Cellular and Molecular Neurophysiology Fourth Edition by Constance Hammond 0123973228 9780123973221

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