receptor (AR)
  • 8.9. The Muscarinic Acetylcholine Receptor (mAChR)
  • 8.10. Metabotropic Glutamate Receptors (mGluRs)
  • 8.11. Neurokinin Receptors (NKRs)
  • 8.12. Cannabinoid Receptors (CBRs)
  • 8.13. Rhodopsin
  • 8.14. Cone Opsins
  • 8.15. Conclusion
  • 9. Pumps
  • 9.1. Energetics
  • 9.2. The Na[superscript +] + K[superscript +] Pump
  • 9.3. The Calcium Pump
  • Box 9.1. Calmodulin
  • 9.4. Other Pumps and Transport Mechanisms
  • 9.5. Conclusion
  • 10. Ligand-gated Ion Channels
  • 10.1. The Nicotinic Acetylcholine Receptor
  • 10.1.1. Structure
  • 10.1.2. Function
  • 10.1.3. Development
  • 10.1.4. Pathologies
  • 10.1.5. CNS Acetylcholine Receptors
  • Box 10.1. Evolution of the nAChRs
  • 10.2. The GABA[subscript A] Receptor
  • 10.2.1. Pathology
  • 10.3. The Glycine Receptor
  • 10.4. Ionotropic Glutamate Receptors (iGluRs)
  • 10.4.1. AMPA Receptors
  • 10.4.2. KA Receptors
  • 10.4.3. NMDA Receptors
  • Box 10.2. The inositol triphosphate (IP[subscript 3] or InsP[subscript 3]) receptor
  • 10.5. Purinoceptors
  • 10.6. Conclusion
  • 11. Voltage-gated Channels
  • 11.1. The KcsA Channel
  • 11.2. Neuronal K[superscript +] Channels
  • 11.2.1. 2TM(1P) Channels; Kir Channels
  • 11.2.2. 4TM(2P) Channels; K[superscript +] Leak Channels
  • 11.2.3. 6TM(1P) Channels; K[subscript v] Channels
  • Box 11.1. Cyclic nucleotide-gated (CNG) channels
  • 11.3. Ca[superscript 2+] Channels
  • 11.3.1. Structure
  • 11.3.2. Diversity
  • 11.3.3. Biophysics
  • 11.4. Na[superscript +] Channels
  • 11.4.1. Structure
  • 11.4.2. Diversity
  • 11.4.3. Biophysics
  • 11.5. Ion Selectivity and Voltage Sensitivity
  • 11.5.1. Ion Selectivity
  • 11.5.2. Voltage Sensitivity
  • 11.6. Voltage-Sensitive Chloride Channels
  • 11.6.1. ClC Channels
  • 11.6.2. Cln Channels
  • 11.6.3. Phospholemman
  • 11.7. Channelopathies
  • 11.7.1. Potassium Channels
  • 11.7.2. Calcium Channels
  • 11.7.3. Sodium Channels
  • 11.7.4. Chloride Channels
  • 11.8. Evolution of Ion Channels
  • 11.9. Conclusion and Forward Look
  • 12. Resting Potentials and Cable Conduction
  • 12.1. Measurement of the Resting Potential
  • 12.2. The Origin of the Resting Potential
  • 12.3. Electrotonic Potentials and Cable Conduction
  • 12.3.1. Length
  • 12.3.2. Diameter
  • 12.4. Conclusion
  • 13. Sensory Transduction
  • 13.1. Chemoreceptors
  • 13.1.1. Chemosensitivity in Prokaryocytes
  • 13.1.2. Chemosensitivity in Vertebrates
  • 13.2. Photoreceptors
  • Box 13.1. Retinitis pigmentosa
  • 13.3. Mechanoreceptors
  • 13.3.1. A Prokaryote Mechanoreceptor
  • 13.3.2. Mechanosensitivity in Caenorhabditis elegans
  • 13.3.3. Mechanosensitivity in Vertebrates: Hair Cells
  • 13.4. Conclusion
  • 14. The Action Potential
  • 14.1. Voltage-clamp Analyses
  • 14.2. Patch-clamp Analyses
  • 14.3. Propagation of the Action Potential
