Synapse Development and Maturation Comprehensive Developmental Neuroscience 1st Edition by Pasko Rakic, ‎John Rubenstein, ‎Bin Che 0128236734 9780128236734

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ISBN-10 :  0128236734 

ISBN-13 :  9780128236734

Author:  Pasko Rakic, ‎John Rubenstein, ‎Bin Che 

Synapse Development and Maturation, the latest release in the Comprehensive Developmental Neuroscience series, presents the latest information on the genetic, molecular and cellular mechanisms of neural development. The book provides a much-needed update that underscores the latest research in this rapidly evolving field, with new section editors discussing the technological advances that are enabling the pursuit of new research on brain development. This volume focuses on the synaptogenesis and developmental sequences in the maturation of intrinsic and synapse-driven patterns.

Synapse Development and Maturation: Comprehensive Developmental Neuroscience 1st Table of contents:

I – Synaptogenesis
1 – Molecular composition of developing glutamatergic synapses
1.1 Introduction
1.2 Molecular composition of glutamatergic synapses
1.2.1 Presynaptic molecular composition
1.2.2 Postsynaptic molecular composition
1.2.3 Trans-synaptic cell adhesion molecules
1.2.4 Immune molecules
1.3 Cellular mechanisms of transport of molecules to developing synapses
1.3.1 Presynaptic proteins
1.3.1.1 Piccolo transport vesicles
1.3.1.2 Synaptic vesicle protein transport vesicles
1.3.2 Postsynaptic proteins
1.3.2.1 N-methyl-d-aspartate receptors
1.3.2.2 α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors
1.3.2.3 Postsynaptic density-95
1.3.2.4 Ion channels
1.3.2.5 Adhesion molecules
1.4 Final thoughts
List of acronyms and abbreviations
Acknowledgments
References
2 – In vivo imaging of synaptogenesis
2.1 Technological advances for in vivo imaging of synaptogenesis
2.2 In vivo analysis of synapse development in the neuromuscular junction
2.2.1 Background and methodology
2.2.2 Synaptogenesis mechanisms
2.3 Small vertebrate model systems: Xenopus and zebrafish
2.3.1 Background and methodology
2.3.2 Imaging synaptogenesis and morphogenesis in the developing spinal cord
2.3.3 Visual system development in fish and frogs
2.4 Visualizing synaptogenesis in mammals
2.4.1 Imaging axons, dendrites, and spines
2.4.2 Somatosensory development and plasticity
2.4.3 Synaptogenesis and plasticity in visual cortex
2.4.4 Imaging synaptogenesis in motor cortex
2.4.5 Integration of new neurons into olfactory circuitry
2.4.6 Structural developmental plasticity in the superior colliculus
2.5 Future perspectives
List of acronyms and abbreviations
References
3 – Astrocytes and synaptogenesis
3.1 Introduction
3.2 Secreted astrocytic factors orchestrate synaptogenesis
3.2.1 Retinal ganglion cells and the discovery of astrocyte-secreted synaptogenic factors
3.2.2 Thrombospondin family proteins as synapse organizers
3.2.3 Hevin, SPARC, and the diversity of synaptogenic modulation by astrocytes
3.2.4 Glypicans and the recruitment of AMPA receptors for functional synapse formation
3.2.5 Control of excitatory synaptic connectivity by transforming growth factor-beta and d-serine
3.2.6 Astrocytes and inhibitory synaptogenesis
3.2.7 Astrocyte synaptogenic heterogeneity
3.3 Astrocyte-neuron interactions as drivers of synaptic development
3.3.1 Glia-neuron interactions in developing circuits: insight from Drosophila and Caenorhabditis el
3.3.2 The role of contact-mediated signaling in astrocyte-induced synaptogenesis
3.3.3 The role of astrocyte lipid metabolism in synaptogenesis
3.3.4 Reciprocal interactions with neurons regulate astrocyte morphology and synaptic connectivity
