Cerebral Cortex

1 Synaptic Interactions between Cortical Neurons.- 1. Introduction.- 1.1. Measures of Synaptic Interactions.- 1.2. Effects of Synaptic Connections.- 2. Visual Cortex.- 2.1. Application of the Cross-Correlation Technique in the Visual System.- 2.2. Geniculocortical Interaction.- 2.3. Corticogeniculate Interaction.- 2.4. Intra- and Intercolumnar Interaction in Single and Adjacent Functional Columns of the Visual Cortex.- 2.5. Transcolumnar Interaction between Distant Columns.- 2.6. Synaptic Interaction Demonstrated by STA.- 2.7. Functional Conclusions.- 3. Auditory Cortex.- 4. Somatosensory Cortex.- 4.1. Cross-Correlation Studies.- 4.2. STA Studies.- 5. Motor Cortex.- 5.1. Cross-Correlation Studies.- 5.2. STA Studies.- 6. Association Cortex.- 7. Hippocampus.- 7.1. Cross-Correlation Studies.- 7.2. STA Studies.- 8. Summary and Conclusions.- 8.1. Common Features of Synaptic Interactions.- 8.2. Future Directions.- 9. References.- 2 The Role of Layer I in Cortical Function.- 1. Introduction.- 2. Behavioral Role of Layer I.- 3. Layer I in Sensory Cortices.- 3.1. Electrophysiology of Layer II Neurons.- 3.2. Afferent Connections and Physiology.- 4. Architecture of Layer I.- 4.1. Subdivisions.- 4.2. Neuronal Composition.- 4.3. Compartmentation of Apical Dendrites.- 5. The Proximal and Distal GABAergic Systems.- 6. Compartmentation of Afferent Connections.- 6.1. Thalamic and Subicular Projections.- 6.2. Serotoninergic Projections to Layer I.- 7. Passive and Active Interactions between Distal and Proximal Dendritic Compartments.- 8. Cholinergic Projections: Organization and Role in Event Holding.- 9. Noradrenergic Projections to Layer I and Memory Consolidation.- 10. What Is the Role of Layer I in Cortical Function?.- 11. References.- 3 Synapse Replacement on Cortical Neurons following Denervation.- 1. Introduction.- 2. The Process of Reinnervation in the Dentate Gyrus of Adult Rats: Nature of the Growth Response of Pre- and Postsynaptic Elements.- 2.1. Documentation of Synapse Replacement on Denervated Neurons Using Quantitative Electron Microscopic Techniques.- 2.2. The Nature of the Growth Response of Pre-and Postsynaptic Elements.- 2.3. Light Microscopic Studies of Afferent Reorganization.- 2.4. Quantitative Electron Microscopic Studies of Terminal Proliferation.- 2.5. Multiple Synapse Formation.- 2.6. Temporal Relationship between Terminal Proliferation and Synapse Replacement.- 2.7. Time Course of Growth of the Participating Systems.- 2.8. Is the Time Course and Extent of Synapse Replacement Constant in Different Settings?.- 2.9. Specificity in the Pattern of Synapse Formation by Reinnervating Fibers.- 2.10. Synapse Formation: Renovation of the Old Synaptic Sites or New Construction.- 2.11. Remodeling the Postsynaptic Cells' Receptive Surface during Reinnervation.- 2.12. Lesion-Induced Growth: Coordinate Growth of Pre- and Postsynaptic Cells.- 3. Role of Glial Cells in Synapse Remodeling.- 3.1. Astrocytes.- 3.2. Microglia.- 4. Cellular and Molecular Mechanisms of Lesion-Induced Growth.- 5. Cellular and Molecular Processes Associated with the Phase of Terminal Degeneration, Dendritic Atrophy, and Glial Proliferation and Hypertrophy.- 5.1. Potential Initiating Signals.- 5.2. Molecular Processes That Lead to Dendritic Atrophy.- 5.3. Molecular Events within Reactive Glial Cells.- 5.4. Changes in Astrocyte Mitogenic and Morphogenetic Factors following Injury.- 6. Cellular and Molecular Processes Associated with the Phase of Terminal Proliferation, Synaptogenesis, and Dendritic Regrowth.- 6.1. Events within Sprouting Neurons.- 6.2. Events within the Postsynaptic Neurons and the Denervated Neuropil.- 6.3. Possible Role of Neuronotrophic Substances and Growth Factors.