The basal ganglia novel perspectives on motor and cognitive functions

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The basal ganglia   novel perspectives on motor and cognitive functions

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Innovations in Cognitive Neuroscience Series Editor: Vinoth Jagaroo Jean-Jacques Soghomonian Editor The Basal Ganglia Novel Perspectives on Motor and Cognitive Functions Innovations in Cognitive Neuroscience More information about this series at http://www.springer.com/series/8817 Jean-Jacques Soghomonian Editor The Basal Ganglia Novel Perspectives on Motor and Cognitive Functions Editor Jean-Jacques Soghomonian Department of Anatomy and Neurobiology Boston University School of Medicine Boston, MA, USA ISSN 2509-730X ISSN 2509-7318 (electronic) Innovations in Cognitive Neuroscience ISBN 978-3-319-42741-6 ISBN 978-3-319-42743-0 (eBook) DOI 10.1007/978-3-319-42743-0 Library of Congress Control Number: 2016948218 © Springer International Publishing Switzerland 2016 This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed The use of general descriptive names, registered names, trademarks, service marks, etc in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made Printed on acid-free paper This Springer imprint is published by Springer Nature The registered company is Springer International Publishing AG Switzerland To Allison and Emilie Preface Descriptions of the deep brain structures that have come to be called the “basal ganglia” can be traced back as far as 350 years based on recorded anatomical observations, notably those published in 1664 by the English anatomist Thomas Willis Yet, for much of this time, the basal ganglia have held a certain enigmatic quality in terms of their functions The conception held late into the twentieth century that the basal ganglia were associated largely with motor control or coordination had a few roots Basal ganglia ablation studies in animals that began in the nineteenth century showed dramatically marked motor symptomatology In clinical neurology, features such as dystonia, dyskinesia, and chorea, manifesting in neurodegenerative disorders with known involvement of the basal ganglia structures, reasonably reinforced the prominence of the motor-centered view Pioneering work in neurobiology conducted in the 1960s and 1970s began the sea of change in the contemporary understanding of the basal ganglia Progress was made possible thanks to the advent of novel investigative methods that permitted more precise analysis of anatomical pathways and the discovery of various neuronal phenotypes throughout the basal ganglia On another front, anatomical and physiological studies carried out in the late 1970s and early 1980s led to the concept of parallel, segregated basal ganglia circuits, while other studies led to the concept of a ventral, “limbic” basal ganglia, and, at a more cellular level, other studies led to the concept of a direct and indirect pathway These advances have been documented in several reviews and volumes By the 1980s, there was early convergence of data from neuroscience and neuropsychology, broadening the conceptual framework of the basal ganglia to include functions of cognition, emotion, and motivation While the inertia in the motorcentered world of the basal ganglia did not fade overnight, studies from diverse avenues of neuroscience, enabled by novel research techniques, began to reveal a complex neural architecture and functional diversity As a complex system of interface between intention and action, the role of the basal ganglia has encroached into processes traditionally associated with the cerebral cortex and hippocampus such as language, memory, reinforcement, and associative learning Its role in the sequencing of learned associations was brought to bear on multiple functional domains vii viii Preface This also highlighted its importance in neurocognitive, neuropsychiatric, and neurodegenerative motor disorders Over the last two decades, the intensification of neuroscience efforts combined with astonishing advances in imaging, genetic, and molecular methods has led to further demystify the basal ganglia and to revise its role in motor and non-motor functions It is now established that the basal ganglia can be subdivided into several anatomical and functional territories that share different connectivity with cortical and subcortical centers These advances combined with a more detailed understanding of the cellular and molecular organization have provided the framework for novel integrative and computational models of the basal ganglia Yet, even with all the progress in understanding the basal ganglia, perspective of its functions as currently understood is neither readily present nor easily articulated in the general