書誌事項

Progress in sensory physiology

editor-in-chief, D. Ottoson ; editor, H. Autrum ... [et al.]

Springer-Verlag, 1981-

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  • v. 8 : gw
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  • v. 9 : gw
  • v. 9 : us
  • v. 10 : gw
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  • v. 11 : gw
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  • v. 11 : softcover
  • v. 12 : us
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  • v. 13 : us
  • v. 13 : gw

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注記

Includes bibliographies and index

Vol. 9--with contributions by G.N. Akocv ... [et al.]

Vol. 12--with contributions by O.R. Anderson...[et al.]

Vol. 13--Editors: H. Autrum ... [et al.], Editor-in-chief: D. Ottoson

内容説明・目次

巻冊次

v. 1 : gw ISBN 9783540084136

内容説明

I fancy that many of you, like myself, have woken up in the night with a "sleeping" arm or leg. It is a very peculiar feeling to have that arm or leg, cold and lifeless, hanging there at your side as if it were something which does not belong to you. In such situations you recover some of the motor functions before the sensory functions, which en- ables you to move the limb like a pendulum. For a few sec- onds the arm functions as an artificial limb - a prosthesis without sensors. In general we are not aware of the importance of our sensory organs until we lose them. You do not feel the pressure of your clothes on the skin or the ring on your finger. In the nineteenth century such phenomena generally named adaptation, were studied to a great extent, partic- ularly in vision, as well as in the so-called lower senses. The question whether sensory adaptation was due to changes in the peripheral sensory receptors or in the central nervous structure remained in general open until the 1920s. Then the development of the electronic arsenal gave us the means to attack the problem by direct observations of the electrical events in the peripheral as well as the central nervous system. But even today there are still some blank areas in our knowledge of adaptation.

目次

Visual Hyperacuity.- Opioid Peptides and Sensory Function.- Ionic Mechanisms and Behavioral Functions of Presynaptic Facilitation and Presynaptic Inhibition in Aplysia: A Model System for Studying the Modulation of Signal Transmission in Sensory Neurons.- Color Vision: A Review from a Neurophysiological Perspective.
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v. 2 : gw ISBN 9783540109235

内容説明

The study of the auditory physiology of reptiles has a relatively long history, but only began in a systematic way in 1956 with the publication of the earliest of Wever's investigations of the cochlear microphonic in reptiles. The long series of experiments which were subsequently undertaken by Wever and his colleagues have been recently conveniently brought together with the publication of Wever's book The Reptile Ear (1978). In the last 10 years, neurophysiological studies at various levels of the auditory system (primarily, however, lower levels), have appeared and produced in a relatively short time a good basis for the discussion of mechanisms. Certainly, a great difference can be noted today between our in- creasing unterstanding in this field and the paucity of data which existed in 1960 when McGill could say Disagreement exists ...as to whether the hearing organs of certain modern reptiles are vestigial or rudimentary. The present state of knowledge of hearing in ...reptiles is not commensurate with the importance of these classes in the study of the evolution of the sense of hearing (McGill 1960). Two main themes dominate the motivation underlying present research in this field. The first, and historically older, theme is a fundamental interest in the evo- lution and systematics of the reptile ear.

目次

Thermoreception and Temperature Regulation in Homeothermic Vertebrates.- A Review of the Auditory Physiology of the Reptiles.- Recent Advances in Structural Correlates of Auditory Receptors.
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v. 4 : gw ISBN 9783540124986

内容説明

The study of the functional organization of the first synapse of the centripetal visual pathway at the outer plexiform layer level (OPL) ought to be made through the application of combined histological, electrophysiological, and neurochemical techniques. A large amount of new evidence has been accumu- lated in the past 20 years on the structure of the retina and on the electrical responses of retinal cells to light stimulus. Also, recently, many substances considered as neurotransmitters in the brain have been found in the retina. The goal of the study of retinal function is to integrate the data obtained by structural and electrophysiological techniques and to identify and determine the role played by neurotransmitters or neuromodulators in the function of the retina. In this study it is important to realize the morphological and biochemical diversi- ty displayed by the visual cells in the vertebrate retina which, according to Cresci- telli (1972), has been produced "through the interaction of natural selection with diversity in the photic environment." The evidence obtained shows that bipolar and especially horizontal cells, closely related to visual cells, display morphologi- cal and probably biochemical differences among classes, genus, and even species according to the photic environment. These differences give peculiarities to the organization of the OPL, which must be taken into account when studying a par- ticular retina with electrophysiological or neurochemical techniques.

