Backpropagation Hypothesis

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Table of contents

Acknowledgements
Summary
1.1 Abstract
1.2 Resume (en francais)
2 Introduction to action potential
2.1 Context and objective of this work
2.2 Currents during action potential
2.2.1 Hodgkin and Huxley Model
2.2.2 Voltage gated channels
2.2.2.1 Sodium channels
2.2.2.2 Potassium channels
2.2.2.3 Other voltage gated channels
2.2.3 Energy eciency
2.3 Role of dierent neuronal segments
2.3.1 Soma
2.3.2 Axon
2.3.3 Axon initial segment
2.3.4 Synapse
2.3.5 Dendrite
2.3.6 Impact of morphology on the ring pattern
2.4 Kink at the initiation, experiments vs models
2.4.1 Cooperativity Hypothesis
2.4.2 Backpropagation Hypothesis
2.4.3 Critical Resistive Coupling Hypothesis
2.5 Signature of a single cell activity in the extracellular potential
2.6 Bursts of action potentials
2.7 Activity of single cell within population
2.8 Sharp Waves as example of network activity
2.9 Malfunction of action potential
2.9.1 Epilepsy
2.9.2 Stroke
2.9.3 Alzheimer’s disease
2.9.4 Other Disease
3 The basis of sharp spike onset in standard biophysical models
3.1 Abstract
3.2 Author summary
3.3 Introduction
3.4 Results
3.4.1 Intracellular and extracellular features of sharp spike initiation in multicompartmental models
3.4.2 Extracellular eld at spike initiation
3.4.3 Currents at spike initiation
3.4.4 Excitability increases with intracellular resistivity
3.4.5 Sharp spike initiation requires a large enough somatodendritic compartment
3.4.6 Backpropagation does not sharpen spikes
3.4.7 Active backpropagation is not necessary for sharp spike initiation
3.4.8 Sharp somatic onset is reproduced by a model with two resistively coupled compartments
3.5 Discussion
3.6 Materials and methods
3.6.1 Detailed neuron models
3.6.1.1 Morphology
3.6.1.2 Channel properties
3.6.2 Two-compartment model
3.6.3 Analysis
3.6.3.1 Voltage-clamp
3.6.3.2 Phase slope
3.6.4 Theoretical prediction of onset rapidness
3.7 Acknowledgments
4 Local eld potential generated by neurons with dierent localisation of axon initial segment
4.1 Results
4.1.1 Soma-axon model
4.1.2 Far-eld dipole approximation
4.1.3 Dipole model { near eld
4.1.4 Two cylinder model
4.2 Discussion
4.3 Methods
4.3.1 Soma-axon model
4.3.2 Linear Source Approximation
4.3.3 Two cylinders model
5 Single CA3 pyramidal cells trigger sharp waves in vitro by exciting interneurones
5.1 Abstract
5.2 Introduction
5.3 Methods
5.3.1 Slice preparation
5.3.2 Drugs
5.3.3 Recordings
5.3.4 Signal analysis
5.3.5 Statistical analysis
5.4 Results
5.4.1 Single pyramidal cells initiate SPWs and eld IPSPs
5.4.2 fIPSPs from perisomatic interneurones are repeated in SPW elds
5.4.3 Excitation of interneurons by single pyramidal cells
5.4.4 Comparison of spontaneous SPWs and SPWs initiated by single cells
5.4.5 Patterns of SPW spread and the activity of identied interneurons
5.5 Discussion
5.5.1 Advantages of an in vitro study
5.5.2 Initiating pyramidal cells excite perisomatic interneurones
5.5.3 Continuation, spread and cellular components of SPWs
6 Conclusions
6.1 Uniqueness of Action Potential
6.2 Role of the axon in neuronal coding
A Recurrent synapses and circuits in the CA3 region of the hippocampus: an associative network
A.1 Abstract
A.2 Recurrent excitatory synapses between CA3 cells: emergence
A.3 Axonal distributions of CA3 pyramidal cells
A.4 CA3 pyramidal cell axon physiology
A.5 CA3 pyramidal cell terminals: numbers, form, contents, channels and release
A.6 Pre- meets post: synapses made by CA3 pyramidal cells with other CA3 cells
A.7 Pre- meets post in dual records
A.8 Short-term and long-term synaptic plasticity in double recordings
A.9 Transmission of recurrent excitatory signals on the membrane of a postsynaptic cell
A.10 Recurrent excitatory contributions to population activities in the CA3 region
A.11 Interictal epileptiform rhythm
A.12 Sharp-wave rhythm
A.13 Theta and gamma rhythms
A.14 Comparison of recurrent connectivity in CA3 and other cortical regions
A.15 The CA3 recurrent system as an associative network