Tseng Cortico-Subcortical Dynamics in Parkinson's Disease

2009
ISBN: 978-1-60327-252-0
Verlag: Humana Press
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 316 Seiten

Reihe: Contemporary Neuroscience

The striatum is the principal input structure of the basal ganglia. Numerically, the great majority of neurons in the striatum are spiny projection neurons, which produce the inhibitory output of the striatum to the globus pallidum and substantia nigra. The major glutamatergic afferents to the striatum from the cerebral cortex make monosynaptic contact with spiny projection neurons. The dopaminergic afferents from the substantia nigra also synapse directly on the spiny projection neurons. Thus, the spiny projection neurons play a crucial role in the input-output operations of the striatum by integrating glutamatergic cortical inputs with dopaminergic inputs and producing the output to other basal ganglia nuclei. Anatomical observations made nearly 30 years ago suggested that inhibitory interactions among the spiny projection neurons of the striatum are very pr- able. Individual spiny projection neurons produce a local axonal plexus in the spheroidal space occupied by their own dendritic trees [1, 2]. Based on the GABAergic nature of these neurons and their synaptic contacts with other spiny neurons, several authors have proposed that the spiny projection neurons form a lateral inhibition type of neural network [3-5]. In the idealised concept of lateral inhibition, each output neuron makes inhibitory synaptic contact with its neighbours [5]. However, there are physical limitations set by the extent of axonal and dendritic trees, and the number of synaptic sites, which mean that lateral inhibition is limited to a local domain of inhibition.

Autoren/Hrsg.

Tseng, Kuei-Yuan

Inhaltsverzeichnis

1;Cortico-Subcortical Dynamics in Parkinson’s Disease;2
1.1;Contemporary Neuroscience;3
1.2;Contents;6
1.3;Contributors;9
1.4;Part 1: Cortico-Subcortical Circuits and Parkinson’s Disease;14
1.4.1;Leading Toward a Unified Cortico-basal Ganglia Functional Model;15
1.4.1.1;Basal Ganglia Circuitry: The Direct and Indirect Pathways;15
1.4.1.2;Functional Changes in the Basal Ganglia After Dopamine Depletion;16
1.4.1.2.1;Glutamate Decarboxylase;17
1.4.1.2.2;Cytochrome Oxidase;17
1.4.1.2.3;2-Deoxyglucose;18
1.4.1.3;Chronic Dopamine Depletion and Basal Ganglia Oscillations;18
1.4.1.3.1;Chronic Dopamine Depletion and Firing Pattern Shift in the Basal Ganglia;19
1.4.1.3.2;Corticostriatal Function and Basal Ganglia Oscillations;21
1.4.1.4;Dopamine-Dependent Regulation of Cortically Driven Oscillatory Activity in the Basal Ganglia and Akinesia;23
1.4.1.5;Integration of the Motor-Limbic Circuits in the Basal Ganglia;25
1.4.1.6;Summary and Conclusions;27
1.4.1.7;References;27
1.4.2;Modeling Parkinson’s Disease: 50 Years Later;35
1.4.2.1;A Turning Point in the History of Neuroscience: The Discovery of l -Dopa Decarboxylase;35
1.4.2.2;Modeling Parkinson’s Disease: From DA Depletion to Genetic Manipulations;36
1.4.2.2.1;Unilateral DA Depletion Induced by Injecting 6-OHDA into the Brain;37
1.4.2.2.2;Modeling PD Pathophysiology with MPTP Intoxication in Mice;38