目次

Sensory Structures in the Viscera.- Schematic Eye Models in Vertebrates.- Organization of the Outer Plexiform Layer of the Tetrapoda Retina.
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v. 5 : gw ISBN 9783540153399

目次

Functional Organization of the Fly Retina.- Mechanoreception in Ciliates.- The Biological Significance of the Earth's Magnetic Field.- Perception of Water Surface Waves: How Surface Waves are Used for Prey Identification, Prey Localization, and Intraspecific Communication.
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v. 6 : gw ISBN 9783540153405

内容説明

1. Themeanrestingmembranepotentialofrattaste cells is - 36 mVunderadap- tation of the tongue to 41.4 mMNaCI and - 50mV under water adaptation. 2. The shapes ofreceptor potentials ofrattastecells inresponsetothe four basic tastestimuli(0.5MNaCI, 0.02 M Q-HCI, 0.01 MHCl, and0.5 M sucrose)are classified into three types, namely (1) a depolarization alone, (2) a depolariza- tion preceded by a transient hyperpolarization, and (3) a hyperpolarization alone. No regenerative spike potentials are evoked in rat taste cells by chemical stimuli. The amplitude of rat taste cell responses increases with increasing concentrationofthe taste stimulus. Mostofthe rat taste cells show a multiple sensitivity in that single cells respond to various combinations of the four basic taste stimuli with depolarizations or hyperpolarizations. 3. The rise and fall times of depolarizing responses to 0.5 M NaCI are much shorter than those of depolarizing responses to the other three stimuli. The fall time of depolarization evoked by 0.01 M HCI is the longest. The rise and fall times of all hyperpolarizing responses are shorter than those of all de- polarizing responses.

目次

Receptor Potential in Rat Taste Cells.- Functional Properties of the Fish Olfactory System.- Homeostasis of Extracellular Fluid in Retinas of Invertebrates and Vertebrates.- Slowly Conducting Afferent Fibers from Deep Tissues: Neurobiological Properties and Central Nervous Actions.
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v. 9 : gw ISBN 9783540502821

内容説明

Sympathetic afferent fibers originate from a visceral organ, course in the thoracolumbar rami communicantes, have cell bodies located in dorsal root ganglia, and terminate in the gray matter of the spinal cord. Sympathetic afferent fibers from the heart transmit information about noxious stimuli associated with myocardial ischemia, i. e. angina pectoris. Previous reviews have described the characteristics of cardiovascular sympathetic afferent fibers (Bishop et al. 1983; Malliani 1982). This review summarizes that work and focuses on the neural mechanisms underlying the complexities of angina pectoris. In order to understand anginal pain, cells forming the classical pain pathway, the spinothalamic tract (STn, were chosen for study. These cells were chosen to address questions about anginal pain because they transmit nociceptive informa- of pain. Antidromic tion to brain regions that are involved in the perception activation of STT cells provided a means of identifying cells involved with trans- mission of nociceptive information in anesthetized animals. Other ascending pathways may also transmit nociceptive information, but many studies show that the STT plays an important role. Visceral pain is commonly referred to overlying somatic structures. The pain of angina pectoris can be sensed over a wide area of the thorax: in the retrosternal, precordial anterior thoracic, and anterior cervical regions of the chest; in the left or sometimes even the right shoulder, arm, wrist, or hand; or in the jaw and teeth (Harrison and Reeves 1968).

目次

Organization of the Spinothalamic Tract as a Relay for Cardiopulmonary Sympathetic Afferent Fiber Activity.- Synaptic Transmission in the Mechano- and Electroreceptors of the Acousticolateral System.- Experimental Models of Sensorineural Hearing Loss - Effects of Noise and Ototoxic Drugs on Hearing.- Sensing of Endogenous Chemicals in Control of Feeding.- Structure and Function of the Vomeronasal System - The Vomeronasal Organ as a Priming Pheromone Receptor in Mammals.
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v. 10 : gw ISBN 9783540513803

内容説明

This monographic work authored by eminent neurophysiologists will be of major interest to researchers investigating the visual system or working in behavioral neuroscience and sleep research. The book deals with the neuronal circuits of the visual thalamocortical system, the brainstem and basal forebrain modulatory systems and their neurotransmitters acting upon these circuits, and the neuronal activities in the visual thalamocortical system as changed during shifts in behavioral states of vigilance from wake to sleep. Data discussed consist of recent studies on light and electron microscopy, extra- and intracellular recordings of thalamic and cortical neurons, neurotransmitter actions, and state-dependent cellular activities in the visual system.

