Cellular and molecular neurobiology:
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
San Diego [u.a.]
Acad. Press
2001
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| Ausgabe: | 2. ed. |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XXIII, 493 S. Ill., graph. Darst. 1 CD-ROM |
| ISBN: | 0123116252 |
Internformat
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| 245 | 1 | 0 | |a Cellular and molecular neurobiology |c C. Hammond |
| 250 | |a 2. ed. | ||
| 264 | 1 | |a San Diego [u.a.] |b Acad. Press |c 2001 | |
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| 650 | 7 | |a Neurobiologie |2 ram | |
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| 650 | 4 | |a Neurobiology | |
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Datensatz im Suchindex
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Contents
Contributors xxii
Acknowledgements xxiv
PART 1 Neurons: Excitable and Secretory Cells that Establish Synapses
Chapter 1 Neurons
C. Hammond
1.1 Neurons have a cell body from which emerge two types of processes: the dendrites and
the axon 3
1.1.1 The somatodendritic tree is the neuron's receptive pole 3
1.1.2 The axon and its collaterals are the neuron's transmitter pole 5
1.2 Neurons are highly polarized cells with a differential distribution of organelles and
proteins 7
1.2.1 The soma is the main site of macromolecule synthesis 7
1.2.2 The dendrites contain free ribosomes and synthesize some of their proteins. 9
1.2.3 The axon, to a large extent, lacks the machinery for protein synthesis 11
1.3 Axonal transport allows bidirectional communication between the cell body and the axon
terminals 11
1.3.1 Demonstration of axonal transport 11
1.3.2 Fast anterograde axonal transport is responsible for the movement of membranous
organelles from cell body towards axon terminals, and allows renewal of axonal proteins 12
1.3.3 Retrograde axonal transport is responsible for the movement of membranous organelles
back from axon terminals to the cell body 15
1.3.4 Slow anterograde axonal transport moves cytoskeletal proteins and cytosoluble proteins 16
1.3.5 Axonal transport of mitochondria allows the turnover of mitochondria in axons and axon
terminals 17
1.4 Neurons connected by synapses form networks or circuits 17
1.4.1 The circuit of the withdrawal medullary reflex 17
1.4.2 The spinothalamic tract or anterolateral pathway is a somatosensory pathway 18
1.5 Summary: the neuron is an excitable and secretory cell presenting an extreme functional
regionalization 18
Appendix 1.1 The cytoskeletal elements in neurons 21
Further reading 22
Chapter 2 Neuron Glial Cell Cooperation
C. Hammond ]
2.1 Astrocytes form a vast cellular network or syncytium between neurons, blood vessels and
the surface of the brain 24
2.1.1 Astrocytes are star shaped cells characterized by the presence of glial filaments in their
cytoplasm 24 ;
2.1.2 Astrocytes maintain the blood brain barrier in the adult brain 25
2.1.3 Astrocytes regulate the ionic composition of the extracellular fluid 26
2.1.4 Astrocytes take part in the neurotransmitter cycle 26
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 26
2.2.1 Processes of interfascicular oligodendrocytes electrically isolate segments of central axons
by forming the lipid rich myelin sheath 27
2.2.2 Myelination enables rapid conduction of action potentials for two reasons 29
2.3 Microglia: ramified microglial cells represent the quiescent form of microglial cells in the
central nervous system; they transform upon injury 30
2.3.1 Ramified microglial cells have long meandering processes 30
2.3.2 Do adult microglial cells play a role in immune processes? 31
2.4 Ependymal cells constitute an active barrier between blood and cerebrospinal fluid 31
2.4.1 Ependymal cells form an epithelium at the surface of the ventricles 31
2.4.2 Ependymal cells of the choroid plexus 31
2.4.3 Extrachoroidal ependymal cells 32
2.5 Schwann cells are the glial cells of the peripheral nervous system; they form the myelin
sheath of axons or encapsulate neurons 33
2.5.1 Myelinating Schwann cells make the myelin sheath of peripheral axons 33
2.5.2 Non myelinating Schwann cells encapsulate the axons and cell bodies of peripheral
neurons 33
Further reading 33
Chapter 3 Ionic Fluxes Across the Neuronal Plasma Membrane
C. Hammond
3.1 Observation and questions 36
3.1.1 There is an unequal distribution of ions across neuronal plasma membrane 36
3.1.2 Neuronal plasma membrane is permeable to ions, allowing both passive and active
transport of ions 37
3.1.3 There is a difference of potential between the two faces of the membrane, called membrane
potential 37
3.1.4 Questions 38
3.2 Na+, K+, Ca2+ and Cl" ions passively cross the plasma membrane through transmembrane
proteins the channels 39
3.2.1 Channels are a particular class of transmembrane proteins 39
3.2.2 Voltage gated channels open in response to a change in membrane potential 40
3.2.3 Ligand gated channels opened by extracellular ligands, and receptor channels opened by
neurotransmitters 41
3.2.4 Ligand gated channels opened by intracellular ligands 41
3.2.5 Mechanically gated channels opened by mechanical stimuli 43
3.2.6 Other channels: junctional channels or gap junctions 43
3.2.7 Distribution of the various channels in the neuronal plasma membrane 44
3.3 The diffusion of ions through an open channel: What is an electrochemical gradient and
an ionic current? 47
3.3.1 The structure of the channel pore determines the type of ion(s) that diffuse passively