arena of behavioral neuroscience This volume presents many of the recent developments relating to neural architecture and functional circuitry of the basal ganglia; the role of the basal ganglia across many of the neurobehavioral domains—motor and cognitive function, emotion, and motivation, etc.; and the manifestations of these basal ganglia-mediated functions in various motor, cognitive, and neuropsychiatric disorders The volume assembles contributions from eminent basal ganglia researchers and covers perspectives across subdisciplines of neuroscience while being grounded in cognitive neuroscience and neurobiology In addition to the basal ganglia and neuroscience research community, the volume should be of interest to practitioners in neuropsychology, neurology, neuropsychiatry, and speech-language pathology Boston, MA Jean-Jacques Soghomonian Acknowledgments I am grateful to my colleagues for their generosity in contributing chapters to this volume I would also like to thank Janice Stern and Christina Tuballes at Springer for their guidance and patience and the series editor Vinoth Jagaroo for his invitation to produce the volume, his constructive feedback, and his unwavering encouragement during the production of this volume I acknowledge Yukiha Maruyama and Kim Wang for their assistance with many aspects of the project especially with preparation of the manuscript and Edith Soghomonian for her artistic renderings of the basal ganglia ix Contents Introduction: Overview of the Basal Ganglia and Structure of the Volume Jean-Jacques Soghomonian and Vinoth Jagaroo Part I Functional and Anatomical Organization of Basal Ganglia: Limbic and Motor Circuits Limbic-Basal Ganglia Circuits Parallel and Integrative Aspects Henk J Groenewegen, Pieter Voorn, and Jørgen Scheel-Krüger Anatomy and Function of the Direct and Indirect Striatal Pathways Jean-Jacques Soghomonian 11 47 The Thalamostriatal System and Cognition Yoland Smith, Rosa Villalba, and Adriana Galvan 69 Dopamine and Its Actions in the Basal Ganglia System Daniel Bullock 87 Part II Motor Function, Dystonia and Dyskinesia Cortico-Striatal, Cognitive-Motor Interactions Underlying Complex Movement Control Deficits 117 Aaron Kucinski and Martin Sarter Interactions Between the Basal Ganglia and the Cerebellum and Role in Neurological Disorders 135 Christopher H Chen, Diany Paola Calderon, and Kamran Khodakhah Signaling Mechanisms in L-DOPA-Induced Dyskinesia 155 Cristina Alcacer, Veronica Francardo, and M Angela Cenci xi xii Contents Part III Perception, Learning and Cognition Cognitive and Perceptual Impairments in Parkinson’s Disease Arising from Dysfunction of the Cortex and Basal Ganglia 189 Deepti Putcha, Abhishek Jaywant, and Alice Cronin-Golomb 10 The Basal Ganglia and Language: A Tale of Two Loops 217 Anastasia Bohsali and Bruce Crosson 11 The Basal Ganglia Contribution to Controlled and Automatic Processing 243 Estrella Díaz, Juan-Pedro Vargas, and Juan-Carlos López 12 Striatal Mechanisms of Associative Learning and Dysfunction in Neurological Disease 261 Shaun R Patel, Jennifer J Cheng, Arjun R Khanna, Rupen Desai, and Emad N Eskandar 13 Alcohol Effects on the Dorsal Striatum 289 Mary H Patton, Aparna P Shah, and Brian N Mathur Part IV Motivation, Decision Making, Reinforcement and Addiction 14 The Subthalamic Nucleus and Reward-Related Processes 319 Christelle Baunez 15 The Basal Ganglia and Decision-Making in Neuropsychiatric Disorders 339 Sule Tinaz and Chantal E Stern 16 Motivational Deficits in Parkinson’s Disease: Role of the Dopaminergic System and Deep-Brain Stimulation of the Subthalamic Nucleus 363 Sabrina Boulet, Carole Carcenac, Marc Savasta, and Sébastien Carnicella 17 The Circuitry Underlying the Reinstatement of Cocaine Seeking: Modulation by Deep Brain Stimulation 389 Leonardo A Guercio and R Christopher Pierce Part V Computational Models and Integrative Perspectives 18 Cognitive and Stimulus–Response Habit Functions of the Neo- (Dorsal) Striatum 413 Bryan D Devan, Nufar Chaban, Jessica Piscopello, Scott H Deibel, and Robert J McDonald 19 Neural Dynamics of the Basal Ganglia During Perceptual, Cognitive, and Motor Learning and Gating 457 Stephen Grossberg ... architecture and functional circuitry of the basal ganglia; the role of the basal ganglia across many of the neurobehavioral domains motor and cognitive function, emotion, and motivation, etc.; and the. .. impact on basal ganglia research These methods have contributed to broaden and deepen our understanding of motor and non -motor functions of the basal ganglia Its functional anatomical organization... of the Volume The objective of this volume is, again, to present recent perspectives on the contributions of the basal ganglia to motor control and cognitive function, emotion, and motivation