3.4 Aberrant synaptogenesis: astrocyte signaling after injury and in disease
3.4.1 Reactive astrocytes
3.4.2 Synaptic remodeling after stroke and brain injury
3.4.3 Astrocytes in the development of neuropathic pain
3.4.4 Epilepsy, seizures, and astrocyte signaling
3.4.5 Deficient astrocyte signaling in neurodevelopment and neurodegeneration
3.4.6 Focusing on human disease: targeting astrocyte-induced synaptogenesis
List of acronyms and abbreviations
References
4 – Genetic analysis of synaptogenesis
4.1 Introduction
4.2 Studying synaptogenesis in genetic model organisms
4.2.1 Genetic approach to the study of the nervous system
4.2.2 Neuromuscular junctions in Caenorhabditis elegans and Drosophila melanogaster as the model sys
4.2.3 Motor behavior screens
4.2.3.1 Modifier drug-resistant screens for locomotion defects in Caenorhabditis elegans
4.2.3.2 Phototaxis-defective mutants with abnormal electroretinograms in the genetic mosaic Drosophi
4.2.3.3 Jump escape defective mutants with disrupted giant fiber flight circuit in Drosophila
4.2.4 Microscopy-based genetic screens for protein misexpression patterns within the synaptic region
4.2.4.1 Microscopy-based screens in Caenorhabditis elegans
4.2.4.2 Microscopy-based screens in the Drosophila neuromuscular junctions
4.2.5 Cell-based genomic screens for promoters and inhibitors of synapse formation
4.3 Molecular genetic tools for screening and analysis of synaptogenesis mutants
4.3.1 Mapping improvements
4.3.2 Transgenesis
4.3.3 Mutagenesis kits
4.3.3.1 Transposon-mediated mutagenesis
4.3.3.2 Locus-specific genome engineering-Targeting-Induced Local Lesions in Genomes and assembly of
4.3.3.3 Locus-specific genome engineering-CRISPR/Cas system
4.3.4 Gene targeting and conditional gene expression by binary systems
4.3.4.1 Combinatorial control of DNA site-specific recombinase activity
4.3.4.1.1 Cre-loxP
4.3.4.1.2 FLP/FLP recognition target
4.3.4.2 Gal4/ upstream activator sequence system
4.3.4.3 Genetic mosaics with conditional knockout
4.4 Perspective
References
Relevant Websites
5 – New imaging tools to study synaptogenesis
5.1 Introduction
5.2 Conventional fluorescence microscopy and electron microscopy
5.2.1 Fluorescence microscopy: pros and cons
5.2.2 Transmission electron microscopy: pros and cons
5.3 Recent advances in fluorescence microscopy: toward superresolution microscopy
5.3.1 Structured illumination microscopy and image scanning microscopy
5.3.2 Stimulated emission depletion microscopy
5.3.3 Localization-based microscopy
5.4 Recent advances in electron microscopy: 3D sectioning techniques and correlative microscopy
5.4.1 3D reconstruction
5.4.2 Cryofixation
5.4.3 Correlative light and electron microscopy
5.5 New developments in genetically encoded photosensitive tools
5.5.1 A brief introduction to photosensitive proteins
5.5.2 Markers of neuronal connectivity
5.5.3 GRASP: a synaptogenic biosensor
5.5.4 Design of photosensitive tools to study the synaptogenic protein EphB
5.6 New compartmentalized microfluidic platforms to culture and image neurons
5.6.1 A microfluidic platform to study synaptogenic cell adhesion molecules in mixed-culture assays
5.6.2 Neuronal microfluidic platforms to study synapses
5.7 Conclusion
References
6 – Wnt signaling
6.1 Introduction
6.2 Wnts and their signaling pathways
6.2.1 Wnt secretion
6.2.2 Wnt signaling pathways
6.3 Regulation of presynaptic differentiation
6.3.1 Axon remodeling and synaptic bouton formation
6.3.2 Cytoskeleton reorganization at the presynaptic terminal
6.3.3 Recruitment of presynaptic components
6.4 Regulation of postsynaptic organization
6.4.1 Postsynaptic assembly of invertebrate peripheral synapses
6.4.2 Vertebrate neuromuscular synapse
