Cellular and Molecular Neurophysiology - 4th Edition - ISBN: 9780123970329, 9780123973221

Cellular and Molecular Neurophysiology

4th Edition

Authors: Constance Hammond
eBook ISBN: 9780123973221
Hardcover ISBN: 9780123970329
Imprint: Academic Press
Published Date: 2nd January 2015
Page Count: 444
Sales tax will be calculated at check-out Price includes VAT/GST
Price includes VAT/GST

Institutional Subscription

Secure Checkout

Personal information is secured with SSL technology.

Free Shipping

Free global shipping
No minimum order.


Cellular and Molecular Neurophysiology, Fourth Edition, is the only up-to-date textbook on the market that focuses on the molecular and cellular physiology of neurons and synapses. Hypothesis-driven rather than a dry presentation of the facts, the book promotes a real understanding of the function of nerve cells that is useful for practicing neurophysiologists and students in a graduate-level course on the topic alike.

This new edition explains the molecular properties and functions of excitable cells in detail and teaches students how to construct and conduct intelligent research experiments. The content is firmly based on numerous experiments performed by top experts in the field

This book will be a useful resource for neurophysiologists, neurobiologists, neurologists, and students taking graduate-level courses on neurophysiology.

Key Features

  • 70% new or updated material in full color throughout, with more than 350 carefully selected and constructed illustrations
  • Fifteen appendices describing neurobiological techniques are interspersed in the text


Neurophysiologists, neurobiologists, and neurologists as well as graduate-level courses on neurophysiology.

Table of Contents

  • Foreword
  • Acknowledgments
  • I: Neurons: excitable and secretory cells that establish synapses
    • Chapter 1: Neurons
      • Abstract
      • 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. Axonal transport allows bidirectional communication between the cell body and the axon terminals
      • 1.4. Neurons connected by synapses form networks or circuits
      • 1.5. Summary: the neuron is an excitable and secretory cell presenting an extreme functional regionalization
    • Chapter 2: Neuron–glial cell cooperation
      • Abstract
      • 2.1. Astrocytes form a vast cellular network or syncytium between neurons, blood vessels and the surface of the brain
      • 2.2. Oligodendrocytes form the myelin sheaths of axons in the central nervous system and allow the clustering of Na+ channels at nodes of Ranvier
      • 2.3. Microglial cells are the macrophages of the central nervous system
      • 2.4. Schwann cells are the glial cells of the peripheral nervous system; they form the myelin sheath of axons or encapsulate neurons
    • Chapter 3: Ionic gradients, membrane potential and ionic currents
      • Abstract
      • 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. How to experimentally change Vrest
      • 3.8. Summary
      • Appendix 3.1. The active transport of ions by pumps and transporters maintain the unequal distribution of ions
      • 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
      • Abstract
      • 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
      • Abstract
      • 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
      • Abstract
      • 6.1. The synaptic complex’s three components: presynaptic element, synaptic cleft and postsynaptic element
      • 6.2. The interneuronal synapses
      • 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
    • Chapter 7: Neurotransmitter release
      • Abstract
      • 7.1. Observations and questions
      • 7.2. Presynaptic processes I: from presynaptic spike to [Ca2+]i increase
      • 7.3. Presynaptic processes II: from [Ca2+] increase to synaptic vesicle fusion
      • 7.4. Processes in the synaptic cleft: from transmitter release in the cleft to transmitter clearance from the cleft
      • 7.5. Summary (Figures 7.16 and  7.17)
  • II: Ionotropic and metabotropic receptors in synaptic transmission
    • Chapter 8: The ionotropic nicotinic acetylcholine receptors
      • Abstract
      • 8.1. Observations
      • 8.2. The torpedo or muscle nicotinic receptor of acetylcholine is a heterologous pentamer α2βγδ
      • 8.3. Binding of two acetylcholine molecules favors conformational change of the protein towards 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. Summary
    • Chapter 9: The ionotropic GABAA receptor
      • Abstract
      • 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-mediated synaptic transmission
      • 9.6. Summary
    • Chapter 10: The ionotropic glutamate receptors
      • Abstract
      • 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 non-NMDA receptors
      • 10.6. Summary
    • Chapter 11: The metabotropic GABAB receptors
      • Abstract
      • 11.1. GABAB receptors were originally discovered because of their insensitivity to bicuculline and their sensitivity to baclofen
      • 11.2. Structure of the GABAB receptor
      • 11.3. Summary
      • 11.4. GABAB receptors are G-protein coupled to a variety of different effector mechanisms
      • 11.5. Summary
      • 11.6. The functional role of GABAB receptors in synaptic activity
      • 11.7. Summary
    • Chapter 12: The metabotropic glutamate receptors
      • Abstract
      • 12.1. The identification of the eight 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 – towards 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
  • III: Somato-dendritic processing and plasticity of postsynaptic potentials
    • Chapter 13: Somato-dendritic processing of postsynaptic potentials I: Passive properties of dendrites
      • Abstract
      • 13.1. Propagation of excitatory and inhibitory postsynaptic potentials through the dendritic arborization
      • 13.2. Summation of excitatory and inhibitory postsynaptic potentials
      • 13.3. Summary
    • Chapter 14: Subliminal voltage-gated currents of the somato-dendritic membrane
      • Abstract
      • 14.1. Observations and questions
      • 14.2. The subliminal voltage-gated currents that depolarize the membrane
      • 14.3. The subliminal voltage-gated currents that hyperpolarize the membrane
      • 14.4. Conclusions
    • Chapter 15: Somato-dendritic processing of postsynaptic potentials II. Role of sub-threshold depolarizing voltage-gated currents
      • Abstract
      • 15.1. Persistent Na+ channels are present in the axo-somatic region of neocortical neurons; INaP boosts EPSPs
      • 15.2. T-type Ca2+ channels are present in the dendrites of cortical neurons; ICaT boosts EPSPs
      • 15.3. The hyperpolarization-activated cationic current Ih is present in dendrites of hippocampal pyramidal neurons; Ih attenuates EPSPs
      • 15.4. A-type K+ channels are present in the dendrites of hippocampal neurons; IA attenuates EPSPs
      • 15.5. Functional consequences
      • 15.6. Conclusions
    • Chapter 16: Somato-dendritic processing of postsynaptic potentials III. Role of high-voltage-activated depolarizing currents
      • Abstract
      • 16.1. 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?
      • 16.2. 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?
      • 16.3. Functional consequences
      • 16.4. Conclusions
    • Chapter 17: Firing patterns of neurons
      • Abstract
      • 17.1. Medium spiny projection neurons of the striatum
      • 17.2. Inferior olivary cells
      • 17.3. Purkinje cells are pacemaker neurons that respond by a complex spike followed by a period of silence
      • 17.4. Thalamic and subthalamic neurons
    • Chapter 18: Synaptic plasticity
      • Abstract
      • 18.1. Short-term potentiation (STP) of a cholinergic synaptic response as an example of short-term plasticity: the cholinergic response of muscle cells to motoneuron stimulation
      • 18.2. Long-term potentiation (LTP) of a glutamatergic synaptic response: example of the glutamatergic synaptic response of pyramidal neurons of the CA1 region of the hippocampus to Schaffer collateral activation
      • 18.3. The long-term depression (LTD) of a glutamatergic response: example of the response of Purkinje cells of the cerebellum to parallel fiber stimulation
      • 18.4. Long-term synaptic modification induced by relative timing between pre- and postsynaptic activity: spike-timing-dependent plasticity (STDP)
      • 18.5. The homeostatic plasticity of a glutamatergic response: example of the synaptic scaling at neocortical gluTaMatergic synapses
  • IV: The hippocampal network
    • Chapter 19: The adult hippocampal network
      • Abstract
      • 19.1. Observations and questions
      • 19.2. The hippocampal circuitry
      • 19.3. Activation of interneurons evokes inhibitory GABAergic responses in postsynaptic pyramidal cells
      • 19.4. Activation of principal cells evokes excitatory glutamatergic responses in postsynaptic interneurons and other principal cells (synchronization in CA3)
      • 19.5. Oscillations in the hippocampal network: example of sharp waves (SPW)
      • 19.6. Summary
    • Chapter 20: Maturation of the hippocampal network
      • Abstract
      • 20.1. GABAergic neurons and GABAergic synapses develop prior to glutamatergic ones
      • 20.2. GABAA receptor-mediated responses differ in developing and mature brains
      • 20.3. Maturation of coherent networks activities
      • 20.4. Conclusions
  • Contributors
  • Index