目次

1 Prologue.- 2 Basic Circuits in the Visual Thalamocortical Systems and Their Physiological Aspects.- 2.1 The Lateral Geniculate-Perigeniculate Thalamic Complex.- 2.1.1 Lateral Geniculate Thalamocortical Cells.- 2.1.2 Lateral Geniculate Local Circuit Inhibitory Cells.- 2.1.3 Perigeniculate Neurons.- 2.1.4 Synaptic Organization of Lateral Geniculate- Perigeniculate Circuits and Their Physiological Aspects.- 2.1.4.1 Lateral Geniculate Glomeruli.- 2.1.4.2 Extraglomerular Lateral Geniculate Neuropil..- 2.1.4.3 The Perigeniculate Sector of the Reticular Nuclear Complex.- 2.1.4.4 Physiological Aspects of Lateral Geniculate- Perigeniculate Circuits.- 2.2 The Visual Cortex.- 2.2.1 Termination Patterns of Geniculocortical Axons.- in Striate and Extrastriate Areas.- 2.2.2 Cell Types in the Visual Cortex.- 2.2.2.1 Long-Axoned Pyramidal Neurons.- 2.2.2.2 Intrinsic Neurons.- 2.2.3 Neuronal Circuits in the Visual Cortex.- 2.2.3.1 Vertical Circuits.- 2.2.3.2 Horizontal Interactions.- 3 Regulatory Systems of the Brain Stem Core, Basal Forebrain, and Hypothalamus.- 3.1 Cholinergic Cell Groups.- 3.1.1 The Innervation of the Visual Thalamus from the Cholinergic Column of the Mesopontine Tegmentum.- 3.1.2 Cholinergic Projections of the Basal Forebrain Towards Visual Cortical Areas.- 3.1.3 Cholinergic Receptors.- 3.2 Catecholaminergic Cell Groups.- 3.2.1 Norepinephrinergic Systems.- 3.2.2 Dopaminergic Projection Systems.- 3.3 Serotonergic Cell Groups.- 3.4 Hypothalamic Cell Groups.- 4 Neurotransmitters.- 4.1 Acetylcholine.- 4.1.1 Lateral Geniculate-Perigeniculate Thalamic Nuclei.- 4.1.2 Visual Cortex.- 4.2 Monoamines.- 4.2.1 Lateral Geniculate-Perigeniculate Thalamic Nuclei.- 4.2.2 Visual Cortex.- 4.3 Amino Acids.- 4.3.1 Excitatory Amino Acids.- 4.3.1.1 Lateral Geniculate Nucleus.- 4.3.1.2 Visual Cortex.- 4.3.2 y-Aminobutyric Acid.- 4.3.2.1 Lateral Geniculate Nucleus.- 4.3.2.2 Visual Cortex.- 4.4 Final Comments.- 5 State Dependency of Visual Thalamic and Cortical Activities.- 5.1 Background Activity: Bursting and Tonic Discharge Patterns.- 5.2 Excitatory-Inhibitory Processes During Sleep Oscillations and Tonically Activated States.- 5.2.1 Responsiveness to Central Stimuli.- 5.2.2. Responsiveness to Photic Stimuli.- 5.2.3 Inhibitory Processes.- 5.2.4 Ponto-geniculo-occipital (PGO) Waves.- 5.2.4.1 Modulation of Lateral Geniculate Cells During PGO Waves and Eye Movement Potentials.- 5.2.4.2 Mechanism of Thalamic PGO Waves.- 5.2.4.3 Functional Significance of the Eye Movement Potentials and PGO Waves During Natural Waking and Sleep States.- 6 References.- 7 Subject Index.
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v. 11 : gw ISBN 9783540525738

内容説明

Rarely have the many mechanisms that might underlie neural plasticity been examined as explicity as they are in this treatment of plasticity in the somato-sensory system. The reader is provided with state-of-the-art knowledge of connections at all levels of the somato-sensory system. The authors examine the propensity for changes of connectivity in both the mature and developing mammal and make clear proposals regarding the mechanisms underlying these changes. Their functional significance to relevant psychophysical and neurological observations is also discussed.