1.4.2.2.3;Environmental Toxins Induce Parkinsonism in Rodents;40
1.4.2.2.4;Genetic Models of PD;40
1.4.2.3;Summary and Conclusions;41
1.4.2.4;References;42
1.5;Part 2: Physiological Studies of the Cortico-subcortical Dynamics and Parkinson’s Disease;47
1.5.1;Phasic Dopaminergic Signaling: Implications for Parkinson’s Disease;48
1.5.1.1;Phasic Dopamine Activation;49
1.5.1.2;Purported Functions of Phasic Dopaminergic Signaling;49
1.5.1.3;Nucleus Accumbens and Associative Learning;52
1.5.1.4;Dorsolateral Striatum and Stimulus-Response Associations;53
1.5.1.5;Prefrontal Cortex and Working Memory;54
1.5.1.6;Dopaminergic Signaling and PD;55
1.5.1.7;Parkinson’s Disease, Motor and Cognitive Impairments, and Phasic Dopaminergic Signaling;56
1.5.1.8;Conclusion;59
1.5.1.9;References;60
1.5.2;Striatal Dendritic Adaptations in Parkinson’s Disease Models;66
1.5.2.1;Introduction;66
1.5.2.2;MSN Dendrites are Excitable;67
1.5.2.3;DA Suppresses While ACh Enhances Dendritic Excitability in the D2 MSNs;69
1.5.2.4;Disconnection of the Indirect Pathway in PD Models;73
1.5.2.5;Functional Implications for the Pathophysiology in PD;76
1.5.2.6;References;77
1.5.3;Diversity of Up-State Voltage Transitions During Different Network States;83
1.5.3.1;Introduction;83
1.5.3.2;Striatal Circuit Arrangement;84
1.5.3.3;The Bistable-Like Behavior of Striatal Medium Spiny Neurons;85
1.5.3.4;Up and Down Voltage Transitions in MSNs;86
1.5.3.5;Up-States: Windows for Ensemble Synchronization;90
1.5.3.6;Conclusions;90
1.5.3.7;References;92
1.5.4;The Corticostriatal Pathway in Parkinson’s Disease;96
1.5.4.1;Introduction;96
1.5.4.2;Corticostriatal Anatomy and Function;96
1.5.4.2.1;Dopaminergic Projections and Receptors in the Motor Striatum;97
1.5.4.2.2;Striatal Organization;98
1.5.4.2.3;Electrophysiological Properties of Striatal D1 and D2 Receptor-Containing MSSNs;99
1.5.4.3;Mouse Models for Parkinsonism;100
1.5.4.4;Effects of Dopamine Deficiency on Postsynaptic Corticostriatal Activity;101
1.5.4.5;Effects of Dopamine Deficiency on Presynaptic Corticostriatal Activity;102
1.5.4.6;Endocannabinoid-Mediated Modulation of the Corticostriatal Pathway;104
1.5.4.7;Acetylcholine-Mediated Modulation of Corticostriatal Afferents;105
1.5.4.8;Summary;106
1.5.4.9;References;107
1.5.5;Cholinergic Interneuron and Parkinsonism;114
1.5.5.1;Introduction;114
1.5.5.2;Cholinergic Interneurons: From Morphological Clues to Functional Evidence;115
1.5.5.3;Animal Models of Parkinson’s Disease;116
1.5.5.3.1;MPTP Model;117
1.5.5.3.2;Rotenone Model;117
1.5.5.3.3;6-Hydroxydopamine Model;118
1.5.5.4;Cholinergic Interneurons and Parkinsonism;118
1.5.5.5;Role of Cholinergic Interneurons in Other Basal Ganglia Disorders;119
1.5.5.6;Future Perspectives;120
1.5.5.7;References;122
1.5.6;Basal Ganglia Network Synchronization in Animal Models of Parkinson’s Disease;125
1.5.6.1;Introduction;125
1.5.6.2;Dopamine Effects on Rate in Basal Ganglia Circuits;126
1.5.6.2.1;Testing Predictions of the Rate-Based Model: Effects of Dopamine Agonists;127
1.5.6.2.2;Testing Predictions of the Rate-Based Model: Effects of Dopamine Loss;128
1.5.6.3;Dopamine Effects on Firing Pattern in Basal Ganglia Circuits;129