through the channel 47
3.3.2 The electrochemical gradient for a particular ion determines the direction of the passive
diffusion of this ion through an open channel 48
3.3.3 The passive diffusion of ions through an open channel is a current 50
3.4 Active transport of Na+, K+, Ca2+ and Cl~ ions by pumps and transporters maintain the
unequal distribution of ions 52
3.4.1 Pumps are ATPases that actively transport ions 52
3.4.2 Transporters use the energy stored in the transmembrane electrochemical gradient of
Na+ or other ions H+ 52
3.5 Summary 53
Appendix 3.1 Hydrophobicity profile of a transmembrane protein 54
Appendix 3.2 The Nernst equation 55
Further reading 56
Chapter 4 Basic Properties of Excitable Cells at Rest
A. Nistri and A. Gutman
4.1 Ionic channels open at rest determine the resting membrane potential 57
4.1.1 The plasma membrane separates two media of different ionic composition 58
4.1.2 At rest most of the channels open are K+channels 58
4.1.3 In muscle cells, K+ and Cl~ ion movements participate equally in resting membrane
potential 59
4.1.4 In central neurons, K+, Cl~ and Na+ ion movements participate in resting membrane
potential: the Goldman Hodgkin Katz equation 60
4.1.5 Some principles related to the derivation of the GHK equation 61
4.2 Membrane pumps are responsible for keeping constant the concentration gradients across
membranes 61
4.3 A simple equivalent electrical circuit for resting membrane properties 62
4.3.1 Membrane potential has an ohmic behaviour at rest 62
4.3.2 Stability, bistability and instability of resting membrane potential 64
4.3.3 An electrical model of resting membrane potential 64
4.4 Advantages and disadvantages of sharp (intracellular) versus patch electrodes for measuring
the resting membrane potential 65
I
4.5 Background currents which flow through voltage gated channels open at resting membrane
potential also participate in Vrest 67
Further reading 67
Chapter 5 The Voltage Gated Channels of Na+Action Potentials
C. Hammond
5.1 Properties of action potentials 69
5.1.1 The different types of action potentials 69
5.1.2 Na+ and K+ ions participate in the action potential of axons 69
5.1.3 Na+ dependent action potentials are all or none and propagate along the axon with the
same amplitude 71
5.1.4 Questions about the Na+ dependent action potential 71
5.2 The depolarization phase of Na+ dependent action potentials results from the transient
entry of Na+ ions through voltage gated Na+ channels 71
5.2.1 The Na+ channel consists of a principal large oc subunit with four internal homologous
repeats and auxiliary P subunits 71
5.2.2 Membrane depolarization favours conformational change of the Na+ channel towards
the open state; the Na+ channel then quickly inactivates 74
5.2.3 The time during which the Na+ channel stays open varies around an average value, to,
called the mean open time ^^
5.2.4 The iNa—V relation is linear: the Na+ channel has a constant unitary conductance yNa 77
5.2.5 The probability of the Na+ channel being in the open state increases with depolarization
to a maximal level 77
5.2.6 The macroscopic Na+ current (7Na) has a steep voltage dependence of activation and
inactivates within a few milliseconds 80
5.2.7 Segment S4, the region between segments S5 and S6, and the region between domains III
and IV play a significant role in activation, ion permeation and inactivation, respectively 83
5.2.8 Conclusion: the consequence of the opening of a population of N Na+ channels is a transient
entry of Na+ ions which depolarizes the membrane above 0 mV 87
5.3 The repolarization phase of the sodium dependent action potential results from Na+ channel
inactivation and partly from K+ channel activation 87
5.3.1 The K+ channel consists of an cc subunit with a single repeat and auxiliary P subunits 87
5.3.2 Membrane depolarization favours the conformational change of the delayed rectifier channel
towards the open state 88
5.3.3 The open probability of the delayed rectifier channel is stable during a depolarization in the
range of seconds 89
5.3.4 The K+ channel has a constant unitary conductance yK 91
5.3.5 The macroscopic delayed rectifier K+ current (/K) has a delayed voltage dependence of
activation and inactivates within tens of seconds 92
5.3.6 Conclusion: during an action potential the consequence of the delayed opening of K+
channels is an exit of K+ ions which repolarizes the membrane to resting potential 93
5.4 Sodium dependent action potentials are initiated at the axon initial segment in response to
a membrane depolarization and then actively propagate along the axon 94
5.4.1 Summary of the Na+ dependent action potential 95
5.4.2 Depolarization of the membrane to the threshold for voltage gated Na+ channel activation
has two origins 95
5.4.3 The site of initiation of Na+ dependent action potentials is the axon initial segment 96
5.4.4 The Na+ dependent action potential actively propagates along the axon to axon terminals 97
5.4.5 Do the Na+ and K+ concentrations change in the extracellular or intracellular media during
firing? 97
5.4.6 The role of the Na+ dependent action potential is to evoke neurotransmitter release 99
5.4.7 Characteristics of the Na+ dependent action potential are explained by the properties of the
voltage gated Na+ channel 99
Appendix 5.1 Current clamp recording 99
Appendix 5.2 Voltage clamp recording 101
Appendix 5.3 Patch clamp recording 102
A5.3.1 The various patch clamp recording configurations 103