- 7. Conclusion.- 8. References.- 4 Olfactory Frontal Cortex and Multiple Olfactory Processing in Primates.- 1. Introduction.- 2. Olfactory Frontal Cortex in Primates.- 2.1. Search for an Olfactory Projection Area in the Neocortex.- 2.2. A Study on the Olfactory Pathway to the LPOF.- 2.3. Search for Another Olfactory Projection Area in the OFC.- 2.4. Search for a Transthalamic Olfactory Pathway.- 2.5. Search for Olfactory Projection Aijeas in the Diencephalon.- 2.6. Studies on the Olfactory Projection to the LHA.- 2.7. Olfactory Nerve Pathways in the Higher Primates and Lower Mammals.- 3. Studies on Multiple Olfactory Processing in Primates.- 3.1. Selection of Eight Odors for Stimulation.- 3.2. Studies on Anesthetized Monkeys.- 3.3. Studies on Unanesthetized Monkeys.- 4. Summary.- 5. Abbreviations.- 6. References.- 5 The Role of the Cerebral Cortex in Pain Sensation.- 1. Introduction.- 2. Clinical Evidence That the Cerebral Cortex Plays a Role in Pain Sensation.- 2.1. The Effects of Lesions of the Cerebral Cortex on Pain.- 2.2. Pain Produced by Stimulation of Neurons in the Cerebral Cortex.- 2.3. Evidence for a Role of Thalamocortical Circuits in Pain.- 3. Experimental Evidence for a Role of the Cerebral Cortex in Pain.- 4. Electrophysiological Evidence for a Role of Cerebral Cortical Neurons in Nociception.- 4.1. Specificity of Nociceptive Transduction in Sensory Receptors.- 4.2. Specificity of Central Transmission in Nociceptive Tracts.- 4.3. Nomenclature of Nociceptive Neurons.- 4.4. Functional Role of WDR and HT Neurons.- 4.5. Nociceptive Responses of Somatosensory Thalamic Neurons.- 4.6. Nociceptive Responses of Neurons in the SI Somatosensory Cortex.- 4.7. Responses of SI Cortical Neurons to Tooth Pulp Stimulation.- 4.8. The Role of the SII Cortex and Area 7b in Nociception.- 5. Role of the Cerebral Cortex in Pain Modulation.- 6. Conclusions.- 7. References.- 6 The Cerebral Organization of Language.- 1. Introduction.- 1.1. Historical Aspects.- 1.2. Contemporary Imaging Technologies.- 2. Metabolic Studies of Language in Normal Volunteers.- 2.1. Nonverbal Auditory Stimuli.- 2.2. Auditory Verbal Stimuli-Word Lists.- 2.3. Complex Auditory Verbal Stimuli.- 2.4. Speech-Automatic Production.- 2.5. Speech-Complex Utterances.- 2.6. Cognitive Processing of Linguistically Complex Stimuli.- 2.7. Sequential Studies of Linguistic Processing.- 3. Metabolic Mapping Studies of Language in Aphasic Patients.- 3.1. PET.- 3.2. rCBF.- 3.3. Recovery of Function in Aphasia.- 3.4. Analysis.- 4. Electrical Stimulation Mapping.- 4.1. Overview.- 4.2. Cortical Stimulation.- 4.3. Thalamic Stimulation.- 4.4. Analysis.- 5. Computerized Axial Tomography.- 5.1. Overview.- 5.2. Broca's Aphasia.- 5.3. Severe Nonfluent Aphasia.- 5.4. Transcortical Motor Aphasia.- 5.5. Auditory Agnosia.- 5.6. Wernicke's Aphasia.- 5.7. Transcortical Sensory Aphasia.- 5.8. Conduction Aphasia.- 5.9. Subcortical Aphasia.- 6. Conclusions.- 6.1. Summary of Brain Imaging Studies in Normals.- 6.2. Summary of Brain Imaging Studies of Aphasia in Patients with Cortical and Subcortical Lesions.- 6.3. Principles Underlying the Cerebral Organization of Language.- 7. References.- 7 Cerebrocortical Asymmetry.- 1. Introduction.- 2. General Issues Concerning Brain Asymmetry.- 3. Gross and Microscopic Cerebral Asymmetries.- 3.1. Asymmetries in the Human Brain.- 3.2. Asymmetries in Nonhuman Brains.- 3.3. Summary.- 4. Asymmetry versus Symmetry of Brain Areas.- 4.1. Volumetric Characteristics of Gross and Architectonic Asymmetry and Symmetry.- 4.2. Cellular Characteristics of Asymmetry and Symmetry.- 4.3. Connectional Characteristics of Asymmetry and Symmetry.- 4.4. Summary.- 5. References.- 8 Alertness, Quiet Sleep, Dreaming.- 1. States of Vigilance.