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  • Dedication

  • Preface

  • Acknowledgments

  • Contents

  • Contributors

  • Abbreviations

  • Chapter 1: Introduction: Overview of the Basal Ganglia and Structure of the Volume

    • 1.1 Why a Volume on the Basal Ganglia?

    • 1.2 Anatomic Layout and Nomenclature

    • 1.3 Structure of the Volume

    • References

  • Part I: Functional and Anatomical Organization of Basal Ganglia: Limbic and Motor Circuits

    • Chapter 2: Limbic-Basal Ganglia Circuits Parallel and Integrative Aspects

      • 2.1 Introduction: The Evolvement of the Concept of the Ventral Striatopallidal System

      • 2.2 What Is the “Limbic” Ventral Striatum?

      • 2.3 Afferent Connections of the “Limbic” Striatum

        • 2.3.1 Hippocampal and Amygdaloid Inputs

        • 2.3.2 Cortical Inputs

        • 2.3.3 Subcortical Inputs

        • 2.3.4 Distribution of Glutamate and GABA Transporters in the Striatum

      • 2.4 Intrinsic Striatal Circuitry

        • 2.4.1 Cholinergic Interneurons

        • 2.4.2 GABAergic Interneurons

      • 2.5 Efferent Connections of the “Limbic” Striatum

        • 2.5.1 Ventral Striatal Efferents

        • 2.5.2 Ventral Striatopallidal Projections: The Extended Circuitry

      • 2.6 Concluding Remarks and Future Perspectives

      • References

    • Chapter 3: Anatomy and Function of the Direct and Indirect Striatal Pathways

      • 3.1 Introduction

      • 3.2 Phenotypic Diversity of Medium Spiny Striatal Neurons

        • 3.2.1 Co-expression of Peptides

        • 3.2.2 Medium Spiny Neurons Connectivity

        • 3.2.3 Segregated Expression of Dopamine Receptors

        • 3.2.4 Membrane Properties of Direct and Indirect Pathway Neurons

      • 3.3 Functions of the Direct and Indirect Pathway

        • 3.3.1 Movement Control

        • 3.3.2 Associative Learning, Social Behavior, and Decision Making

        • 3.3.3 Addiction and Obesity

      • 3.4 Conclusions

      • References

    • Chapter 4: The Thalamostriatal System and Cognition

      • 4.1 Introduction

      • 4.2 Anatomy of the CM/PF-Striatal System

      • 4.3 The Dual CM/Pf-Versus Non-CM/Pf-Striatal Systems

      • 4.4 The CM/Pf-Striatal System Regulates Activity of Striatal Cholinergic Interneurons

      • 4.5 Differential Role of CM and Pf Neurons in Cognition

      • 4.6 CM/Pf Cell Loss in Neurodegenerative Diseases: Potential Impact upon Early Cognitive Impairments

      • 4.7 The CM/PF as a Target for Neurosurgical Interventions in Brain Disorders

      • 4.8 Concluding Remarks

      • References

    • Chapter 5: Dopamine and Its Actions in the Basal Ganglia System

      • 5.1 Introduction: Consensus Summary of Dopamine’s Actions in the Circuitry of the Basal Ganglia

      • 5.2 The Dopamine-Acetylcholine Cascade in Striatum

      • 5.3 Multiple Components Found in Dopamine Neuron Signals

        • 5.3.1 Dopamine as an Internal Reinforcement Signal

        • 5.3.2 Reward Prediction Errors, Punishment Prediction Errors, or Both?

        • 5.3.3 Dopamine Cell Firing Rate Is Only One Factor Controlling Dopamine Release Amounts

        • 5.3.4 Does the Magnitude of Dopamine Release Indicate the Subjective Utility of an Option?