A5.3.2 Principles of the patch clamp recording technique 105
A5.3.3 The unitary current i is a rectangular step of current 107
A5.3.4 Determination of the conductance of a channel 107
A5.3.5 Mean open time of a channel 108
Further reading 109
Chapter 6 The Voltage Gated Channels of Ca2+ Action Potentials: Generalization
C. Hammond
6.1 Properties of Ca2+ dependent action potentials 111
6.1.1 Ca2+ and K+ ions participate in the action potential of endocrine cells 111
6.1.2 Questions about the Ca2+ dependent action potential 111
6.2 The depolarizing or plateau phase of Ca2+ dependent action potentials results from the
transient entry of Ca2+ ions through voltage gated Ca2+ channels 112
6.2.1 The voltage gated Ca2+ channels are a diverse group of multisubunit proteins 113
6.2.2 The L, N and P type Ca2+ channels open at membrane potentials positive to 20 mV; they
are high threshold Ca2+ channels 115
6.2.3 Macroscopic L, N and P type Ca2+ currents activate at a high threshold and inactivate with
different time courses 118
6.3 The repolarization phase of Ca2+ dependent action potentials results from the activation
of K+ currents JK and JK(Ca) 123
6.3.1 The Ca2+ activated K+ currents are classified as big K (BK) channels and small K (SK)
channels 124
6.3.2 Ca2+ entering during the depolarization or the plateau phase of Ca2+ dependent action
potentials activates K(Ca) channels 126
6.4 Calcium dependent action potentials are initiated in axon terminals or in dendrites 128
6.4.1 Depolarization of the membrane to the threshold for the activation of L , N and P type
Ca+ channels has two origins 128
6.4.2 The role of the calcium dependent action potentials is to provide a local and transient
increase of [Ca2+]j to trigger secretion, contraction and other Ca2+ gated processes 130
6.5 A note on voltage gated channels and action potentials 131
Appendix 6.1 Fluorescence measurements of intracellular Ca2+ concentration 131
Y. Tan A6.1.1 The interaction of light with matter 131 I
A6.1.2 The return from the excited state 133 :
A6.1.3 Fluorescence measurements: general points 134
A6.1.4 Fluorescence imaging hardware 135
A6.1.5 Methods of calcium measurement by fluorescence 135
A6.1.6 Two photon absorption 137
A6.1.7 Measurement of other ions by fluorescence techniques 138
Appendix 6.2 Tail currents 139
Further reading 140
Chapter 7 The Chemical Synapses
C. Hammond
7.1 The synaptic complex's three components: presynaptic element, synaptic cleft and
postsynaptic element 142
7.1.1 The pre and postsynaptic elements are morphologically and functionally specialized 142
7.1.2 General functional model of the synaptic complex 144
7.1.3 Complementarity between the neurotransmitter stored and released by the presynaptic
element and the nature of receptors in the postsynaptic membrane 146
7.2 The interneuronal synapses 149
7.2.1 In the CNS the most common synapses are those where an axon terminal is the presynaptic
element 149
7.2.2 At low magnification, the axo dendritic synaptic contacts display features implying various
functions 149
7.2.3 Interneuronal synapses display ultrastructural characteristics that vary between two
extremes: types 1 and 2. 150
7.3 The neuromuscular junction is the group of synaptic contacts between the terminal
arborization of a motor axon and a striated muscle fibre 152
7.3.1 In the axon terminals, the synaptic vesicles are concentrated at the level of the electron
dense bars; they contain acetylcholine 153
7.3.2 The synaptic cleft is narrow and occupied by a basal lamina which contains
acetylcholinesterase 153
7.3.3 Nicotinic receptors for acetylcholine are abundant in the crests of the folds in the
postsynaptic membrane 155
7.3.4 Mechanisms involved in the accumulation of postsynaptic receptors in the folds of the
postsynaptic muscular membrane 155
7.4 The synapse between the vegetative postganglionic neuron and the smooth muscle cell 156
7.4.1 The presynaptic element is a varicosity of the postganglionic axon 156
7.4.2 The width of the synaptic cleft is very variable 158
7.4.3 The autonomous postganglionic synapse is specialized to ensure a widespread effect of the
neurotransmitter 158
7.5 Example of a neuroglandular synapse 159
7.6 Summary 160
Appendix 7.1 Neurotransmitters, agonists and antagonists 160
A7.1.1 Criteria to be satisfied before a molecule can be identified as a neurotransmitter 161
A7.1.2 Types of neurotransmitter 161
A7.1.3 Agonists and antagonists of a receptor 162
Appendix 7.2 Identification and localization of neurotransmitters and their receptors 162
M. Esclapez
A7.2.1 Immunocytochemistry 162
A7.2.2 In situ hybridization 166
Further reading 167
Chapter 8 Neurotransmitter Release
C. Hammond
8.1 Observations and questions 169
8.1.1 Quantitative data on synapse morphology and synaptic transmission 169
8.1.2 Ways of estimating neurotransmitter release in central mammalian synapses 171
8.1.3 Questions 174
8.2 Presynaptic processes I: From presynaptic spike to [Ca2+]; increase 174
8.2.1 The presynaptic Na+ dependent spike depolarizes the presynaptic membrane, opens
presynaptic Ca2+ channels and triggers Ca2+ entry 174
8.2.2 Ca2+ enters the presynaptic bouton during the time course of the presynaptic spike through
high voltage activated Ca2+ channels (N and P/Q types) 174
8.2.3 Presynaptic [Ca2+]; increase is transient and restricted to micro or nanodomains close to
docked vesicles 175
8.2.4 Ca2+ clearance makes presynaptic [Ca2+]; increase transient: it shapes its amplitude and
