Cellular and Molecular Neurophysiology

5th Edition - May 30, 2024
Imprint: Academic Press
Author: Constance Hammond
Language: English
Hardback ISBN:
9 7 8 - 0 - 3 2 3 - 9 8 8 1 1 - 7
eBook ISBN:
9 7 8 - 0 - 3 2 3 - 9 8 6 1 3 - 7

Unveiling the latest research in neurophysiology, Cellular and Molecular Neurophysiology, Fifth Edition continues to stand as the only resource in the field. This book remains the… Read more

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Unveiling the latest research in neurophysiology, Cellular and Molecular Neurophysiology, Fifth Edition continues to stand as the only resource in the field. This book remains the standard for those who seek to explore the intricate molecular and cellular physiology of neurons and synapses.

Notably, this new edition delves even deeper into the molecular properties and functions of excitable cells, offering unparalleled insights. In this edition, there are two groundbreaking chapters. The first reviews metabotropic receptors for olfactory transduction, while the second presents cutting-edge techniques for neuroscience research. Hypothesis-driven rather than a dry presentation of facts, the content firmly based on numerous experiments performed by top experts in the field, teaches students how to build and conduct intelligent research experiments.

This book promotes a true understanding of nerve cell function and will be a useful resource for practicing neurophysiologists, neurobiologists, neurologists, and students in a graduate-level course on the topic alike.