        • 5.3.5 Dopaminergic Control of Synaptic Plasticity

        • 5.3.6 Dynamics of DA Signaling Across Ventromedial to Dorsolateral Striatum in Habit Formation

        • 5.3.7 Formal Models for Learned Control of DA Release, and Learning Effects of DA Release

        • 5.3.8 The Role of Dopamine in Electrical Coupling and Synchronous Oscillations

      • 5.4 Conclusions: Dopamine’s Broad Implications

      • References

  • Part II: Motor Function, Dystonia and Dyskinesia

    • Chapter 6: Cortico-Striatal, Cognitive-Motor Interactions Underlying Complex Movement Control Deficits

      • 6.1 Introduction

      • 6.2 Cortico-Striatal, Cognitive-Motor Deficits in Parkinson’s Disease

      • 6.3 Modeling Falls and Cognitive-Motor Deficits with Dual Cholinergic and Dopaminergic System Losses

      • 6.4 Falls Resulting from Extensive Striatal Dopamine Loss

      • 6.5 Preventing Falls

      • 6.6 Conclusions and Future Directions

      • References

    • Chapter 7: Interactions Between the Basal Ganglia and the Cerebellum and Role in Neurological Disorders

      • 7.1 The Cerebellum

      • 7.2 The Basal Ganglia

      • 7.3 Cerebellar-Basal Ganglia Interactions: Historical Perspective

      • 7.4 Basal Ganglia to Cerebellar Communication

      • 7.5 Pathological Consequences of Aberrant Interaction Between the Cerebellum and Basal Ganglia

        • 7.5.1 Rapid Onset Dystonia Parkinsonism (DYT12)

        • 7.5.2 Aberrant Cerebellar Activity May Prompt Dystonia in Other Pathologies

          • 7.5.2.1 Myoclonus Dystonia (DYT11)

          • 7.5.2.2 Early Onset Primary Dystonia (DYT1)

          • 7.5.2.3 Whispering Dysphonia (DYT4)

          • 7.5.2.4 Syndromes Associated with Mutations in the α3 sodium pump

        • 7.5.3 Parkinson’s Disease

        • 7.5.4 Psychiatric Disorders

      • Conclusion

      • References

    • Chapter 8: Signaling Mechanisms in l-DOPA-Induced Dyskinesia

      • 8.1 Introduction

      • 8.2 Dopamine D1 Receptor Supersensitivity

        • 8.2.1 Increased Coupling of D1R to G Protein and Enhanced Adenylyl Cyclase Activity in LID

        • 8.2.2 Altered Trafficking of D1 Receptors

        • 8.2.3 Formation of Novel Signaling Complexes

      • 8.3 Intracellular Signaling Pathways

        • 8.3.1 Canonical cAMP-Related Pathways

        • 8.3.2 Non-canonical Pathways

        • 8.3.3 Nuclear Signaling Events

        • 8.3.4 Protein Translation Pathways

      • 8.4 Striatal Synaptic Plasticity

      • 8.5 Changes in the Phosphorylation and Trafficking of Glutamate Receptors

      • 8.6 Profiles of Genes and Protein Expression

        • 8.6.1 Changes in Expression and Regulation of Transcription Factors and Immediate Early Genes

        • 8.6.2 Gene Expression Profiles Associated with LID

      • 8.7 Non-neuronal Mechanisms

        • 8.7.1 Gliovascular Mechanisms

        • 8.7.2 Changes in BBB Permeability

      • 8.8 Summary and Conclusions

      • References

  • Part III: Perception, Learning and Cognition

    • Chapter 9: Cognitive and Perceptual Impairments in Parkinson’s Disease Arising from Dysfunction of the Cortex and Basal Ganglia