duration 179
8.3 Presynaptic processes II: From [Ca2+]; increase to synaptic vesicle fusion 180
8.3.1 Overview of the hypothetical vesicle cycle in presynaptic terminals 180
8.3.2 Docking: a subpopulation of synaptic vesicles is docked to the active zone close to Ca2+
channels by means of specific pairing of vesicular and plasma membrane proteins 182
8.3.3 Three to four Ca2+ ions must bind to Ca2+ receptor(s) to initiate vesicle fusion (exocytosis) 185
8.3.4 Fusion: from Ca2+binding to exocytosis 186
8.3.5 Pharmacology of neurotransmitter release 187
8.4 Processes in the synaptic cleft: from transmitter release in the deft to transmitter clearance
from the cleft 188
8.4.1 The amount of neurotransmitter released in the synaptic cleft 188
8.4.2 Transmitter time course in the synaptic cleft is brief and depends mainly on transmitter
binding to target proteins 190
8.5 Summary 191
Appendix 8.1 Quantal nature of neurotransmitter release 193
A8.1.1 Spontaneous release of acetylcholine at the neuromuscular junction evokes
miniature endplate potentials: the notion of quanta 193
A8.1.2 The quantal composition of EPSPs and IPSPs 194
Appendix 8.2 The probabilistic nature of neurotransmitter release 194
1
I
A8.2.1 The neuromuscular junction as a model 194 f
A8.2.2 Inhibitory synapses between interneurons and the Mauthner cell in the teleost fish
bulb, as a model 196
Further reading 198
PART 2 Ionotropic and Metabotropic Receptors in Synaptic Transmission and
Sensory Transduction
Chapter 9 The Ionotropic Nicotinic Acetylcholine Receptors
C. Hammond
9.1 Observations
9.2 The torpedo or muscle nicotinic receptor of acetylcholine is a heterologous pentamer a2P"y8 202
9.2.1 Nicotinic receptors have a rosette shape with an aqueous pore in the centre 203
9.2.2 The four subunits of the nicotinic receptor are assembled as a pentamer cc2py8 203
9.2.3 Each subunit presents two main hydrophilic domains and four hydrophobic domains 205
9.2.4 Each a subunit contains one acetylcholine receptor site located in the hydrophilic NH2
terminal domain 206
9.2.5 The pore of the ion channel is lined by the M2 transmembrane segments of each of the
five subunits 207
9.3 Binding of two acetylcholine molecules favours conformational change of the protein
towards the open state of the cationic channel 207
9.3.1 Demonstration of the binding of two acetylcholine molecules 207
9.3.2 The nicotinic channel has a selective permeability to cations: its unitary conductance is
constant 208
9.3.3 The time during which the channel stays open varies around an average value to, the mean
open time, and is a characteristic of each nicotinic receptor 212
9.4 The nicotinic receptor desensitizes 214
9.5 nAChR mediated synaptic transmission at the neuromuscular junction 217
9.5.1 Miniature and endplate synaptic currents are recorded at the neuromuscular junction 217
9.5.2 Synaptic currents are the sum of unitary currents appearing with variable delays and
durations 219
9.6 Nicotinic transmission pharmacology 220
9.6.1 Nicotinic agonists 220
9.6.2 Competitive nicotinic antagonists 220
9.6.3 Channel blockers 221
9.6.4 Acetylcholinesterase inhibitors 222
9.7 Summary 223
Appendix 9.1 The neuronal nicotinic receptors 223
Further reading 225
Chapter 10 The lonotropic GABAA Receptor
C. Hammond
10.1 Observations and questions 227
10.2 GABAA receptors are hetero oligomeric proteins with a structural heterogeneity 227
10.2.1 The diversity of GABAA receptor subunits 227
10.2.2 Subunit composition of native GABAA receptors and their binding characteristics 228
10.3 Binding of two GABA molecules leads to a conformational change of the GABAA receptor
into an open state; the GABAA receptor desensitizes 230
10.3.1 GABA binding site 230
10.3.2 Evidence for the binding of two GABA molecules 230
10.3.3 The GABAA channel is selectively permeable to Cl" ions 230
10.3.4 The single channel conductance of GABAA channels is constant in symmetrical Cl" solutions,
but varies as a function of potential in asymmetrical solutions 233
10.3.5 Mean open time of the GABAA channel 234
10.3.6 The GABAA receptor desensitizes 235
10.4 Pharmacology of the GABAA receptor 237
10.4.1 Bicuculline and picrotoxin reversibly decrease total GABAA current; they are respectively
competitive and non competitive antagonists of the GABAA receptor 237
10.4.2 Benzodiazepines, barbiturates and neurosteroids reversibly potentiate total GABAA current;
they are allosteric agonists at the GABAA receptor 238
10.4.3 P carbolines reversibly decrease total GABAA current; they bind at the benzodiazepine site
and are inverse agonists of the GABAA receptor 242
10.5 GABAA mediated synaptic transmission 243
10.5.1 The GABAergic synapse 243
10.5.2 The synaptic GABAA mediated current is the sum of unitary currents appearing with
variable delays and durations 244
10.5.3 The consequences of the synaptic activation of GABAA receptors depend on the relative
values of Ea and Vm 246
10.5.4 What shapes the decay phase of GABAA mediated currents? 247
10.6 Summary 249
Appendix 10.1 Mean open time and mean burst duration of the GABAA single channel current 249
Further reading 250
Chapter 11 The lonotropic Glutamate Receptors
C. Hammond
11.1 The three different types of ionotropic glutamate receptors have a common structure and
participate in fast glutamatergic synaptic transmission 251
11.1.1 Ionotropic glutamate receptors have the name of their selective or preferential agonist 251