  • Box 14.1. Early history of the impulse
  • 14.4. Initiation of the Impulse
  • Box 14.2. Switching off neurons by manipulating K[superscript +] channels
  • 14.5. Rate of Propagation
  • 14.6. Conclusion
  • 15. The Neuron as a Secretory Cell
  • 15.1. Neurons and Secretions
  • 15.2. Synthesis in the Perikaryon
  • 15.2.1. Co-translational Insertion
  • 15.2.2. The Golgi Body and Post-translational Modification
  • 15.3. Transport Along the Axon
  • 15.3.1. Microfilaments
  • 15.3.2. Intermediate Filaments (IFs)
  • Box 15.1. Subcellular geography of protein biosynthesis in neurons
  • 15.3.3. Microtubules (MTs)
  • 15.3.4. The Axonal Cytoskeleton
  • 15.3.5. Axoplasmic Transport Summarised
  • 15.4. Exocytosis and Endocytosis at the Synaptic Terminal
  • 15.4.1. Vesicle Mustering
  • 15.4.2. The Ca[superscript 2+] Trigger
  • 15.4.3. Vesicle Docking
  • 15.4.4. Transmitter Release
  • 15.4.5. Dissociation of Fusion Complex and Retrieval and Reconstitution of Vesicle Membrane
  • 15.4.6. Refilling of Vesicle
  • Box 15.2. Vesicular neurotransmitter transporters
  • 15.4.7. Termination of Transmitter Release
  • 15.4.8. Modulation of Release
  • 15.5. Conclusion
  • 16. Neurotransmitters and Neuromodulators
  • 16.1. Acetylcholine
  • Box 16.1. Criteria for neurotransmitters
  • 16.2. Amino Acids
  • 16.2.1. Excitatory Amino Acids (EAAs): Glutamic Acid and Aspartic Acid
  • 16.2.2. Inhibitory Amino Acids (IAAs): [gamma]-Aminobutyric Acid and Glycine
  • Box 16.2. Otto Loewi and vagusstoff
  • 16.3. Serotonin (=5-Hydroxytryptamine, 5-HT)
  • 16.4. Catecholamines
  • 16.4.1. Dopamine (DA)
  • 16.4.2. Noradrenaline (=Norepinephrine, NE)
  • 16.5. Purines
  • 16.6. Cannabinoids
  • Box 16.3. Reuptake neurotransmitter transporters
  • 16.7. Peptides
  • 16.7.1. Substance P
  • 16.7.2. Enkephalins
  • 16.8. Cohabitation of Peptides and Non-peptides
  • 16.9. Nitric Oxide (NO)
  • 16.10. Conclusion
  • 17. The Postsynaptic Cell
  • 17.1. Synaptosomes
  • 17.2. The Postsynaptic Density
  • 17.3. Electrophysiology of the Postsynaptic Membrane
  • 17.3.1. The Excitatory Synapse
  • Box 17.1. Cajal, Sherrington and the beginnings of synaptology
  • 17.3.2. The Inhibitory Synapse
  • 17.3.3. Interaction of EPSPs and IPSPs
  • 17.4. Ion Channels in the Postsynaptic Membrane
  • 17.5. Second Messenger Control of Ion Channels
  • 17.6. Second Messenger Control of Gene Expression
  • 17.7. The Pinealocyte
  • 17.8. Conclusion and Forward Look
  • 18. Developmental Genetics of the Brain
  • 18.1. Introduction: 'Ontology Recapitulates Phylogeny'
  • 18.2. Establishing an Anteroposterior (A-P) Axis in Drosophila
  • 18.3. Initial Subdivision of the Drosophila Embryo
  • 18.4. The A-P Axis in Vertebrate Central Nervous Systems
  • 18.5. Segmentation Genes in Mus musculus