6.4.3 Prepatterning of acetylcholine receptors in muscle cells
6.4.4 Assembly of the neuromuscular synapse
6.4.5 Postsynaptic assembly at central synapses
6.5 Wnt proteins as antisynaptogenic factors
6.5.1 Regulation of synaptic distribution
6.5.2 Wnt/β-catenin signaling at the vertebrate neuromuscular junction
6.5.3 Inhibition of synapse formation at central synapses
6.6 Wnt signaling and activity-mediated synaptic remodeling
6.6.1 Neuronal activity, Wnts, and their receptors
6.6.2 Synaptic remodeling in the adult hippocampus
6.6.3 Emerging roles for Wnts
List of abbreviations
Glossary
Acknowledgments
References
Relevant website
7 – Neurotrophin and synaptogenesis
7.1 Introduction
7.2 One neurotrophin, three ligands at the synapse
7.2.1 Pro-brain-derived neurotrophic factor
7.2.2 Cleavage of pro-brain-derived neurotrophic factor
7.2.3 The prodomain
7.3 Which side of the synapse produces neurotrophins?
7.3.1 Presynaptic source of brain-derived neurotrophic factor
7.3.2 Postsynaptic source of brain-derived neurotrophic factor
7.3.3 Nonneuronal source of synaptic brain-derived neurotrophic factor
7.4 What are the modes of neurotrophin synaptic release?
7.4.1 Secretion of pro-brain-derived neurotrophic factor
7.4.2 Secretion of the mature brain-derived neurotrophic factor
7.4.3 Secretion of the prodomain
7.5 Receptors for neurotrophin ligands
7.5.1 Receptors for proneurotrophins
7.5.2 Receptors for mature neurotrophins
7.5.3 Receptors for the prodomain
7.6 Signaling mechanisms of Trk and p75NTR
7.6.1 Presynaptic responses
7.6.2 Postsynaptic responses
7.6.3 Rapid and slow responses
7.6.4 Balancing act on excitation and inhibition
7.7 Specificity of neurotrophin actions at the synapse
7.8 Conclusion and perspectives
References
8 – Neuroligins and neurexins
8.1 Introduction
8.2 Along came a spider: discovery of neurexin and neuroligin proteins
8.3 Extensive diversification: gene and protein structures
8.3.1 The neurexin and neuroligin gene families
8.3.2 Protein topology and domain organization
8.4 Crystal clear: structural insights into neuroligin-neurexin interactions
8.4.1 Structures of neurexin and neuroligin proteins
8.4.2 Regulation of neurexin-neuroligin binding affinities by alternative splicing
8.5 Spatiotemporal modifications: regulation of alternative splicing
8.6 Nonexclusive partners: a hub for synaptic proteins
8.7 Acting locally: polarized transport and synapse-specific localization
8.8 More than glue: synaptic functions of neuroligin-neurexin complexes
8.8.1 Synaptogenic functions
8.8.2 Cell biological mechanisms of neurexin and neuroligin functions
8.8.3 Synaptic functions in invertebrates
8.9 From synapses to behavior: disruption of the neurexin-neuroligin complex in neurodevelopmental d
8.9.1 Disorder-associated mutations and copy number variations
8.9.2 Mouse models of autism spectrum disorder and schizophrenia
8.9.3 Disease and neuron specificity
8.10 Twenty five years and on: outlook
Acknowledgment
References
9 – Synapse formation in the developing vertebrate retina
9.1 Introduction
9.2 Synaptic development in the outer plexiform layer
9.2.1 Synaptic organization of the mature outer plexiform layer
9.2.2 Assembly and maintenance of the photoreceptor ribbon
9.2.3 Postsynaptic targeting and differentiation in the outer plexiform layer
9.2.3.1 Development of horizontal cell connectivity
9.2.3.2 Development of bipolar cell connectivity in the outer plexiform layer
9.3 Synaptogenesis in the inner plexiform layer
9.3.1 Synaptic organization in the mature inner plexiform layer
9.3.2 Sequence of synapse formation in the inner plexiform layer
9.3.3 Assembly of conventional synapses from amacrine cells to amacrine cells and retinal ganglion c