11.1.2 The three ionotropic receptors participate in fast glutamatergic synaptic transmission 251
11.2 AMPA receptors are an ensemble of cationic receptor channels with different permeabilities
to Ca2+ ions 253
11.2.1 The diversity of AMPA receptors results from subunit combination, alternative splicing and
post transcriptional nuclear editing 253
11.2.2 The native AMPA receptor is permeable to cations and has a unitary conductance of 8 pS 254
11.2.3 AMPA receptors are permeable to Na+, K+ and Ca2+ ions unless the edited form of GluR2
is present; in the latter case, AMPA receptors are impermeable to Ca2+ ions 257
11.2 A The presence of flip or flop isoforms plays a role on the amplitude of the total AMPA
current 257
11.3 Kainate receptors are an ensemble of cationic receptor channels with different permeabilities
to Ca2+ ions 257
11.3.1 The diversity of kainate receptors 257
11.3.2 Native kainate receptors are permeable to cations 258
11.4 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 259
11.4.1 Molecular biology of NMDA receptors 259
11.4.2 Native NMDA receptors have a high unitary conductance of 40 50 pS 261
11.4.3 The NMDA channel is highly permeable to monovalent cations and to Ca2+ 261
11.4.4 NMDA channels are blocked by physiological concentrations of extracellular Mg2+ ions; this
block is voltage dependent 262
11.4.5 Glycine is a co agonist of NMDA receptors 265
11.4.6 Conclusions on NMDA receptors 265
11.5 Synaptic responses to glutamate are mediated by NMDA and non NMDA receptors 267
11.5.1 Glutamate receptors are co localized in the postsynaptic membrane of glutamatergic
synapses 267
11.5.2 The glutamatergic postsynaptic current is inward and can have at least two components
in the absence of extracellular Mg2+ ions 268
11.5.3 The glutamatergic postsynaptic depolarization (EPSP) has at least two components in the
absence of extracellular Mg2+ ions 270
11.5.4 Synaptic depolarization recorded in physiological conditions: factors controlling NMDA
receptors activation 270
11.6 Summary 272
Further reading 272
Chapter 12 lonotropic Mechanoreceptors: the Mechanosensitive Channels
C. Bourque
12.1 Mechanoreception in sensory neurons is associated with the production of a receptor
potential 274
12.2 Discovery of mechanosensitive ion channels provided a potential molecular mechanism for
mechanotransduction 274
12.3 Structural basis for the mechanical gating of ion channels 275
12.3.1 Intrinsic and extrinsic forms of mechanical gating 275
12.3.2 Channels regulated by coupling molecules oriented orthogonally to the membrane 275
12.3.3 Channels regulated by coupling molecules parallel to the membrane 275
12.3.4 Other gating configurations 276
12.4 Classification of stretch sensitive ion channels 276
12.4.1 Patch clamp experiments reveal the existence of stretch activated and stretch inactivated
channels 276
12.4.2 Ionic permeability of stretch sensitive channels 277
12.5 Mechanosensitive ion channels and mechanotransduction 278
12.6 Osmoreceptors in the central nervous system 278
12.6.1 Electrical activity and neurohypophyseal hormone secretion 279
12.6.2 Magnocellular neurosecretory cells in the hypothalamus are intrinsic osmoreceptors 280
12.7 Osmoreception in magnocellular neurosecretory cells 281
12.7.1 Osmoreceptor potentials reflect the modulation of a non selective cationic conductance 281
12.7.2 Changes in cell volume directly regulate the macroscopic cationic conductance in
magnocellular neurosecretory cells 281
12.7.3 Magnocellular neurosecretory cells express stretch inactivated cationic channels 282
12.7.4 The inhibitory effects of Gd3+ provide pharmacological evidence for the involvement of the
stretch inactivated cation channels in osmoreception 283
12.7.5 Molecular basis for mechanotransduction in osmoreceptors 283
12.8 Conclusions 284
Further reading 286
Chapter 13 The Metabotropic GABAB Receptors
D. Mott
13.1 GABAB receptors were originally discovered because of their insensitivity to bicuculline and
their sensitivity to badofen 287
13.2 Structure of the GABAB receptor 288
13.2.1 GABAB receptors belong to family 3 G protein coupled receptors 288
13.2.2 GABAB receptors are heterodimers 291
13.2.3 GABAB receptors are located throughout the brain at both presynaptic and postsynaptic sites 292
13.2.4 Summary 292
13.3 GABAB receptors are G protein coupled to a variety of different effector mechanisms 292
13.3.1 GABAB receptors are coupled to inhibitory G proteins 293
13.3.2 GABAB receptors regulate the activity of adenylyl cyclase 294
13.3.3 GABAB receptor activation inhibits voltage dependent calcium channels 296
13.3.4 GABAB receptors activate potassium channels 302
13.3.5 Summary 308
13.4 The functional role of GABAB receptors in synaptic activity 308
13.4.1 Postsynaptic GABAB receptors produce an inhibitory postsynaptic current 309
13.4.2 Presynaptic GABAB receptors inhibit the release of many different transmitters 310
13.5 Summary 312
Further reading 313
Chapter 14 The Metabotropic Glutamate Receptors
G. Bhave and R. Gereau
14.1 What is the receptor underlying glutamate stimulated PI hydrolysis? The cloning of
metabotropic glutamate receptor genes 314
14.2 How do metabotropic glutamate receptors carry out their function? Structure function
studies of metabotropic glutamate receptors 315
14.3 What biochemical means do metabotropic glutamate receptors utilize to elicit physiological
changes in the nervous system? Signal transduction studies of metabotropic glutamate