1.5.6.3.1;Multisecond Oscillations;129
1.5.6.3.1.1;Dopamine Agonist Effects on Incidence and Frequency of Multisecond Oscillations;130
1.5.6.3.1.2;Dopamine Agonist Effects on Synchronization of Multisecond Oscillations in GPe, STN and SNpr;131
1.5.6.3.2;1 Hz Oscillations;132
1.5.6.3.2.1;Dopamine Cell Lesion Effects on 1 Hz Oscillations in the Basal Ganglia;133
1.5.6.3.2.2;Dopamine Cell Lesion Effects on Phase Relationships of 1 Hz Oscillations in Basal Ganglia Circuits;135
1.5.6.3.3;4-30 Hz Oscillations;138
1.5.6.3.3.1;Dopamine Cell Lesion Effects on 4-30 Hz Oscillations;138
1.5.6.4;Conclusion;140
1.5.6.5;References;141
1.5.7;Converging into a Unified Model of Parkinson’s Disease Pathophysiology;151
1.5.7.1;Slow Waves Versus Activation or Silent Versus Depolarized Network States?;152
1.5.7.2;Spontaneous Activity Downstream the Striatum;155
1.5.7.3;Electrical Stimulation as a Tool to Study the Dynamic Activation of Trans-striatal and Trans-subthalamic Pathways;157
1.5.7.4;Evoked Activity Downstream the Striatum;158
1.5.7.5;Conclusions;160
1.5.7.6;References;162
1.5.8;The Corticostriatal Transmission in Parkinsonian Animals: In Vivo Studies;165
1.5.8.1;Introduction;165
1.5.8.2;Cortical Inputs to Striatonigral and Striatopallidal Neurons in Intact Animals;165
1.5.8.2.1;The Direct and Indirect Striatal Output Pathways;165
1.5.8.2.2;Segregation of D1 and D2 Receptors in Striatonigral and Striatopallidal Neurons: Recent Evidence;166
1.5.8.2.3;Cortical Inputs to Striatonigral and Striatopallidal Neurons;167
1.5.8.2.4;Spontaneous MSN Discharge Activities Generated by Cortical Inputs;168
1.5.8.2.5;MSNs Activities Evoked by Cortical Stimulation;169
1.5.8.2.6;Feedforward Inhibition of MSNs by FS Interneurons;169
1.5.8.3;Effects of the Dopaminergic Depletion on the Corticostriatal Transmission;172
1.5.8.3.1;Effects of DA Depletion on Striatonigral and Striatopallidal Neurons;172
1.5.8.3.2;Effects of DA Depletion on Feedforward Inhibition;172
1.5.8.3.3;Origin of the Striatal Dysfunctions;173
1.5.8.4;Conclusion and Future Prospects;173
1.5.8.5;References;174
1.5.9;Striatal Nitric Oxide-cGMP Signaling in an Animal Model of Parkinson’s Disease;178
1.5.9.1;Parkinson’s Disease;178
1.5.9.2;Striatal Circuitry;179
1.5.9.3;Role of NO-GC Signaling in Motor Behavior;180
1.5.9.4;Impact of Partial Striatal DA Depletions on Motor Behavior;180
1.5.9.5;Impact of DA Depletion on NO-GC Signaling;182
1.5.9.6;Impact of DA Depletion on Striatal MSN Activity and Striatal Output;184
1.5.9.7;Conclusions;188
1.5.9.8;References;188
1.5.10;Dopamine-Endocannabinoid Interactions in Parkinson’s Disease;192
1.5.10.1;Introduction;192
1.5.10.2;Overview of the Endogenous Cannabinoid Signaling System;192
1.5.10.2.1;Cannabinoid Receptor Distribution in the Brain;193
1.5.10.2.2;Endogenous Cannabinoids;194
1.5.10.2.3;Endogenous Cannabinoids: Mode of Action in the CNS;195
1.5.10.3;Dopamine, Cannabinoids and Movement;196
1.5.10.3.1;The Role of the Basal Ganglia in Movement;196
1.5.10.3.2;Dopamine D1 Receptor-Mediated Changes in Motor Activity;198
1.5.10.3.3;Dopamine D2 Receptor-Mediated Changes in Motor Activity;198