9.3.4 Assembly of bipolar cell ribbon synapses
9.3.5 Formation of presynaptic inhibition of bipolar cell terminals by amacrine cells
9.3.6 Emergence of synaptic laminae and wiring specificity through dendritic patterning
9.3.7 Functional circuit assembly, specificity, and refinement in the inner plexiform layer
9.4 Conclusion
References
10 – Synaptogenesis in the adult CNS-Hippocampus
10.1 Plasticity in the hippocampus
10.2 Hippocampal circuits
10.3 Neurogenesis and stem cells
10.4 Methods to identify adult neurogenesis
10.5 Functional development of adult-born GCs
10.6 Intrinsic membrane properties of new GCs
10.7 Developing GCs at phase I: GABAergic synaptogenesis
10.8 Developing GCs at phase II: glutamatergic synaptogenesis
10.9 Developing GCs at phase III: hyperactivity and synaptic plasticity
10.10 Developing GCs at phase IV: maturation and reduced excitability
10.11 Development of synaptic output
10.12 Activity-dependent regulation of neuronal connectivity
10.13 Aging and adult neurogenesis
10.14 Impact of adult neurogenesis on the architecture of preexisting dentate circuitry
10.15 Conclusions
List of acronyms and abbreviations
Acknowledgments
References
11 – Synaptogenesis in the adult CNS-olfactory system
11.1 Introduction
11.2 Olfaction-a central sense driving behavior
11.3 Basic architecture of the olfactory bulb
11.3.1 The olfactory bulb
11.3.2 Cell types in the olfactory bulb
11.3.3 Synapses and connectivity patterns
11.3.4 Beyond the olfactory bulb
11.4 Synaptogenesis in the adult olfactory bulb
11.4.1 The dynamic nature of the adult olfactory bulb
11.4.2 New synapses in the adult olfactory bulb
11.4.3 Neonatally born versus adult-born synaptogenesis
11.5 Mechanisms of synaptogenesis in the adult olfactory bulb
11.5.1 Mechanisms preceding synaptogenesis in the adult olfactory bulb (proliferation, survival, and
11.5.2 Sensory experience and synaptogenesis
11.5.3 In vivo functional properties of adult-born neurons in the olfactory bulb
11.6 Future perspective
Acknowledgments
References
II – Developmental sequences in the maturation of intrinsic and synapse-driven patterns
12 – The GABA developmental shift in health and disease
12.1 Introduction
12.2 GABA depolarizes, produces a rise of [Ca2+]I, and can generate sodium spikes in immature neuron
12.3 The developmental shift is mediated by chloride cotransporters NKCC1 and KCC2
12.4 GABAergic signals develop before glutamatergic ones in many brain structures
12.5 A parallel developmental sequence of brain patterns
12.6 Trophic actions of GABA and the checkpoint concept
12.7 Pathological shifts of [Cl-]I levels and the neuroarchaeology concept
12.8 An oxytocin-mediated shift of [Cl-]I during labor and birth that is abolished in autism spectru
12.9 Treating autism spectrum disorders with bumetanide: novel therapeutic avenues based on a reduct
12.10 General conclusions
Acknowledgments
References
13 – Chloride homeodynamics underlying pathogenic modal shifts of GABA actions
13.1 Developmental and dynamic shifts of Cl- homeostasis change GABA actions
13.1.1 Modal shifts of GABA actions attributed to Cl- homeodynamics
13.1.2 Developmental shifts of Cl- homeostasis
13.1.3 Dynamic shifts of Cl- homeostasis
13.1.4 Cation-Cl- cotransporters are responsible for hyperpolarizing or depolarizing GABAergic respo
13.1.5 Astrocytic Cl- buffering system regulates postsynaptic Cl- homeodynamics
13.2 Pathological models of dynamic Cl- homeostasis perturbation
13.2.1 NKCC1 transporter facilitates neonatal seizures
13.2.2 Perturbed Cl- homeostasis is the general mechanism for seizures in animal models of epilepsy
13.2.3 Ischemia results in acute and chronic perturbation of Cl- homeostasis