Cover image
Title page
Table of Contents
Copyright
Dedication
Foreword
Acknowledgments
Section I. Neurons: Excitable and secretory cells that establish synapses
Chapter 1. Neurons
1.1. Neurons have a cell body from which emerge two types of processes: the dendrites and the axon
1.2. Neurons are highly polarized cells with a differential distribution of organelles and proteins
1.3. Neurons are categorized based on their molecular signature, morphology, connectivity and physiology
1.4. Axonal transport allows bidirectional communication between the cell body and the axon terminals
1.5. Neurons connected by synapses form networks or circuits
1.6. Summary: the neuron is an excitable and secretory cell presenting an extreme functional regionalization
Chapter 2. Neuron–glial cell cooperation
2.1. Astrocytes are in a unique position between blood vessels and synapses
2.2. Oligodendrocytes form the myelin sheaths of axons in the central nervous system and contribute to cellular and functional plasticity
2.3. Microglial cells
Chapter 3. Ionic gradients, membrane potential and ionic currents
3.1. There is an unequal distribution of ions across the neuronal plasma membrane. The notion of concentration gradient
3.2. There is a difference of potential between the two faces of the membrane, called membrane potential (Vm)
3.3. Concentration gradients and membrane potential determine the direction of the passive movements of ions through ionic channels: the Electrochemical gradient
3.4. The passive diffusion of ions through an open channel creates a current
3.5. A particular membrane potential, the resting membrane potential, Vrest
3.6. A simple equivalent electrical circuit for the membrane at rest
3.7. Summary
Appendix 3.1 The active transport of ions by pumps and transporters maintain the unequal distribution of ions (Fig. A3.1)
Appendix 3.2 The passive diffusion of ions through an open channel
Appendix 3.3 The Nernst equation
Chapter 4. The voltage-gated channels of Na+ action potentials
4.1. Properties of action potentials
4.2. The depolarization phase of Na+-dependent action potentials results from the transient entry of Na+ ions through voltage-gated Na+ channels
4.3. The Repolarization phase of the sodium-dependent action potential results from Na+ channel inactivation and partly from K+ channel activation
4.4. Sodium-dependent action potentials are initiated at the axon initial segment in response to a Membrane depolarization and then actively propagate along the axon
Chapter 5. The voltage-gated channels of Ca2+ action potentials: generalization
5.1. Properties of Ca2+-dependent action potentials
5.2. The transient entry of Ca2+ ions through voltage-gated Ca2+ channels is responsible for the depolarizing phase or the plateau phase of Ca2+-dependent action potentials
5.3. The repolarization phase of Ca2+-dependent action potentials results from the activation of K+ currents IK and IKCa
5.4. Calcium-dependent action potentials are initiated in axon terminals and in dendrites
5.5. A note on voltage-gated channels and action potentials
Chapter 6. The chemical synapses
6.1. The synaptic complex's three components: presynaptic element, synaptic cleft, and postsynaptic element
6.2. The interneuronal synapses of the central nervous system
6.3. The neuromuscular junction is the group of synaptic contacts between the terminal arborization of a motor axon and a striated muscle fiber
6.4. The synapse between the vegetative postganglionic neuron and the smooth muscle cell
6.5. Example of a neuroglandular synapse
6.6. Summary
Appendix 6.1 Neurotransmitters, agonists, and antagonists
Chapter 7. Neurotransmitter release
7.1. The concept of vesicular release. Observations and questions
7.2. The molecular machinery underlying the synaptic vesicle cycle
7.3. The regulation of the intracellular Ca2+ concentration at active zones
7.4. The different pools of synaptic vesicle
7.5. Pharmaclogy of neurotransmitter release
7.6. Summary
Appendix 7.1: Quantal nature of neurotransmitter release
Appendix 7.2: Methods of neurotransmitter release measurements
Appendix 7.3: Variance analysis and quantification of parameters of neurotransmitter release
Appendix 7.4: Lipids as novel actors in neurotransmitter release
Appendix 7.5: SNAREopathies
Section II. Ionotropic and metabotropic receptors in synaptic transmission
Chapter 8. The ionotropic nicotinic acetylcholine receptors
8.1. Observations
8.2. The torpedo or muscle nicotinic receptor of acetylcholine is a heterologous pentamer α2βγδ or α2βεδ
8.3. Binding of two acetylcholine molecules favors conformational change of the protein toward the open state of the cationic channel
8.4. The nicotinic receptor desensitizes
8.5. nAChR-mediated synaptic transmission at the neuromuscular junction
8.6. Nicotinic transmission pharmacology
8.7. Neuronal nicotinic receptors and interneuronal nicotinic synaptic transmission
8.8. Summary
Chapter 9. The ionotropic GABAA receptor
9.1. Observations and questions
9.2. GABAA receptors are hetero-oligomeric proteins with a structural heterogeneity
9.3. Binding of two GABA molecules leads to a conformational change of the GABAA receptor into an open state; the GABAA receptor desensitizes
9.4. Pharmacology of the GABAA receptor
9.5. GABAA receptor-mediated synaptic transmission
9.6. Summary
Appendix 9.1 Mean open time and mean burst duration of the GABAA single-channel current
Appendix 9.2 Noninvasive measurements of membrane potential and of the reversal potential of the GABAA current using cell-attached recordings of single channels
Chapter 10. The ionotropic glutamate receptors
10.1. There are three different types of ionotropic glutamate receptors. They have a common structure and all participate in fast glutamatergic synaptic transmission
10.2. AMPA receptors are an ensemble of cationic receptor-channels with different permeabilities to Ca2+ ions
10.3. Kainate receptors are an ensemble of cationic receptor channels with different permeabilities to Ca2+ ions
10.4. NMDA receptors are cationic-receptor-channels highly permeable to Ca2+ ions; they are blocked by Mg2+ ions at voltages close to the resting potential, which confers strong voltage dependence
10.5. Synaptic responses to glutamate are mediated by NMDA and nonNMDA receptors