1.5.10.3.4;Cannabinoid Receptor Activation and Movement;199
1.5.10.3.5;Convergence of Dopamine and Cannabinoid Receptor Activation: Implications for Motor Control;200
1.5.10.4;Dopamine and Endogenous Cannabinoid Interactions in Striatum;201
1.5.10.4.1;Cannabinoids Exert Excitatory Control over Dopamine Neurotransmission;201
1.5.10.4.2;Endogenous Cannabinoid and Dopamine Dynamics in the Hypodopaminergic State;202
1.5.10.5;Potential for Therapeutic Use of Cannabinoid Receptor Modulators for Parkinson’s Disease;203
1.5.10.5.1;Role of Endogenous Cannabinoid Signaling in Parkinson’s Disease;203
1.5.10.5.2;Therapeutic Use of CB1 Receptor Antagonists;204
1.5.10.5.3;Therapeutic Use of CB1 Receptor Agonists;205
1.5.10.6;Concluding Remarks;205
1.5.10.7;References;206
1.5.11;Glutamate Plasticity in an Animal Model of Parkinson’s Disease;213
1.5.11.1;Time-Dependent Changes in Striatal Glutamate Following Loss of Dopamine;214
1.5.11.1.1;Electron Microscopy/Immunocytochemistry;214
1.5.11.1.2;In Vivo Microdialysis;218
1.5.11.2;Glutamate Plasticity in the Substantia Nigra Pars Reticulata;221
1.5.11.3;Alterations in Glutamate in the Subthalamic Nucleus;223
1.5.11.4;Overall Conclusion;229
1.5.11.5;Reference;230
1.6;Part 3: Computational Analyses of the Cortico-Subcortical Dynamics and Parkinson’s Disease;237
1.6.1;Neuromodulation and Neurodynamics of Striatal Inhibitory Networks: Implications for Parkinson’s Disease;238
1.6.1.1;Introduction;239
1.6.1.2;Electrophysiology of Inhibitory Interactions Between Spiny Projection Neurons;240
1.6.1.3;Competitive Dynamics Among Spiny Projection Neurons;241
1.6.1.4;Neuromodulation of Lateral Inhibition by Dopamine and Adenosine;243
1.6.1.5;Conclusion;245
1.6.1.6;References;245
1.6.2;Dopaminergic Modulation of Corticostriatal Interactions and Implications for Parkinson’s Disease;249
1.6.2.1;Intrinsic Properties and Membrane Behavior of MSP Neurons;250
1.6.2.2;Computational Model;250
1.6.2.3;Functional role of MSP Cells and DA Modulation;251
1.6.2.4;Modulation Conditions;252
1.6.2.5;D1-Receptor-Mediated Modulation and Nonlinearity in the Model MSN;253
1.6.2.6;Excitatory/Inhibitory Properties of DA Modulation;254
1.6.2.7;Dopamine and Temporal Integration Properties of the MSN;256
1.6.2.8;Local and Network Level Inhibition;257
1.6.2.9;Implications of MSN Responses for BG Models;258
1.6.2.10;Implications for Parkinson’s Disease;259
1.6.2.11;References;260
1.7;Part 4: Neurobiology and Pathophysiology of Parkinson’s Disease;263
1.7.1;Pathogenesis of Oxidative Stress and the Destructive Cycle in the Substantia Nigra in Parkinson’s Disease;264
1.7.1.1;Fundamental Aspects of Reactive Oxygen Species;264
1.7.1.2;Can Cell Death in Substantia Nigra be Caused by Oxidative Damage?;264
1.7.1.3;Substantia Nigra is Subjected to Oxidative Stress in PD: The Destructive Toxic Cycle;267
1.7.1.4;Mitochondrial Dyisfunction and the ‘‘Toxic Cycle’’;269
1.7.1.5;Excitotoxic Damage: Role of Glutamate;270
1.7.1.6;Neuroinflammatory Phenomena in the Substantia Nigra;271
1.7.1.7;Conclusions;272
1.7.1.8;References;272
1.7.2;Regulation of G-Protein-Coupled Receptor (GPCR) Trafficking in the Striatum in Parkinson’s Disease;275