  • 18.6. Homeosis and Homeotic Mutations
  • 18.7. Homeobox Genes
  • 18.8. Homeobox Genes and the Early Development of the Brain
  • 18.9. POU Genes and Neuronal Differentiation
  • 18.10. Sequential Expression Of Transcription Factors in Drosophila CNS
  • 18.11. Pax-6: Developmental Genetics of Eyes and Olfactory Systems
  • 18.12. Other Genes Involved in Neuronal Differentiation
  • 18.13. Conclusion
  • 19. Epigenetics of the Brain
  • 19.1. The Origins of Neurons and Glia
  • 19.2. Neural Stem Cells
  • 19.3. Tracing Neuronal Lineages
  • 19.3.1. Retrovirus Tagging
  • 19.3.2. Enhancer Trapping
  • 19.4. Morphogenesis of Neurons
  • 19.5. Morphogenesis of the Drosophila Compound Eye
  • 19.6. Growth Cones
  • 19.7. Pathfinding
  • Box 19.1. Eph receptors and ephrins
  • 19.8. Cell Adhesion Molecules (CAMs)
  • 19.9. Growth Factors and Differential Survival
  • Box 19.2. Neurotransmitters as growth factors
  • 19.10. Morphopoietic Fields
  • 19.11. Functional Sculpting
  • 19.12. Conclusion
  • 20. Memory
  • 20.1. Some Definitions
  • 20.1.1. Classical Conditioning
  • 20.1.2. Operant Conditioning
  • 20.2. Short- and Long-term Memory
  • 20.2.1. Relation Between STM and LTM
  • 20.3. Where is the Memory Trace Located?
  • 20.4. Invertebrate Systems
  • 20.4.1. Thermal Conditioning in C. elegans
  • 20.4.2. Drosophila
  • 20.4.3. Aplysia and the Molecular Biology of Memory
  • 20.5. The Memory Trace in Mammals
  • 20.5.1. Post-tetanic Potentiation and Long-term Potentiation
  • 20.5.2. Fibre Pathways in the Hippocampus
  • 20.5.3. Perforant and Schaffer Collateral Fibres
  • 20.5.4. The CRE Site Again
  • 20.5.5. Mossy Fibre Pathway
  • 20.5.6. Histology
  • 20.5.7. Non-genomic Mechanisms
  • Box 20.1. Dendritic spines
  • 20.6. Conclusion
  • 21. Some Pathologies
  • 21.1. Neuroses, Psychoses and the Mind/Brain Dichotomy
  • 21.2. Prions and Prion Diseases
  • 21.3. Phenylketonuria (PKU)
  • 21.4. Fragile X Syndrome (FraX)
  • 21.5. Neurofibromatoses
  • 21.6. Motor Neuron Disease (MND)
  • 21.7. Huntington's Disease (=Chorea) (HD)
  • 21.8. Depression
  • 21.8.1. Endogenous Depression
  • 21.8.2. Exogenous Depression
  • 21.8.3. Neurochemistry of Depression
  • 21.8.4. Stress and Depression
  • 21.9. Parkinson's Disease (PD)
  • Box 21.1. [alpha]-Synuclein
  • 21.10. Alzheimer's Disease (AD)
  • 21.10.1. Diagnosis
  • 21.10.2. Aetiology
  • 21.10.3. Molecular Pathology
  • 21.10.4. Environmental Influences: Aluminium
  • 21.10.5. The BAPtist Proposal: an Amyloid Cascade Hypothesis
  • 21.10.6. Therapy
  • 21.11. Conclusion
  • Appendix 1. Molecules and Consciousness
  • Appendix 2. Units
  • Appendix 3. Data
  • Appendix 4. Genes
  • Appendix 5. Physical Models of Ion Conduction and Gating
  • Acronyms and Abbreviations
  • Glossary
  • Bibliography
  • Index of Neurological Disease
  • Index