receptors 317
14.4 What are the functions of metabotropic glutamate receptors in the nervous system?
Physiological and genetic studies of mGluRs 319
14.5 How are metabotropic glutamate receptors specifically localized in neurons to execute their
functions? Studies of mGluR postsynaptic localization 323
14.6 How is the activity of metabotropic glutamate receptors modulated? Studies of mGluR
desensitization 324
14.7 Summary 325
Further reading 325
Chapter 15 The Metabotropic Olfactory Receptors
C. Hammond
15.1 The olfactory receptor cells are sensory neurons located in the olfactory neuroepithelium 327
15.1.1 The olfactory neurons are bipolar cells that project to the olfactory bulb 327
15.1.2 Odorants diffuse through the extracellular mucous matrix before interacting with the
chemosensory membrane of olfactory receptor neurons 329
15.2 The response of olfactory receptor neurons to odours is a membrane depolarization which
elicits action potential generation 329
15.3 Odorants bind to a family of G protein linked receptors which activate adenylate cyclase 330
15.3.1 Odorant receptors are a family of G protein linked receptors 330
15.3.2 The activation of odorant receptors leads to the activation of adenylate cyclase and the rapid
formation of cAMP via the activation of a Gs like protein 331
15.4 cAMP opens a cyclic nudeotide gated channel and generates an inward current 332
15.4.1 The olfactory cyclic nucleotide gated channel is a ligand gated channel composed of at least
two different subunits 332
15.4.2 cAMP directly opens a cyclic nucleotide gated channel 333
15.4.3 The activation of N cyclic nucleotide gated channels evokes an inward depolarizing current
carried by cations 338
15.4.4 The cyclic nucleotide gated conductance and the odour gated conductance are identical 342
15.4.5 Conclusions 342
15.5 The odorant evoked inward current evokes a membrane depolarization that spreads
electronically to the axon hillock where it can elicit action potentials 343
15.5.1 The odorant induced inward current depolarizes the membrane of olfactory receptors: the
generator potential 343
15.5.2 The odorant induced depolarization takes place in the cilia; spikes are initiated in the
soma initial axon segment, and the pattern of spike discharge propagated codes for the
concentration and duration of the odorant stimulus 344
15.5.3 The nature of the odorant would be coded by the nature of the olfactory neuron stimulated
and the synaptic arrangements in the olfactory bulb 344
15.6 Conclusions 345
Further reading 345
PART 3 Somato Dendritic Processing and Plasticity of Postsynaptic Potentials
Chapter 16 Somato Dendritic Processing of Postsynaptic Potentials.
I: Passive Properties of Dendrites
C. Hammond
16.1 Propagation of excitatory and inhibitory postsynaptic potentials through the dendritic
arborization 350
16.1.1 The complexity of synaptic organization (Figure 16.1) 350
16.1.2 Passive decremental propagation of postsynaptic potentials 351
16.1.3 Passive and non decremental propagation of postsynaptic potentials 351
16.2 Summation of excitatory and inhibitory postsynaptic potentials 351
16.2.1 Linear and nonlinear summation of excitatory postsynaptic potentials 351
16.2.2 Linear and nonlinear summation of inhibitory postsynaptic potentials 354
16.2.3 The integration of excitatory and inhibitory postsynaptic potentials partly determines the
configuration of the postsynaptic discharge 354
16.3 Summary 354
Further reading 355
Chapter 17 Subliminal Voltage Gated Currents of the Somato Dendritic Membrane
C. Hammond
17.1 Observations and questions 359
17.2 The subliminal voltage gated currents that depolarize the membrane 359
17.2.1 The persistent inward Na+ current, /NaP 359
17.2.2 The low threshold transient Ca2+ current, 1^ 361
17.2.3 The hyperpolarization activated cationic current, Jh, 7f, JQ 364
17.3 The subliminal voltage gated currents that hyperpolarize the membrane 367
17.3.1 The rapidly inactivating transient K+ current: JA or lKi 367
17.3.2 The slowly inactivating transient K+ current, JD or JAs 368
17.3.3 The K+ currents activated by intracellular Ca2+ ions, IKCa 369
17.3.4 The K+ current sensitive to muscarine, IM 369
17.3.5 The inward rectifier K+ current, JKir 371
17.4 Conclusions 372
Further reading 372
Chapter 18 Somato Dendritic Processing of Postsynaptic Potentials.
II. Role of Subliminal Depolarizing Voltage Gated Currents
C. Hammond
18.1 Persistent Na+ channels are present in soma and dendrites of neocortical neurons; JNaP boosts
EPSPs in amplitude and duration 375
18.1.1 Persistent Na+ channels are present in the dendrites and soma of pyramidal neurons of the
neocortex 375
18.1.2 Dendritic persistent Na+ channels are activated by EPSPs; in turn, JNaP boosts EPSP
amplitude 376
18.2 T type Ca2+ channels are present in dendrites of neocortical neurons; 7CaT boosts EPSPs in
amplitude and duration 378
18.2.1 T type Ca2+ channels are present in dendrites of pyramidal neurons of the hippocampus 378
18.2.2 Dendritic T type Ca2+ channels are activated by EPSPs; in turn, 7CaT boosts EPSPs amplitude 378
18.3 The hyperpolarization activated cationic current Ihis present in dendrites of hippocampa
pyramidal neurons; for EPSPs, dendritic Jh decreases the current transmitted from the
dendrites to the soma 382
18.3.1 H type cationic channels are expressed in dendrites of pyramidal neurons of the
hippocampus 382
18.3.2 Dendritic H type cationic channels are activated by IPSPs; in turn, 7h decreases EPSPs
amplitude 383
18.4 Functional consequences 386
18.4.1 Amplification of distal EPSPs by 7NaP and JCaT counteracts their attenuation owing to passive
propagation to the soma; it also favours temporal summation versus spatial summation 386
18.4.2 Activation of dendritic /CaT generates a local dendritic [Ca2+]; transient 386
18.4.3 Activation of dendritic Jh, 7NaP and 7CaT alter the local membrane resistance and time
constant 386
18.5 Conclusions 386
Further reading 387
Chapter 19 Somato Dendritic Processing of Postsynaptic Potentials.