目次

  • Plasticity in the peripheral somato-sensory nervous system
  • plasticity and the mystacial vibrissae of rodents
  • plasticity and the spinal dorsal horn (with notes on homologous regions of the trigeminal nuclei)
  • plasticity and the dorsal column nuclei
  • plasticity and the somato-sensory thalamus
  • plasticity and the somato-sensory cerebral cortex.
巻冊次

v. 12 : gw ISBN 9783540529859

内容説明

The objective of this series is to provide concise and critical information on current advances in the different domains of sensory physiology. It will be of interest to all who want to keep abreast of the latest developments in the field - from the level of the receptor to that of the cortex, including neuropsychological and psychophysical aspects.

目次

Opioid Regulation of Pituitary Function.- The Development of Projections from Cerebral Cortex.- Neurocognitive Models of Information Processing and Knowledge Acquisition.- Cortical Organization of Language and Verbal Memory Based on Intraoperative Investigations.
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v. 13 : gw ISBN 9783540545538

内容説明

Stability of the internal environment in which neuronal elements are situated is unquestionably an important prerequisite for the effective transmission of information in the nervous system. During the past decade our knowledge on the microenvironment of nerve cells has expanded. The conception that the microenvironment of neurones comprises a fluid with a relatively simple and stable composition is no longer accepted; the microenvironment is now envisaged as a dynamic structure whose composition, shape, and volume changes, thereby significantly influencing neuronal function and the trans- mission of information in the nervous system. The modern conception of the neuronal microenvironment is based on the results of research over the last 20 years. The extracellular space (ECS) is comprehended not only as a relatively stable microenvironment containing neurones and glial cells (Bernard 1878), but also as a channel for communica- tion between them. The close proximity of the neuronal elements in the CNS and the narrowness of the intercellular spaces provides a basis not only for interaction between the elements themselves, but also between the elements and their microenvironment. Substances which can cross the cell membranes can easily find their way through the microenvironment to adjacent cellular elements. In this way the microenvironment can assure non-synaptic com- munication between the relevant neurones. Signalization can be coded by modulation of the chemical composition of the ECS in the vicinity of the cell membrane and does not require classic connection by axones, dendrites, and synapses.