1.7.2.1;Dopamine Receptor Trafficking Under Homologous Stimulation in the Striatum;276
1.7.2.2;D1R Trafficking;276
1.7.2.3;Striatal D2R Trafficking;277
1.7.2.4;Dopamine Receptor Trafficking in Parkinson’s Disease;277
1.7.2.5;Glutamate and Dopamine Receptor Trafficking Under Heterologous Stimulation;279
1.7.2.6;Conclusions;280
1.7.2.7;References;280
1.7.3;Atypical Parkinsonism in the French West Indies: The Plant Toxin Annonacin as a Potential Etiological Factor;284
1.7.3.1;Introduction;285
1.7.3.2;Clinical Features of the Disease Entity;285
1.7.3.2.1;Guadeloupean Atypical Parkinsonism Has Two Distinct Phenotypes;285
1.7.3.2.2;Neuroimaging Features of Atypical Parkinsonian Patients;286
1.7.3.2.3;Neuropathological Data;286
1.7.3.2.4;REM Sleep Behavior Disorder in Patients with Guadeloupean Parkinsonism;286
1.7.3.3;Candidate Etiological Factors;287
1.7.3.3.1;Plant Toxins;287
1.7.3.3.2;Other Potential Etiological Factors;287
1.7.3.4;The Complex I Inhibitor Annonacin as a Possible Etiological Factor;288
1.7.3.4.1;Neurodegenerative Changes Induced by Annonacin;288
1.7.3.4.2;Can Annonacin Intoxication Reproduce the Tau Pathology of the Disease?;289
1.7.3.5;References;290
1.7.4;Cognitive Deficits in Parkinson’s Disease;292
1.7.4.1;Introduction;292
1.7.4.2;Epidemiology;293
1.7.4.3;Cognitive Features in Parkinson’s Disease;294
1.7.4.4;Neuropsychiatric Symptoms in Parkinson’s Disease;295
1.7.4.5;Functional Changes Underlying Cognitive Deficits in Parkinson’s Disease;296
1.7.4.6;Genetics of PDD;297
1.7.4.7;Pathological Correlations;298
1.7.4.8;Summary and Conclusions;300
1.7.4.9;References;300
1.8;Part 5: Pharmacological and Non-Pharmacological Treatments in Parkinson’s Disease;307
1.8.1;Dopamine Replacement Therapy in Parkinson’s Disease: Past, Present and Future;308
1.8.1.1;L-DOPA Pharmacotherapy in Perspective;308
1.8.1.2;Current Options for a Dopaminergic Pharmacotherapy in PD;310
1.8.1.3;The Concept of Continuous Dopamine Stimulation and the Ways to Achieve It;314
1.8.1.3.1;Continuous Duodenal or jeujenal Infusion of l-DOPA;315
1.8.1.3.2;Transdermal Drug Delivery;316
1.8.1.3.3;‘‘Enzyme Replacement Therapy’’ by Gene Transfer;316
1.8.1.3.4;Neural Transplantation;317
1.8.1.4;Adjunct Treatments to Prevent or Treat Motor Complications;318
1.8.1.5;The Challenge of l-DOPA-Resistant Symptoms;320
1.8.1.6;Current Treatment Options for l-DOPA-Resistant Symptoms;322
1.8.1.6.1;Cognitive Dysfunction;322
1.8.1.6.2;Dopamine Dysregulation Syndrome and Impulse Control Disorders;322
1.8.1.6.3;Psychosis;322
1.8.1.6.4;Depression;323
1.8.1.6.5;Sleep;323
1.8.1.6.6;Autonomic Symptoms;323
1.8.1.6.7;L-DOPA-Resistant Gait, Freezing and Balance Problems;323
1.8.1.7;Concluding Remarks;324
1.8.1.8;References;325
1.8.2;Molecular, Cellular and Electrophysiological Changes Triggered by High-Frequency Stimulation of the Subthalamic Nucleus in Animal Models of Parkinson’s Disease;334
1.8.2.1;Introduction;334
1.8.2.1.1;Deep Brain Stimulation and Parkinson’s Disease;334
1.8.2.1.2;Experimental Models of Parkinson’s Disease;337
1.8.2.1.2.1;Reserpine;337
1.8.2.1.2.2;Haldol/Haloperidol;337
1.8.2.1.2.3;6-OHDA;338
1.8.2.1.2.4;MPTP;338
1.8.2.1.3;Electrophysiological Properties of STN Neurons;338