III. Role of High Voltage Activated Depolarizing Currents
C. Hammond
19.1 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? 390
19.1.1 High voltage activated Na+ channels are present in some dendrites 390
19.1.2 Dendritic Na+ channels are opened by EPSPs and the resultant Na+ current boosts EPSPs in
amplitude and duration 392
19.1.3 Dendritic Na+ channels are opened by backpropagating Na+ action potentials 394
19.2 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? 398
19.2.1 High voltage activated Ca2+ channels are present in some dendrites 398
19.2.2 High voltage activated Ca2+ channels of Purkinje cell dendrites are opened by climbing fibre
EPSP; this initiates Ca2+ action potentials in the dendritic tree of Purkinje cells 400
19.2.3 Dendritic high voltage activated Ca2+ channels are opened by backpropagating Na+ action
potentials 403
19.3 Functional consequences 403
19.3.1 Amplification of distal synaptic responses by dendritic HVA currents counteracts their
attenuation due to passive propagation to the soma 403
19.3.2 Active backpropagation of Na+ spikes in the dendritic tree depolarizes the dendritic
membrane, with multiple consequences 404
19.3.3 Initiation of Ca2+ spikes in the dendritic tree of Purkinje cells evokes a widespread
intradendritic [Ca2+] increase 405
19.4 Conclusions 405
Further reading 406
Chapter 20 Firing Patterns of Neurons
C. Hammond
20.1 Medium spiny neurons of the neostriatum are silent neurons that respond with a long
latency 407
20.1.1 Medium spiny neurons are silent at rest owing to the activation of an inward rectifier K+
current 407
20.1.2 When activated, the response of medium spiny neurons is a long latency regular discharge 409
20.2 Inferior olivary cells are silent neurons that can oscillate 410
20.2.1 Inferior olivary cells are silent at rest in the absence of afferent activity 410
20.2.2 When depolarized, inferior olivary cells oscillate at a low frequency (3 6 Hz) 411
20.2.3 When hyperpolarized, inferior olivary cells oscillate at a higher frequency (9 12 Hz) 413
20.3 Purkinje cells are pacemaker neurons that respond by a complex spike followed by a period
of silence 414
20.3.1 Purkinje cells present an intrinsic tonic firing that depends on a persistent Na+ current 414
20.3.2 Purkinje cells respond to climbing fibre activation by a complex spike 414
20.4 Thalamic and subthalamic neurons are pacemaker neurons with two intrinsic firing modes:
a tonic and a bursting mode 417
20.4.1 The intrinsic tonic (single spike) mode depends on a persistent Na+ current 419
20.4.2 The bursting mode depends on a cascade of subliminal inward currents: /h, /CaT, JCaN 420
20.4.3 The transition from one mode to the other in response to synaptic inputs 420
Further reading 423
Chapter 21 Synoptic Plasticity
C. Hammond
21.1 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 424
21.2 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 collaterals activation 425
21.2.1 The Schaffer collaterals are axon collaterals of CA3 pyramidal neurons which form
glutamatergic excitatory synapses with dendrites of CA1 pyramidal neurons 425
21.2.2 Observation of the long term potentiation of the Schaffer collateral mediated EPSP 427
21.2.3 Long term potentiation (LTP) of the glutamatergic EPSP recorded in CA1 pyramidal
neurons results from an increase of synaptic efficacy (or synaptic strength) 427
21.2.4 Induction of LTP results from a transient enhancement of glutamate release and a rise in
postsynaptic intracellular Ca2+ concentration 429
21.2.5 Expression of LTP (also called maintenance) involves a persistent enhancement of the
AMPA component of the EPSP 434
21.2.6 Multiple ways to induce LTP, multiple forms of LTP and multiple ways to block LTP
induction 435
21.2.7 Summary: principal features of LTP in the Schaffer collateral pyramidal cell glutamatergic
transmission 437
21.3 The long term depression (LTD) of a glutamatergic response: example of the response of
Purkinje cells of the cerebellum to parallel fibre stimulation 437
21.3.1 The long term depression of a postsynaptic response (EPSC or EPSP) is a decrease of
synaptic efficacy 437
21.3.2 Induction of LTD requires a rise in postsynaptic intracellular Ca2+concentration and the
activation of postsynaptic AMPA receptors 438
21.3.3 The expression of LTD involves a persistent desensitization of postsynaptic AMPA receptors 443
21.3.4 Second messengers are required for LTD induction: examples of protein kinases C and nitric
oxide (NO) 443
21.3.5 The different ways to induce or block cerebellar LTD 446
21.3.6 Summary: Principal features of LTD in parallel fibre/Purkinje cell glutamatergic transmission 448
Further reading 448
PART 4 Activity and Development of Networks: The Hippocampus as an Example
Chapter 22 The Adult Hippocampal Network
C. Hammond
22.1 Observations and questions 451
22.2 The hippocampal circuitry 453
22.2.1 Ammon's horn 453
22.2.2 The dentate gyrus 454
22.2.3 Principal cells form a tri neural excitatory circuit 457
22.2.4 Extrinsic afferences to principal cells and interneurons 457
22.3 Activation of interneurons evoke inhibitory GABAergic responses in postsynaptic pyramidal
cells 458
22.3.1 Experimental protocol to study pairs of neurons 458