13.3 Pathological models of developmental Cl- homeostasis disorders
13.3.1 Differential developmental patterns of Cl- transporters in various brain regions
13.3.2 Modal shifts of Cl- homeostasis and GABA actions underlying neocortical malformation
13.3.3 Modal shifts of Cl- homeostasis in human epileptic tissue
13.3.3.1 Decreased KCC2 expression in human epileptic focal cortical dysplasia
13.3.3.2 Perturbed NKCC1 and/or KCC2 expressions in other human epileptic tissues
13.3.4 Altered Cl- homeostasis during perturbed brain development
13.3.4.1 Disturbed NKCC1 and/or KCC2 which lowers [Cl-]i underlies abnormal synapse formation and ne
13.3.4.2 Failures in depolarizing GABAA receptor activation disturb migration
13.3.4.3 Failures in depolarizing GABAA receptor activation disturb neurogenesis
13.4 Pathological models of regenerating immature Cl- homeostasis induced by injury
13.4.1 Injuries induce regeneration of immature Cl- homeostasis for survival and repair
13.4.2 Regeneration of immature Cl- homeostasis may contribute to pathogenesis
13.5 Perspectives of possible involvement of Cl- homeodynamics in pathogenesis
13.5.1 Psychiatric disorders and Cl- homeodynamics
13.5.2 Potential risks of early exposure to anesthesia in childhood
13.6 Conclusion
List of Abbreviations
Symbols
References
14 – Multimodal GABAA receptor functions in the development of the central nervous system
14.1 Developmental shifts of GABAA receptor subunit composition
14.1.1 Developmental changes in GABAA receptor subunits in neocortex
14.1.2 Developmental changes in GABAA receptor subunits in hippocampus
14.1.3 Developmental changes in GABAA receptor subunits in thalamus
14.1.4 Developmental changes in GABAA receptor subunits in basal ganglia
14.1.5 Developmental changes in GABAA receptor subunits in cerebellum
14.1.6 Developmental changes in GABAA receptor subunits in spinal cord
14.1.7 Developmental changes in GABAA receptor subunits in other brain regions
14.2 GABAA receptor function on neurogenesis
14.3 GABAA receptor function on migration
14.3.1 Neocortex
14.3.2 Neuronal precursor migration in the anterior subventricular zone and the rostral migratory st
14.3.3 Hippocampus
14.3.4 Other neurons
14.4 GABAA receptor function on synaptogenesis
14.5 GABAA receptor function on excitatory neurotransmission
14.6 When does inhibitory GABAA receptor-mediated neurotransmission emerge?
14.6.1 Neocortex
14.6.2 Brainstem and spinal cord
14.7 Multimodal GABAA receptor function in neurodevelopmental disorders
14.7.1 Schizophrenia
14.7.2 Epilepsy and cortical malformations
14.7.3 Autism spectrum disorders (ASD)
14.7.4 Down syndrome
14.8 Conclusion
List of acronyms and abbreviations
Glossary
References
15 – GABAergic signaling at newborn mossy fiber-CA3 synapses: short and long-term activity-dependent
15.1 Mossy fiber synapses
15.2 Corelease of glutamate and GABA from mossy fiber terminals
15.3 GABA is the main neurotransmitter released from immature mossy fiber terminals
15.4 Criteria for identifying single MF-CA3 responses
15.4.1 Paired-pulse facilitation
15.4.2 Short-term frequency-dependent facilitation
15.4.3 Sensitivity to group II and III metabotropic glutamate receptor agonists
15.5 Presynaptic modulation of GABA release
15.5.1 Glutamate receptors
15.5.2 GABA-A and GABA-B receptors
15.5.3 Tonic GABA
15.6 Activity-dependent changes in synaptic efficacy at immature MF-CA3 synapses
15.6.1 Functional role of giant depolarizing potentials-associated calcium transients
15.6.2 The direction of synaptic plasticity is controlled by the prion protein PrPC
15.6.3 Functional role of spike-time-dependent plasticity
15.7 Neurodevelopmental disorders associated with alterations of GABAergic signaling at MF-CA3