目次

1 Introduction.- 2 Ion-Selective Microelectrodes.- 3 K+ Homeostasis in the ECS.- 3.1 Stability of K+ in the Extracellular Fluid.- 3.2 Sources of [K+]e Increases.- 3.3 Redistribution of Extracellularly Accumulated K+.- 3.3.1 Role of Active Transport.- 3.3.2 Role of Glial Cells in K+ Homeostasis.- 3.3.2.1 The Spatial Buffer Mechanism.- 3.3.2.2 Active K+ Transport.- 3.3.2.3 Channel-Mediated KCl Uptake.- 3.3.3 K+ Diffusion in the ECS.- 3.3.4 K+ Exchange Between Extracellular Fluid and Blood.- 4 Dynamic [K+]e Changes.- 4.1 Dynamic [K+]e Changes in the Spinal Cord...- 4.1.1 [K+]e Changes Induced by Electrical Stimulation of Peripheral Nerves.- 4.1.2 Depth Profile of [K+]e Changes in the Spinal Cord.- 4.1.3 Electrical Stimulation of Descending Pathways.- 4.1.4 [K+]e Changes Induced by Adequate Stimulation.- 4.1.4.1 Acute Nociceptive and Non-Nociceptive Stimuli.- 4.1.4.2 Chronic Nociceptive Stimuli.- 4.1.5 [K+]e Changes Associated with Spontaneous Activity in the Dorsal Horns of the Spinal Cord.- 4.1.6 [K+]e Changes Induced by Systemic Administration of Drugs, Transmitters, and Neuropeptides.- 4.2 Dynamic [K+]e Changes in the Brain.- 4.2.1 Dynamic [K+]e Changes in the Cerebral Cortex and Striatum.- 4.2.2 Dynamic [K+]e Changes in the Mesencephalic Reticular Formation.- 4.2.3 Dynamic [K+]e Changes in the Cerebellum and Hippocampus.- 4.3 Functional Significance of [K+]e Changes in the CNS.- 4.3.1 Role of K+ in Presynaptic Inhibition.- 4.3.1.1 Depolarization of Primary Afferents.- 4.3.1.2 Effect of Picrotoxin and Bicuculline.- 4.3.2 Effect of K+ Accumulation on Synaptic Transmission.- 4.3.2.1 Effect of K+ on Neuronal Membrane Potential.- 4.3.2.2 Effect of K+ on Synaptic Potentials and Spontaneous Activity.- 4.3.2.3 Effect of K+ on Flexor Reflex.- 4.3.3 K+ Accumulation and Glial Cell Function.- 4.3.4 K+ Accumulation and the Therapeutic Effect of Electrostimulation.- 4.3.5 Other Functional Correlates of a [K+]e Increase.- 4.3.6 K+ Accumulation and Its Functional Significance in Pathological Processes.- 4.3.6.1 [K+]e Changes During Ischaemia and Hypoxia.- 4.3.6.2 K+, Epilepsy, and Epileptiform Activity.- 4.3.6.3 [K+]e and Spreading Depression.- 4.4 Dynamic K+ Changes in the Organ of Corti.- 4.4.1 Resting K+ Concentration in the Inner Ear.- 4.4.2 Dynamic Changes in K+ Concentration in the Organ of Corti Evoked by Acoustic Stimuli.- 4.4.3 Functional Significance of Dynamic [K+]e Changes in the Organ of Corti.- 4.5 Changes in K+ Concentration in the Retina.- 4.5.1 Regulation of [K+]e by Glial Cells in the Retina.- 5 Dynamic Changes in Extracellular Na+, Cl-, and Ca2+ Concentration.- 5.1 Changes Induced in Resting [Ca2+]e During Stimulation of Afferent Input.- 5.2 [Ca2+]e Changes in Pathological States.- 5.3 Functional Significance of Dynamic [Ca2+]e Changes.- 6 Dynamic pHe Changes.- 6.1 Extracellular Buffering Power.- 6.2 Activity-Related Dynamic pHe Changes in Nervous Tissue.- 6.2.1 Resting pHe.- 6.2.2 pHe Changes Evoked by Stimulation of Afferent Input.- 6.2.2.1 pHe Changes Evoked by Adequate Stimulation of Skin Nociceptors.- 6.2.3 Effect of Block of Synaptic Transmission on pHe Changes.- 6.2.4 pHe Changes Induced by K+ Depolarization.- 6.3 Mechanisms of pHe Changes in the CNS.- 6.3.1 Effect of Sodium Fluoride.- 6.2.3 Effect of Ouabain.- 6.3.3 Effect of Amiloride.- 6.3.4 Effect of SITS and DIDS.- 6.3.5 Effect of Acetazolamide.- 6.3.6 Effect of Furosemide.- 6.3.7 Effect of Block of H+ Channels.- 6.4 Role of Glial Cells in pHe Homeostasis.- 6.5 pHe Changes in the Retina.- 6.6 pHe Changes During Anoxia, Ischaemia, Epilepsy, and SD.- 6.7 Functional Significance of pHe Changes.- 7 Dynamic Changes in Size of the ECS.- 7.1 Measurement of Changes in Size of the ECS by Means of K+-ISMs.- 7.2 Changes Induced in Size of the ECS by Electrical Stimulation.- 7.3 Changes Induced in Size of the ECS by Adequate Stimulation.- 7.4 Mechanisms of Dynamic Changes in Size of the ECS.- 7.4.1 Volume Changes Induced by Changes in Extracellular Osmolarity.- 7.4.2 Volume Changes During Neuronal Activity.- 7.4.3 Transport Systems of Glial Cells and Regulation of Their Volume.- 7.4.4 Changes in Cell Volume Induced by Inhibition of Na+/K+ ATPase.- 7.5 Functional Significance of Dynamic Volume Changes in the Microenvironment of Nerve Cells.- 8 Conclusion.- References.
巻冊次

v. 11 : softcover ISBN 9783642757037

内容説明

Rarely have the many mechanisms that might underlie neural plasticity been examined as explicitly as they are in this broad, lavishly illustrated treatment of plasticity in the somatosensory system. The reader is provided with state-of-the-art knowledge of connections at all levels of the somatosensory system. The authors examine the propensity for changes of connectivity in both the mature and developing mammal and make clear proposals regarding the mechanisms underlying these changes. Their functional significance to relevant psychophysical and neurological observations is also discussed.