      • 9.1 Introduction

      • 9.2 Cortico-Striatal Connectivity and Cognition

      • 9.3 Cognition in Parkinson’s Disease

      • 9.4 Visual Perception in Parkinson’s Disease

      • 9.5 Relation of Visual Perception to Cognition in Parkinson Disease

      • 9.6 Perception-Action Coupling in PD

      • 9.7 Concluding Remarks

      • References

    • Chapter 10: The Basal Ganglia and Language: A Tale of Two Loops

      • 10.1 Introduction

      • 10.2 Anatomy

        • 10.2.1 Broca’s Area–Basal Ganglia Loops

        • 10.2.2 Pre-SMA–Basal Ganglia Loops

        • 10.2.3 Connections Between Pre-SMA and Broca’s Area

      • 10.3 Function

        • 10.3.1 Pre-SMA–Basal Ganglia Loops

        • 10.3.2 Broca’s Area–Basal Ganglia Loops

        • 10.3.3 Interactions Between Pre-SMA and Broca’s Area Loops

      • 10.4 Conclusions

      • References

    • Chapter 11: The Basal Ganglia Contribution to Controlled and Automatic Processing

      • 11.1 Automatic and Controlled Processes: A Historical View

      • 11.2 Controlled Versus Automatic: A Continuum Processes?

        • 11.2.1 Learning Based on the Predictive Value of a CS

        • 11.2.2 The Operant as a Tool for the Study of Goal-Directed and Automatic Responses

      • 11.3 Implications of Striatal Networks in Maladaptive Behavior

        • 11.3.1 Drug Addition and Automatic Response to Environmental Stimuli

        • 11.3.2 Degenerative Diseases of Nigrostriatal System Support a Double Mechanism of Learning

      • 11.4 Striatal Networks and Interference Processes

      • 11.5 Dorsolateral Striatal Activity and the Increases in Conditioning: More Than an S-R Function

      • 11.6 Theoretical Implications to Learning Models: Interference vs. Attentional Decreases

        • 11.6.1 Recovery or Acquisition Failure?

        • 11.6.2 The Interference as an Action Mechanism in the Dorsal Striatum

      • 11.7 Conclusions

      • References

    • Chapter 12: Striatal Mechanisms of Associative Learning and Dysfunction in Neurological Disease

      • 12.1 Introduction: Basal Ganglia Anatomy

      • 12.2 Basal Ganglia Models

      • 12.3 Neuropsychological and Cellular Mechanisms of Learning

      • 12.4 Dysfunctions of Associative Learning in Pathology

        • 12.4.1 Parkinson’s Disease

        • 12.4.2 Schizophrenia

        • 12.4.3 Obsessive-Compulsive Disorder

        • 12.4.4 Huntington’s Disease

        • 12.4.5 Other Disorders

      • 12.5 Future Directions and Conclusions

      • References

    • Chapter 13: Alcohol Effects on the Dorsal Striatum

      • 13.1 Introduction

      • 13.2 Effects of Acute Ethanol on Physiology in the Dorsal Striatum

      • 13.3 Effects of Chronic Ethanol on Dorsal Striatum Physiology

      • 13.4 Effects of Ethanol on Striatal-Mediated Behaviors

      • 13.5 Conclusions

      • References

  • Part IV: Motivation, Decision Making, Reinforcement and Addiction

    • Chapter 14: The Subthalamic Nucleus and Reward-­Related Processes

      • 14.1 Introduction

      • 14.2 Anatomy and Connectivity of the Subthalamic Nucleus: From a Motor Relay Structure to a Limbic Structure

        • 14.2.1 Inputs to the STN

        • 14.2.2 Outputs from the STN

        • 14.2.3 STN in the Reward Circuit

      • 14.3 Subthalamic Nucleus and Primary Processes of Motivation: Consumption

        • 14.3.1 Food Consumption

        • 14.3.2 Alcohol Consumption

        • 14.3.3 Drug Consumption

      • 14.4 STN and Secondary Processes of Motivation

        • 14.4.1 STN and Reward-Related Information: Electrophysiological Data

        • 14.4.2 Incentive Motivation

          • 14.4.2.1 Food Reward

          • 14.4.2.2 Drugs and Other Rewards: Towards Addiction

            • Cocaine and Psychostimulants

            • Alcohol

            • Heroin

            • Sex

            • Conclusions

      • 14.5 STN and Addiction

      • 14.6 Conclusions

      • References

    • Chapter 15: The Basal Ganglia and Decision-Making in Neuropsychiatric Disorders