15.8 Conclusions
List of abbreviations
Acknowledgments
References
16 – Retinal waves and their role in visual system development
16.1 Introduction
16.2 Spatiotemporal patterns of retinal waves
16.2.1 Discovery of retinal waves
16.2.2 Development of retinal wave patterns
16.3 Influence of waves on retinal development
16.4 Retinal waves and retinotopic refinement
16.5 Retinal waves and eye-specific segregation
16.6 Retinal waves and ON/OFF segregation in the dLGN
16.7 Retinal waves influence the developing V1
16.8 Conclusions
References
17 – Neurotransmitter phenotype plasticity: from calcium signaling to functional consequences
17.1 Introduction
17.2 Calcium spiking
17.2.1 Calcium spikes in the Xenopus brain
17.2.2 Characteristics of calcium spikes
17.2.3 Temporal expression of calcium spikes
17.2.4 Physiological triggers of calcium spiking
17.2.5 Calcium spikes in the mammalian brain
17.3 Neurotransmitter phenotype specification: intrinsic determinants
17.3.1 GABA and glutamate
17.3.2 Dopamine
17.3.3 Serotonin
17.4 Neurotransmitter phenotype plasticity: from neurotransmitter respecification to neurotransmitte
17.4.1 Early indications of neurotransmitter phenotype plasticity
17.4.2 Neurotransmitter phenotype plasticity in the developing Xenopus central nervous system
17.4.3 Neurotransmitter phenotype plasticity in the developing mammalian central nervous system
17.4.4 Activation of neurotransmitter phenotype plasticity through synaptic activity in the Xenopus
17.4.5 Activation of neurotransmitter phenotype plasticity through synaptic activity in the mammalia
17.4.6 Neurotransmitter switching
17.5 Molecular mechanisms
17.5.1 Calcium-dependent regulation of transcription
17.5.2 Physiological regulation of calcium spiking: non-cell-autonomous mechanisms
17.5.3 Regulation of neurotransmitter phenotype plasticity by microRNAs
17.5.4 The reserve pool hypothesis
17.5.5 Neurotransmitter receptor expression plasticity
17.6 Functional relevance of neurotransmitter phenotype plasticity
17.6.1 Functional relevance of neurotrophic phenotype: serotonin and dopamine in the Xenopus central
17.6.2 Functional relevance of neurotrophic phenotype: dopamine in the rat central nervous system
17.7 Perspectives
17.7.1 Optogenetic dissection of neurotransmitter phenotype plasticity and in vivo imaging
17.7.2 Implications of neurotransmitter phenotype plasticity in the developing brain
17.7.3 Applications of neurotransmitter phenotype plasticity in the mature brain
17.8 Summary
References
18 – Developmental sequences in the maturation of intrinsic and synapse-driven patterns
18.1 Postnatal and experience-dependent maturation of sensory cortex
18.2 Postnatal maturation of inhibitory synaptic transmission
18.3 Opening and closure of critical periods and maturation of GABAergic inhibition
18.4 Postnatal maturation of cortical excitatory synapses
18.5 Developmental changes in synaptic plasticity at excitatory and inhibitory synapses
18.6 Coregulation of excitatory and inhibitory synapses during postnatal development
18.7 Conclusions
Acknowledgments
References
19 – Functional maturation of neocortical inhibitory interneurons
19.1 Introduction
19.2 Embryonic origins of interneuron diversity
19.2.1 The medial ganglionic eminence lineage
19.2.2 The caudal ganglionic eminence lineage
19.2.3 Differences in interneuron origin in humans
19.3 Postnatal maturation of interneurons
19.3.1 Passive properties
19.3.2 Active properties
19.3.3 Synaptic outputs
19.3.4 Cell death
19.3.5 Specializations in humans and other primates
19.3.6 Variability in interneuron development with local activity
19.4 The role of interneuron maturation in patterning cortex
19.5 Conclusions
Acknowledgments
References