目次

1 Introductory Remarks.- 2 Plasticity in the Peripheral Somatosensory Nervous System.- 2.1 Aspects of Plasticity in the Peripheral Nervous System.- 2.2 Survival and Loss of Sensory Neurons After Lesions of the Peripheral Nervous System.- 2.2.1 Effect of Crush or Transection of Peripheral Nerve on Neurons of Sensory Ganglia.- 2.2.2 Trophic Dependence of Immature Sensory Neurons on the Periphery.- 2.2.3 Effect of Peripheral Nerve Transection on Different Types of Sensory Neurons in Dorsal Root Ganglia.- 2.2.4 Effect of Peripheral Nerve Section on Fibre Composition of Dorsal Roots.- 2.2.5 Fate of the Lost neurons.- 2.2.6 Sensory Cell Loss After Chemical Lesions of Afferent Fibres.- 2.3 Collateral Sprouting of Primary Afferent Fibres in the Periphery.- 2.3.1 Collateral Reinnervation of the Skin in Adult Mammals.- 2.3.2 Collateral Sprouting in Neonates.- 2.3.3 Effect of Neural Activity on Collateral Sprouting.- 2.3.4 Collateral Sprouting of Trigeminal Afferents.- 2.3.5 Collateral Sprouting and Sensory Recovery in Man.- 2.3.6 Fate of Collateral Sprouts After Regeneration of Original Nerve.- 2.4 Regeneration of Somatic Sensory Afferent Fibres.- 2.4.1 Numbers of Axons in Nerves Regenerating After Crush or Transection.- 2.4.2 Size of Regenerated Axons.- 2.4.3 Effect of Denervation on Specialized Cutaneous Mechanoreceptors.- 2.4.4 Reinnervation of Cutaneous Receptors by Regenerating Sensory Fibres.- 2.5 Modality Specificity of Somatosensory Nerve Regeneration.- 2.5.1 Regeneration of Myelinated Afferent Fibres to Hairy Skin.- 2.5.2 Regeneration of Myelinated Afferent Fibres to Glabrous Skin.- 2.5.3 Regeneration of Unmyelinated Afferent Fibres..- 2.6 Major Conclusions.- 3 Plasticity and the Mystacial Vibrissae of Rodents.- 3.1 General Account of Pathway.- 3.2 Normal Development of the Vibrissae and Their Neural Connections to the Cerebral Cortex.- 3.3 Effects of Lesions and Manipulations in Prenatal, Neonatal and Developing Animals.- 3.3.1 Damage of the Infraorbital Nerve.- 3.3.2 Lesions to One or More Vibrissae.- 3.3.3 The Effects of Supernumerary Vibrissae.- 3.3.4 The Effects of Lesioning Unmyelinated Afferents.- 3.3.5 Hyper- and Hypostimulation of Vibrissa Afferents.- 3.3.6 Cortical Alterations.- 3.4 Plasticity in the Vibrissa System of Adult Animals.- 3.4.1 The SI Cortex.- 3.4.2 The Ventral Posterior Medial Nucleus.- 3.5 Major Conclusions.- 4 Plasticity and the Spinal Dorsal Horn (with Notes on Homologous Regions of the Trigeminal Nuclei).- 4.1 Experimental Strategies for Demonstration of Plasticity in the Dorsal Horn of the Spinal Cord and Trigeminal Nuclei.- 4.2 Overview of Dorsal Horn Organization.- 4.2.1 Laminar Cytoarchitectonic Organization.- 4.2.2 Laminar Organization of the Termination of Primary Afferent Fibres.- 4.2.3 Microanatomical Organization of Low-Threshold Cutaneous Afferents.- 4.2.4 Relation of Functional Properties to Lamination of the Dorsal Horn.- 4.2.5 Inhibitory Receptive Fields.- 4.3 Somatotopic Organization of the Dorsal Horn.- 4.3.1 Dorsal Horn Neurons.- 4.3.2 Somatotopy and Lamination.- 4.3.3 Relation of Primary Afferent Projections to Dorsal Horn Somatotopy.