1.8.2.2;High-Frequency Stimulation of the STN: In Vitro Approaches;342
1.8.2.2.1;Electrophysiological Effects of In Vitro STN HFS;342
1.8.2.2.2;Other Effects of STN HFS;346
1.8.2.2.3;Main Contributions of In Vitro Approaches;347
1.8.2.3;High-Frequency Stimulation of the STN: In Vivo Approaches;348
1.8.2.3.1;Effects Ex Vivo;349
1.8.2.3.1.1;Brain Metabolism;349
1.8.2.3.1.2;Neuronal Activity and Plasticity in the STN;349
1.8.2.3.1.3;Neuronal Activity and Plasticity Outside the STN;350
1.8.2.3.1.4;Neuroprotective and Dopaminergic Effects of STN HFS;351
1.8.2.3.1.5;Electrophysiological Effects of STN HFS;352
1.8.2.3.2;Effects In Vivo;353
1.8.2.3.2.1;Electrophysiological Effects of STN HFS in the STN;353
1.8.2.3.2.2;Electrophysiological Effects of STN HFS Outside the STN;355
1.8.2.3.2.3;Biochemical Effects of STN HFS;360
1.8.2.3.3;Main Contributions of In Vivo Approaches;361
1.8.2.4;References;362
1.8.3;Surgical Strategies for Parkinson’s Disease Based on Animal Model Data: GPi and STN Inactivation on Various Aspects of Behavior (Motor, Cognitive and Motivational Processes);370
1.8.3.1;Introduction;370
1.8.3.2;The Internal Globus Pallidus (GPi);371
1.8.3.2.1;Motor Behavior;371
1.8.3.2.1.1;Lesion and Pharmacological Data in the Monkey;371
1.8.3.2.1.2;GPi HFS Data in the Monkey;372
1.8.3.2.1.3;Lesion Data and Pharmacological Manipulations in the Rat;372
1.8.3.2.1.4;EP HFS Data in the Rat;374
1.8.3.2.2;Cognitive Behavior: What Is Available in Animal Models?;374
1.8.3.3;The STN;374
1.8.3.3.1;Motor Behavior;375
1.8.3.3.1.1;Lesion Data in Monkeys;375
1.8.3.3.1.2;STN HFS Data in Monkeys;375
1.8.3.3.1.3;Lesion and Pharmacological Data in Rats;375
1.8.3.3.1.4;STN HFS Data in Rats;377
1.8.3.3.2;Cognitive Behavior;379
1.8.3.3.2.1;Lesions or STN HFS Data in Monkeys;380
1.8.3.3.2.2;Lesion Data in Rats;380
1.8.3.3.2.3;STN HFS Data in Rats;382
1.8.3.3.3;Motivational Behavior and Psychiatric Models;384
1.8.3.4;Conclusion;386
1.8.3.5;References;386
1.8.4;Antidromic Cortical Activity as the Source of Therapeutic Actions of Deep Brain Stimulation;391
1.8.4.1;Introduction;391
1.8.4.2;A Direct Test of the Idea in Anaesthetised Animals;392
1.8.4.3;Some Experiments on Alert Animals;395
1.8.4.4;Resonance as the Explanation for Frequency Dependence;396
1.8.4.5;Some Suggestions for Future Work;398
1.8.4.6;References;399
1.8.5;Cell-Based Replacement Therapies for Parkinson’s Disease;402
1.8.5.1;Introduction;402
1.8.5.2;Grafts Based on Cells of the Sympathoadrenal Cell Lineage;404
1.8.5.2.1;Sympathetic Neurons;405
1.8.5.2.2;Adrenal Chromaffin Cells;406
1.8.5.2.3;Extra-Adrenal Chromaffin Cells;408
1.8.5.2.4;Advantages of Transplanting SA Lineage Cells;411
1.8.5.3;Carotid Body Dopamine Cells;411
1.8.5.4;Fetal Mesencephalic Neurons;412
1.8.5.5;Stem Cells;414
1.8.5.5.1;Generation of DA Neurons from VM Neural Stem/Progenitor Cells (NSC/NP);415
1.8.5.5.2;Generation of DA Neurons from Other NSCs;415
1.8.5.5.3;Generation of DA Neurons from Embryonic Stem Cells (ESCs);416
1.8.5.6;Neural Xenotransplantation;418
1.8.5.7;Genetically Engineered Autologous Tissue;419
1.8.5.8;Retinal Pigmental Epithelial Cells;419
1.8.5.9;References;420
1.9;Index;429