20 – The role of brain-derived neurotrophic factor in neural circuit development and function
20.1 Introduction to neurotrophins
20.2 BDNF transcription, translation, processing, and signaling
20.2.1 Gene structure and transcriptional regulation
20.2.2 Epigenetic regulation of BDNF
20.2.3 Translation and processing
20.2.4 Constitutive and activity-dependent secretion
20.2.5 Pre- and postsynaptic release
20.2.6 Receptors and intracellular cascades
20.2.7 Effector and target of local protein synthesis
20.3 BDNF functions in the nervous system
20.3.1 Dendritic and axonal development
20.3.2 Cell health and survival
20.3.3 Neuronal differentiation, synapse formation, and maturation
20.3.4 Cellular plasticity
20.4 BDNF’s role in behavior and disease
20.4.1 Learning and memory
20.4.1.1 Hippocampal memory consolidation and persistence
20.4.1.2 BDNF roles in cortical memory formation
20.4.2 Stress, depression-like behavior, and antidepressant efficacy
20.4.3 Neurodevelopmental disorders
20.4.3.1 Rett Syndrome
20.4.3.2 Fragile X syndrome
20.4.4 Neurodegenerative diseases
20.4.4.1 Alzheimer’s disease
20.4.4.2 Huntington’s disease
20.5 Conclusions
List of acronyms and abbreviations
Glossary
References
21 – Striatal circuit development and synapse maturation
21.1 Introduction
21.2 Early patterning of the striatum
21.2.1 Morphogenesis
21.2.2 Neurogenesis of striatal neurons
21.2.3 Compartmentalization of the striatum
21.2.4 Extrinsic trophic support and regulation of apoptosis
21.3 Development of striatal afferents
21.3.1 Development of corticostriatal pathways
21.3.2 Development of thalamostriatal projections
21.3.3 Maturation of neuromodulatory projections
21.4 Development of SPN physiological properties
21.4.1 Electrophysiological maturation of SPNs
21.4.2 The genesis of synapses on striatal SPNs
21.5 Concluding statements
References
Further reading
22 – Cajal-Retzius and subplate cells: transient cortical neurons and circuits with long-term impact
22.1 Introduction
22.2 Cajal-Retzius neurons
22.2.1 Morphological and molecular properties of Cajal-Retzius neurons
22.2.2 Developmental origin of Cajal-Retzius neurons
22.2.3 Electrophysiological properties of Cajal-Retzius neurons
22.2.3.1 Intrinsic membrane properties
22.2.3.2 Synaptic connectivity
22.2.3.3 Function in early network activity
22.2.4 Role of Cajal-Retzius neurons in early cortical development
22.2.5 Developmental destiny of Cajal-Retzius neurons
22.2.6 Patho(physio)logy of Cajal-Retzius neurons
22.2.7 Cajal-Retzius neurons in the hippocampus
22.2.8 Summary on Cajal-Retzius neurons
22.3 Subplate neurons
22.3.1 Morphological and molecular properties of subplate neurons
22.3.2 Developmental origin of subplate neurons
22.3.3 Electrophysiological properties of subplate neurons
22.3.3.1 Intrinsic membrane properties
22.3.3.2 Synaptic connectivity
22.3.3.3 Function in early network activity
22.3.4 Role of subplate neurons in early cortical development
22.3.5 Developmental destiny of subplate neurons
22.3.6 Patho(physio)logy of subplate neurons
22.3.7 Summary on subplate neurons
22.4 Conclusions and perspectives
Acknowledgments
References
23 – AMPA receptor trafficking in the developing and mature glutamatergic synapse
23.1 Introduction
23.2 Glutamatergic synaptogenesis during development
23.3 AMPAR subunit-specific structure, localization, and function
23.4 AMPAR assembly and intracellular trafficking along the secretory pathway
23.5 Surface trafficking of AMPARs
23.5.1 Exocytosis from intracellular pools
23.5.2 Lateral diffusion and capture at synaptic sites
23.5.3 Endocytosis and endosomal trafficking
23.6 Conclusion and future perspective

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