      • 15.1 Introduction

      • 15.2 Definitions

        • 15.2.1 Decision-Making

        • 15.2.2 Reward

        • 15.2.3 Expected Value

        • 15.2.4 Expected Utility

        • 15.2.5 Prediction Error

        • 15.2.6 Uncertainty, Risk, and Ambiguity

        • 15.2.7 Prospect Theory

        • 15.2.8 Temporal Discounting

      • 15.3 Neural Correlates

        • 15.3.1 Reward Magnitude, Probability, Delay, and Reward Prediction Error

        • 15.3.2 Reward Uncertainty

        • 15.3.3 Reward Context

      • 15.4 Problems with Decision-Making in Neuropsychiatric Disorders

        • 15.4.1 Parkinson’s Disease

        • 15.4.2 Attention Deficit Hyperactivity Disorder

        • 15.4.3 Obsessive Compulsive Disorder

        • 15.4.4 Tourette Syndrome

        • 15.4.5 Schizophrenia

        • 15.4.6 Mood Disorders

      • 15.5 Conclusion

      • References

    • Chapter 16: Motivational Deficits in Parkinson’s Disease: Role of the Dopaminergic System and Deep-­Brain Stimulation of the Subthalamic Nucleus

      • 16.1 Introduction

      • 16.2 Nosology and Pathophysiology of Apathy

        • 16.2.1 Nosology of Apathy

        • 16.2.2 A “Two-Head” Pathophysiological Hypothesis of Apathy in Parkinson’s Disease

      • 16.3 The Dopaminergic Nigrostriatal System and Motivational Deficits in Parkinson’s Disease

        • 16.3.1 Functional Dissociation of the Dopaminergic Mesocorticolimbic and Nigrostriatal Systems

        • 16.3.2 Bilateral Partial Dopaminergic Lesions of the SNc, but not of the VTA, Specifically Impair Motivated and Affective Behaviors

        • 16.3.3 Reversal of the Behavioral Deficits Resulting from Nigrostriatal Dopaminergic Denervation by Dopaminergic Medications: Implication of the Dopamine D3 Receptor

        • 16.3.4 Conclusions

      • 16.4 Motivational Deficits in Parkinson’s Disease Patients Under Deep-Brain Stimulation of the Subthalamic Nucleus: Is the Dopaminergic System Implicated?

        • 16.4.1 Non-motor Symptoms Associated with STN-DBS in PD Patients

        • 16.4.2 Motivational and Affective Deficits and STN-DBS: What Can We Learn from Experimental Studies

        • 16.4.3 Proposed Mechanism for the Motivational Deficits Associated with STN-DBS: The Role of the Dopaminergic System

        • 16.4.4 Conclusions

      • 16.5 Concluding Remarks

      • References

    • Chapter 17: The Circuitry Underlying the Reinstatement of Cocaine Seeking: Modulation by Deep Brain Stimulation

      • 17.1 Introduction

      • 17.2 Neuronal Circuitry Underlying Cocaine Reinstatement

      • 17.3 The Role of the Nucleus Accumbens in Cocaine Seeking

        • 17.3.1 Priming-Induced Reinstatement of Cocaine Seeking in the Nucleus Accumbens

        • 17.3.2 Cue-Induced Reinstatement of Cocaine Seeking in the Nucleus Accumbens

        • 17.3.3 Stress-Induced Reinstatement of Cocaine Seeking in the Nucleus Accumbens

        • 17.3.4 Non-pharmacological Manipulations of the Nucleus Accumbens in the Reinstatement of Cocaine-Seeking Behavior

      • 17.4 The Role of the mPFC in the Reinstatement of Cocaine Seeking

        • 17.4.1 Priming-Induced Reinstatement of Cocaine Seeking in the mPFC

        • 17.4.2 Cue-Induced Reinstatement of Cocaine Seeking in the mPFC

        • 17.4.3 Stress-Induced Reinstatement of Cocaine Seeking in the mPFC

        • 17.4.4 Non-pharmacological Manipulations of the mPFC in the Reinstatement of Cocaine-Seeking Behavior

      • 17.5 The Role of the Hippocampus in the Reinstatement of Cocaine Seeking

        • 17.5.1 Priming-Induced Reinstatement of Cocaine Seeking in the Hippocampus

        • 17.5.2 Cue-Induced Reinstatement of Cocaine Seeking in the Hippocampus

        • 17.5.3 Non-pharmacological Manipulations of the Hippocampus in the Reinstatement of Cocaine-­Seeking Behavior