No. of pages:
© Academic Press 2015
Academic Press
eBook ISBN:
Hardcover ISBN:

About the Author

Constance Hammond

Constance Hammond

Constance Hammond is an INSERM director of research at the Mediterranean Institute of Neurobiology. A renowned Parkinson's disease investigator, in 2012 she became a Chevalier of the Légion d'Honneur in recognition for her services to scientific communication. Studying biology at the University of Pierre and Marie Curie and the Ecole Normale Supérieure in Paris she completed her thesis in neurosciences at the Marey Institute in Paris, directed by Prof. D. Albe-Fessard. Guided by her curiosity and her constant desire to learn, she changed lab and research domains several times. With the knowledge of other systems and the mastering of other techniques she finally came back to her first and preferred subject of research; the role of the subthalamic nucleus in the basal ganglia system in health and Parkinson's disease.

After many years of lecturing neurobiology to biology and psychology students it became apparent that students were in need of a book to help understand the basic principles of cell electrophysiology. Discussions with Philippe Ascher convinced her that the best way to approach the subject was to explain ionic currents and potential changes in terms of single channels and unitary currents, describing pioneering neurobiological experiments. This first book "Neurobiologie Cellulaire" (written in French with her colleague Danièle Tritsch) appeared in 1990. Its immediate success inspired her to completely revise the book content and publish it in English giving it to a larger audience; Appearing in 1996 the fist edition of "Cellular and Molecular Neuroscience" was born.

Affiliations and Expertise

Director of Research INSERM U901, Institut de Neurobiologie de la Méditerranée, Marseilles, France


"This is an excellent work on the cellular and molecular physiology of nerve cells. I would highly recommend it for universities, neuroscience libraries, and physiology departments. Score: 100 - 5 Stars"--Doody's, Cellular and Molecular Neurophysiology, Fourth Edition

Reviews for the previous edition:

"In its third internationally acclaimed edition, this textbook provides an unrivaled account of the basic foundations of molecular and cellular neurophysiology. For those of us who were inclined to believe that the unprecedented development of neuroscience made neurophysiology disposable, Constance Hammond proves us with conviction and elegance that this is just not the case!"--Dr. Robert Dantzer, Professor of Psychoneuroimmunology, Integrative Immunology and Behavior Program University of Illinois at Urbana-Champaign
"More than any similar volume that I have come across in recent years, this one has the potential of luring students of neuroscience and even students from other fields to build a career in neurophysiology."--György Buzsáki, M.D., Ph.D., Board of Governors Professor, Center for Molecular and Behavioral Neuroscience, Rutgers University

Ratings and Reviews