- 1.1. Brain-Activated and Brain-Deafferented States.- 1.2. Stable and Transitional States.- 2. Physiological Bases of Rhythmic Electrical Activity.- 2.1. Synchronization, Desynchronization, and Generator Sources.- 2.2. Sleep Spindles, Augmenting and Recruiting Waves.- 2.3. Alpha Rhythm.- 2.4. Fast Synchronous Cortical Oscillations.- 2.5. Theta Waves.- 3. State Dependency of Sensory Processing and Motor Control.- 3.1. Methodological Considerations.- 3.2. Evoked Potential Studies in Animals and Man.- 3.3. Neuronal Excitability.- 3.4. Inhibitory Processes.- 3.5. Phasic Events during Alertness and REM Sleep.- 4. Brain-Stem and Basal Forebrain Modulatory Systems.- 4.1. Brain-Stem and Basal Forebrain Projections.- 4.2. Synaptic Effects of Modulatory Systems and Transmitter Actions upon Thalamic and Cortical Neurons.- 4.3. A View of Brain-Stem, Thalamic, Hypothalamic, and Basal Forebrain Networks Controlling the Genesis of the Sleep-Waking Cycle and the State-Related Activities in the Cerebral Cortex.- 5. References.- 9 Coma and Related Global Disturbances of the Human Conscious State.- 1. Neurologic Aspects of Coma.- 1.1. Consciousness Depends on Diffuse Ascending and Focal Cerebral Mechanisms.- 1.2. Global Impairments of Consciousness Defined.- 1.3. Causes and Implications of Coma.- 1.4. Coma Is Always a Transient State if Mammals Survive.- 1.5. Normal Sleep Patterns and Metabolism in Humans.- 1.6. Historical Clinical Concepts of Coma and Related States.- 2. Experimental Studies of Arousal Mechanisms.- 2.1. Pre-1949: Prologues to Understanding the EEG.- 2.2. 1949-1980: Concepts of Ascending Nonspecific Systems Stimulating Behavioral and EEG "Arousal".- 2.3. Neurotransmitter Systems and Arousal.- 3. Human Studies on Pathologically Altered States of Sleep, Coma, and Related Abnormalities.- 3.1. Qualifying Factors.- 3.2. Electrophysiologic Changes in Coma.- 3.3. Anatomy of Brain Dysfunction Altering Sleep or Arousal.- 3.4. Upper Brain Stem and Diencephalic Lesions Causing Coma.- 3.5. Cerebral Damage in Human Coma.- 3.6. Brain Metabolic Mapping after Focal Tissue Injuries Shows Multiple Deactivated Systems.- 3.7. Wakeful Unconsciousness-The Vegetative State.- 4. Dementia as a Global Reduction in Human Consciousness.- 5. Summary and Conclusion, Sections 3 and 4.- 6. References.- 10 Epilepsy and the Cortex: Anatomy.- 1. Introduction.- 2. Descriptive Studies of Brains from Humans with Epilepsy.- 2.1. Historical Description of Temporal Lobes.- 2.2. Recent Studies of Human Brains Using Immunocytochemical Methods.- 3. Experimental Models of Epilepsy.- 3.1. Types of Experimental Models of Epilepsy.- 3.2. Alumina Gel Model of Cortical Focal Epilepsy.- 3.3. Loss of GABAergic Terminals in the Isolated Cortical Slab of Cats.- 3.4. Other Chronic Cortical Models of Focal Epilepsy.- 3.5. Acute Models of Cortical Epilepsy.- 3.6. Models of Epilepsy Produced by Kindling or Sustained Electrical Stimulation.- 3.7. Genetic Models of Epilepsy.- 4. Functional Significance.- 4.1. Gliosis and the Cellular Milieu.- 4.2. Loss of GABAergic Inhibition in Focal Epilepsy.- 4.3. Excitotoxicity and Increased Recurrent Excitation as Causes of Hyperexcitability.- 4.4. NE Hyperinnervation May Create Synchrony in Cortical Neurons.- 5. Future Challenges.- 6. References.- 11 Aging in Monkey Cerebral Cortex.- 1. Life Span of the Rhesus Monkey.- 2. Neuronal Population Changes in Cerebral Cortex.- 3. Changes in Neuronal Perikarya with Age.- 4. Changes in Neuroglial Cells during Aging.- 5. Changes with Age in the Neuropil.- 6. Neuritic Plaques.- 7. Conclusion.- 8. References.- 12 Down Syndrome.- 1. Introduction.- 2. Brain Weight, Appearance, and Postnatal Growth.- 3. Microscopic Anatomy.- 4. Age-Related Changes.- 5. References.