      • 17.6 The Role of the Basolateral Amygdala in the Reinstatement of Cocaine Seeking

        • 17.6.1 Priming-Induced Reinstatement of Cocaine Seeking in the BLA

        • 17.6.2 Cue-Induced Reinstatement of Cocaine Seeking in the Basolateral Amygdala

        • 17.6.3 Non-pharmacological Manipulations of the Basolateral Amygdala in the Reinstatement of Cocaine-Seeking Behavior

      • 17.7 Concluding Remarks

      • References

  • Part V: Computational Models and Integrative Perspectives

    • Chapter 18: Cognitive and Stimulus–Response Habit Functions of the Neo- (Dorsal) Striatum

      • 18.1 Introduction: A Historical Perspective

      • 18.2 Neuroanatomy

      • 18.3 Neurochemical Compartmentalization

        • 18.3.1 Compartmental Interactions and Reinforcement Learning

        • 18.3.2 Neurobehavioral Integration

        • 18.3.3 Summary

      • 18.4 In-Vivo Electrophysiological Techniques

        • 18.4.1 More Recent Electrophysiological Approaches

        • 18.4.2 Summary

      • 18.5 Bayesian Computational Approaches

        • 18.5.1 Thomas Bayes

        • 18.5.2 Bayesian Approaches Applied to Sensorimotor Learning

        • 18.5.3 Which Learning and Memory System Controls Behavior?: Systems Behavioral Neuroscience Combined with Bayesian Approaches

        • 18.5.4 Model-Free and Model-Based Controllers for Instrumental Learning: Bayesian Approaches

        • 18.5.5 Seminal Computations

        • 18.5.6 Other Variants

        • 18.5.7 How Well Do These Models Fit with the Data?

          • 18.5.7.1 Behavior and Neural Correlates

          • 18.5.7.2 Strategy Selection

          • 18.5.7.3 Changes in Task Parameters

          • 18.5.7.4 External Factors

          • 18.5.7.5 Individual Differences

          • 18.5.7.6 Pathologies

          • 18.5.7.7 Are Model-Free and Model-Based Behaviors Dissociable?

        • 18.5.8 Summary

      • 18.6 Final Conclusions

      • References

    • Chapter 19: Neural Dynamics of the Basal Ganglia During Perceptual, Cognitive, and Motor Learning and Gating

      • 19.1 Introduction

        • 19.1.1 Linking Brain to Mind with Neural Models: Method of Minimal Anatomies

        • 19.1.2 Modeling the Basal Ganglia

        • 19.1.3 Complementary Computing and Laminar Computing

      • 19.2 Neural Models for Reinforcement Learning and Action Selection and Planning

      • 19.3 Adaptively Timed Reinforcement Learning in Response to Unexpected Rewards

        • 19.3.1 Balancing Fast Excitatory Conditioning Against Adaptively Timed Inhibitory Conditioning

        • 19.3.2 Spectral Adaptively Timed Inhibitory Conditioning by Ca2+ and mGluR

        • 19.3.3 Spectrally Timed Learning in Basal Ganglia, Hippocampus, and Cerebellum

        • 19.3.4 Neural Relativity: Space and Time in the Entorhinal-­Hippocampal System

      • 19.4 Associative and Reinforcement Learning of Eye Movements

        • 19.4.1 Eye Movements as a Model System for Understanding Movement and Cognition

        • 19.4.2 How Does the Brain “Know Before It Knows”? Gating Reactive and Planned Behaviors

        • 19.4.3 Frontal–Parietal Resonance Codes Plan Choice and Leads to Planned Gate Opening

        • 19.4.4 Spatially Invariant Object Categories Control Spatially Directed Actions

      • 19.5 Basal Ganglia Gating of Variable-Speed Arm Movements: Synergy, Synchrony, and Speed

        • 19.5.1 VITE Model of Arm Trajectory Formation

        • 19.5.2 Variable-Speed Arm Movements Due to Variable-Size GO Signals

        • 19.5.3 Motor-Equivalent Reaching and Arm Movements Given Perturbations and Obstacles