10.6. Summary
Chapter 11. The metabotropic GABAB receptors
11.1. Introduction
11.2. GABAB receptors were originally discovered because of their insensitivity to bicuculline and their sensitivity to baclofen
11.3. Structure of the GABAB receptor
11.4. GABAB receptor pharmacology
11.5. Summary
11.6. GABAB receptors are G-protein-coupled to a variety of different effector mechanisms
11.7. Summary
11.8. The functional role of GABAB receptors in synaptic activity
11.9. Summary
Chapter 12. The metabotropic glutamate receptors
12.1. The identification of the metabotropic glutamate receptor subtypes
12.2. How do metabotropic glutamate receptors carry out their function? Structure–function studies of metabotropic glutamate receptors
12.3. How to identify selective compounds acting at the metabotropic glutamate receptor—toward the Development of new therapeutic drugs
12.4. What biochemical means do metabotropic glutamate receptors utilize to elicit physiological changes in the nervous system? Signal transduction studies of metabotropic glutamate receptors
12.5. How is the activity of metabotropic glutamate receptors modulated? Studies of mGluR desensitization
12.6. Metabotropic glutamate receptors modulate neuronal excitability
12.7. Metabotropic glutamate receptors mediate and modulate synaptic transmission
12.8. Pre- and postsynaptic functional assembly of metabotropic glutamate receptors
12.9. Physiological roles of metabotropic glutamate receptor—a study of knockout models
12.10. Summary
Chapter 13. The metabotropic olfactory receptors
13.1. General view on olfactory transduction
13.2. Odorants bind to specific odorant receptors
13.3. The second messenger cAMP opens a cyclic nucleotide gated channel and generates an inward cationic current
13.4. The third messenger, intracellular Ca2+ ions, activates a calcium-sensitive chloride channel and generates an inward chloride current
13.5. The transduction current is transient and shows adaptation
13.6. Coding of odorant concentration
13.7. Summary
Section III. Somato-dendritic processing and plasticity of postsynaptic potentials
Chapter 14. Somatodendritic processing of postsynaptic potentials I: passive properties of dendrites
14.1. Propagation of excitatory and inhibitory postsynaptic potentials through the dendritic arborization
14.2. Summation of excitatory and inhibitory postsynaptic potentials
14.3. Summary
Chapter 15. Subliminal voltage-gated currents of the somatodendritic membrane
15.1. Observations and questions
15.2. The subliminal voltage-gated currents that depolarize the membrane
15.3. The subliminal voltage-gated currents that hyperpolarize the membrane
15.4. General conclusion
Chapter 16. Somatodendritic processing of postsynaptic potentials II. Role of subthreshold voltage-gated currents
16.1. Persistent Na+ channels are present in the axosomatic region of neocortical neurons; INaP boosts EPSPs
16.2. T-type Ca2+ channels are present in the dendrites of cortical neurons; ICaT boosts EPSPs
16.3. The hyperpolarization-activated cationic channels are present in dendrites of cortical pyramidal neurons; Ih has a dual action on EPSPs
16.4. A-type K+ channels are present in the dendrites of hippocampal neurons; IA attenuates EPSPs
16.5. Functional consequences
16.6. Conclusions
Chapter 17. Somatodendritic processing of postsynaptic potentials III. Role of high-voltage–activated currents
17.1. High-voltage–activated Na+ and/or Ca2+ channels are present in the dendritic membrane of some CNS neurons, but are they distributed with comparable densities in soma and dendrites?
17.2. High-voltage–activated Ca2+ channels are present in the dendritic membrane of some CNS neurons, but are they distributed with comparable densities in soma and dendrites?
17.3. Functional consequences
17.4. Conclusions
Chapter 18. Firing patterns of neurons
18.1. Spiny projection neurons of the striatum
18.2. Inferior olivary cells
18.3. Purkinje cells of the cerebellar cortex
18.4. Thalamic and subthalamic neurons
18.5. Summary
Chapter 19. Synaptic plasticity
19.1. Short-term potentiation: example of the cholinergic synaptic response of muscle cell to motoneuron stimulation
19.2. Long-term potentiation: example of the glutamatergic synaptic response of pyramidal neurons of the CA1 region of the hippocampus to Schaffer collateral activation
19.3. Long-term depression: example of the glutamatergic synaptic response of Purkinje cells of the cerebellum to parallel fiber stimulation
19.4. Short- and long-term depression mediated by endogenous cannabinoids
19.5. Spike-timing-dependent plasticity, a long-term plasticity induced by relative timing between pre- and postsynaptic spikes
19.6. The homeostatic plasticity example of the synaptic scaling at the glutamatergic synapses of the neocortex
Section IV. The hippocampal network
Chapter 20. The adult hippocampal network
20.1. Observations and questions
20.2. The hippocampal circuitry
20.3. Activation of Interneurons evokes inhibitory gabaergic responses in postsynaptic pyramidal cells
20.4. Activation of Pyramidal neurons evokes excitatory glutamatergic responses in postsynaptic interneurons and in other pyramidal neurons (synchronization in CA3)
20.5. Oscillations in the hippocampal network: example of sharp waves and ripples
20.6. Coding properties of CA1 pyramidal neurons during spatial exploration
Chapter 21. Morphogenesis and maturation of the hippocampal network
21.1. Hippocampal circuits are sculpted by development
21.2. GABAergic neurons and synapses develop prior to glutamatergic ones
21.3. GABA receptors-mediated responses differ in developing and mature brain neurons
21.4. Maturation of coherent network activities
21.5. Concluding remarks
Chapter 22. Chapter techniques
22.1. Identification and localization of neurotransmitters and their receptors (Monique Esclapez)
22.2. Patch clamp recording techniques (Constance Hammond)
22.3. How to depolarize or hyperpolarize the recorded membrane?
22.4. Optogenetic or chemogenetic excitation or inhibition of tagged neurons in a network (Clement Menuet and Andrew Allen)
22.5. Imaging intracellular calcium changes (François Michel)
Index

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