22.3.2 Unitary inhibitory postsynaptic currents (IPSCs) evoked by different types of interneurons
are all GABAA mediated but have different kinetics when recorded at the level of the soma 458
22.3.3 GABAA mediated IPSCs generate IPSPs in postsynaptic pyramidal cells 461
22.3.4 GABAB mediated IPSPs are also recorded in pyramidal neurons in reponse to strong
interneuron stimulation 464
22.4 Activation of principal cells evokes excitatory glutamatergic responses in postsynaptic
interneurons and other principal cells (synchronization in CA3) 464
22.4.1 Pyramidal neurons evoke AMPA mediated EPSPs in interneurons 465
22.4.2 EPSPs in interneurons lead to feedback inhibition of pyramidal neurons 466
22.4.3 CA3 pyramidal neurons are monosynaptically connected via glutamatergic synapses 466
22.4.4 Overview of intrinsic hippocampal circuits 466
22.5 Oscillations in the hippocampal network: example of sharp waves (SPW) 466
22.6 Summary 470
Further reading 471
Chapter 23 Maturation of the Hippocampal Network
Y. Ben Ari and C. Hammond
23.1 GABAergic neurons and GABAergic synapses develop prior to glutamatergic ones 472
23.1.1 GABAergic interneurons divide and arborize prior to pyramidal neurons and granular cells 472
23.1.2 GABAergic synapses are the first synapses established on to pyramidal cells 473
23.1.3 Sequential expression of GABA and glutamate synapses is also observed in the hippocampus
of subhuman primates in utero 47'4
23.1.4 Questions about the sequential maturation of GABA and glutamate synapses 476
23.2 GABAA and GABAB mediated responses differ in developing and mature brains 476
23.2.1 Activation of GABAA receptors is depolarizing and excitatory in immature networks because
of a high intracellular concentration of chloride 476
23.2.2 GABAB receptor mediated IPSCs have a delayed expression in immature neurons 479
23.3 Network driven giant depolarizing potentials (GDPs) provide most of the synaptic activity
in the neonatal hippocampus 480
23.3.1 Giant depolarizing potentials result from GABAergic and glutamatergic synaptic activity 481
23.3.2 Giant depolarizing potentials are generated in the septal pole of the immature hippocampus
and then propagate to the entire structure 482
23.4 Hypotheses on the role of the sequential expression of GABA and glutamate mediated
currents and of giant depolarizing potentials 483
23.5 Conclusions 483
Further reading 484
Index 485 |
| any_adam_object | 1 |
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| dewey-tens | 570 - Biology |
| discipline | Biologie |
| edition | 2. ed. |
| format | Book |
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| genre_facet | Aufsatzsammlung |
| id | DE-604.BV013861952 |
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| indexdate | 2024-12-02T15:02:20Z |
| institution | BVB |
| isbn | 0123116252 |
| language | English |
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| spelling | Cellular and molecular neurobiology C. Hammond 2. ed. San Diego [u.a.] Acad. Press 2001 XXIII, 493 S. Ill., graph. Darst. 1 CD-ROM txt rdacontent n rdamedia nc rdacarrier Biologie moléculaire ram Neurobiologie ram Molecular neurobiology Neurobiology Neurons Neurobiologie (DE-588)4041871-6 gnd rswk-swf Neurophysiologie (DE-588)4041897-2 gnd rswk-swf Cytologie (DE-588)4070177-3 gnd rswk-swf Neurochemie (DE-588)4041872-8 gnd rswk-swf Molekularbiologie (DE-588)4039983-7 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Neurobiologie (DE-588)4041871-6 s Molekularbiologie (DE-588)4039983-7 s DE-604 Neurophysiologie (DE-588)4041897-2 s Neurochemie (DE-588)4041872-8 s Cytologie (DE-588)4070177-3 s 1\p DE-604 Hammond, Constance Sonstige (DE-588)1342460391 oth HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=009481222&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis 1\p cgwrk 20201028 DE-101 https://d-nb.info/provenance/plan#cgwrk |
| spellingShingle | Cellular and molecular neurobiology Biologie moléculaire ram Neurobiologie ram Molecular neurobiology Neurobiology Neurons Neurobiologie (DE-588)4041871-6 gnd Neurophysiologie (DE-588)4041897-2 gnd Cytologie (DE-588)4070177-3 gnd Neurochemie (DE-588)4041872-8 gnd Molekularbiologie (DE-588)4039983-7 gnd |
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| title | Cellular and molecular neurobiology |
| title_auth | Cellular and molecular neurobiology |
| title_exact_search | Cellular and molecular neurobiology |
| title_full | Cellular and molecular neurobiology C. Hammond |
| title_fullStr | Cellular and molecular neurobiology C. Hammond |
| title_full_unstemmed | Cellular and molecular neurobiology C. Hammond |
| title_short | Cellular and molecular neurobiology |
| title_sort | cellular and molecular neurobiology |
| topic | Biologie moléculaire ram Neurobiologie ram Molecular neurobiology Neurobiology Neurons Neurobiologie (DE-588)4041871-6 gnd Neurophysiologie (DE-588)4041897-2 gnd Cytologie (DE-588)4070177-3 gnd Neurochemie (DE-588)4041872-8 gnd Molekularbiologie (DE-588)4039983-7 gnd |
| topic_facet | Biologie moléculaire Neurobiologie Molecular neurobiology Neurobiology Neurons Neurophysiologie Cytologie Neurochemie Molekularbiologie Aufsatzsammlung |
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