      • 19.6 Basal Ganglia Gating of Speech Perception

        • 19.6.1 cARTWORD Model, Resonant Wave, Conscious Speech, and Phonemic Restoration

        • 19.6.2 Adaptive Resonance Theory, Language Learning, and the Stability-Plasticity Dilemma

        • 19.6.3 Simulations of Phonemic Restoration

      • 19.7 Complementary Roles of Basal Ganglia and Amygdala in Reinforcement Learning

        • 19.7.1 MOTIVATOR Model

        • 19.7.2 Basal Ganglia Learning Affects Sensory-Amygdala-�Orbitofrontal Motivated Performance

        • 19.7.3 Influences of Amygdala and Orbitofrontal Lesions on Learning and Behavior

      • 19.8 Item-Order-Rank Working Memory and Basal Ganglia Gating of Behavioral Sequences

        • 19.8.1 Basal Ganglia Control of Sequential Learning and Performance of Saccades

        • 19.8.2 Item-Order-Rank Working Memories Store Sequences Using Activity Gradients

        • 19.8.3 All Working Memories Are Variations of the Same Circuit Design

        • 19.8.4 Supplementary Eye Fields Select Saccadic Targets from Sequences Stored in Spatial Working Memory

        • 19.8.5 Basal Ganglia Regulation of Saccade Sequence Learning and Performance

      • 19.9 Basal Ganglia Gating of Perceptual and Cognitive Processes

        • 19.9.1 From Top-Down Attentional Priming to Suprathreshold Activation

        • 19.9.2 Visual Imagery, Thinking, Planning, and Searching

        • 19.9.3 From Phasic to Tonic Gate Opening: Hallucinations

        • 19.9.4 Working Memory Storage and the Useful Field of View of Spatial Attention

      • 19.10 Concluding Remarks

      • References

    • Chapter 20: The Basal Ganglia and Hierarchical Control in Voluntary Behavior

      • 20.1 Introduction

        • 20.1.1 Basic Facts

        • 20.1.2 Conservation of BG Circuitry

      • 20.2 Basal Ganglia Activity During Behavior

        • 20.2.1 SNr Outputs Map Instantaneous Position of the Animal

        • 20.2.2 Striatal Activity and Movement Velocity

        • 20.2.3 DA Neurons Represent Movement Velocity and Acceleration

        • 20.2.4 Departures from Previous Models

      • 20.3 Negative Feedback and Closed Loop Control

        • 20.3.1 Control of Input

      • 20.4 Neural Implementation of the Control Hierarchy

        • 20.4.1 Muscle Tension Control and the Final Common Path

        • 20.4.2 Muscle Length Control

        • 20.4.3 Position Control: Joint Angle and Body Configuration

        • 20.4.4 Locomotion and Gait

        • 20.4.5 Orientation Control and the Tectum

        • 20.4.6 Nigrotectal Projections Send Descending Reference Signals

        • 20.4.7 Turning and Steering

      • 20.5 Transition Control

        • 20.5.1 Cascade Organization and Velocity Control

        • 20.5.2 Direct and Indirect Pathways

        • 20.5.3 Role of Dopamine

        • 20.5.4 Dopamine Depletion and Symptoms of Parkinson’s Disease

      • 20.6 How Can the BG be Commanded?

        • 20.6.1 Cortical Organization

        • 20.6.2 Goals and Perceptual Representations

        • 20.6.3 Imagination

        • 20.6.4 Neural Implementation of the Imagination Mode

        • 20.6.5 Action Observation and Simulation

      • 20.7 Cortico-BG Networks

        • 20.7.1 Sensorimotor (Somatic) Network

        • 20.7.2 The Associative Cortico-Basal Ganglia Network

        • 20.7.3 Differences Between Associative and Sensorimotor Network

        • 20.7.4 Limbic Network: Nucleus Accumbens

        • 20.7.5 Proximity Control

        • 20.7.6 Consummatory Network

        • 20.7.7 Reward and Aversion

        • 20.7.8 Mesolimbic Dopamine

      • 20.8 Integrative Action of the Cortico-Basal Ganglia Networks

      • 20.9 Conclusions

      • References

  • Index

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