- 4.3.4 Relation Between Dorsal Horn Cell Dendritic Morphology and Receptive Field.- 4.4 Effect of Lesions on Somatotopic Organization.- 4.4.1 Dorsal Rhizotomy.- 4.4.2 Chronic Spinal Lesions.- 4.4.3 Peripheral Nerve Transection or Crush.- 4.5 Mechanisms Underlying the Somatotopic Reorganization of Dorsal Horn Neurons.- 4.5.1 Physiological and Pharmacological Evidence for the Existence of Normally Ineffective.- Afferent Connections.- 4.5.2 Spontaneous Changes of Receptive Fields.- 4.5.3 Plasticity of Receptive Fields Induced by Afferent Activity.- 4.5.4 Involvement of Unmyelinated Afferents in the Somatotopic Reorganization After Peripheral Nerve Injury.- 4.5.5 Sprouting of Primary Afferent Fibres and Other Neurons as a Basis for Somatotopic Reorganization.- 4.6 Plasticity of the Developing Dorsal Hor.- 4.6.1 Development of Dorsal Horn Neurons and Primary Afferents.- 4.6.2 Functional Plasticity in Development.- 4.6.3 Somatotopic Reorganization Following Neonatal Peripheral Nerve Lesions.- 4.6.4 Anatomical Plasticity of Neonatal Afferent Projections.- 4.7 Major Conclusions.- 5 Plasticity and the Dorsal Column Nuclei.- 5.1 Advantages of the Dorsal Column Nuclei for Studies of Plasticity.- 5.2 Organization of the Dorsal Column Nuclei.- 5.2.1 Cytoarchitectonics.- 5.2.2 Ascending Afferent Pathways.- 5.2.3 Responses of Neurons to Natural Stimulation.- 5.2.4 Core and Shell Organization.- 5.2.5 Somatotopic Organization.- 5.3 Alterations of Inputs to the Nuclei.- 5.3.1 Section of Ascending Pathways.- 5.3.2 Effects of Dorsal Rhizotomy.- 5.3.3 Peripheral Nerve Section.- 5.4 Evidence for Ineffective Afferent Connections.- 5.4.1 Projections of Dorsal Roots and Peripheral Nerves.- 5.4.2 Projections of Single Afferent Fibres.- 5.4.3 Dendritic Spread of Cuneate Neurons.- 5.4.4 Electrical Stimulation and Widefield Neurons..- 5.4.5 Pharmacological Alterations of Receptive Fields.- 5.5 Recovery from Sensorimotor Deficits Following Dorsal Column Lesions.- 5.6 Plasticity of the DCN During Development.- 5.6.1 Effects of Prenatal Lesions.- 5.6.2 Effect of Neonatal Destruction of Unmyelinated Afferents.- 5.7 Major Conclusions.- 6 Plasticity and the Somatosensory Thalamus.- 6.1 Experimental Strategies and Plasticity in the Ventral Posterior Nuclei of the Thalamus.- 6.2 Anatomical Organization of Inputs and Outputs of the Ventral Posterior Nuclei.- 6.2.1 Primate and Cat.- 6.2.2 Raccoon.- 6.2.3 Rat.- 6.3 Responses of Neurons to Cutaneous Stimulation and the Effects of Anaesthetics and Other Drugs.- 6.4 Somatotopic Organization of the VPL and VPM.- 6.5 Effects of Alteration of Input on Somatotopic Organization.- 6.5.1 Reversible Blockade of Afferents and the Immediate Expression of New Inputs.- 6.5.2 Chronic Lesion of Afferent Pathways and Sprouting of Thalamic Afferents.- 6.6 Major Conclusions.- 7 Plasticity and the Somatosensory Cerebral Cortex.- 7.1 Experimental Strategies and Cortical Plasticity..- 7.2 Plasticity in the Cortex of Adult and Developing Primates.- 7.2.1 Multiple Representations.- 7.2.2 Thalamic Input and Intracortical Connectivity..- 7.2.3 Responses of Cortical Neurons to Natural Stimulation.- 7.2.4 Somatotopic Representation of the Hand in Areas 3b and 1.- 7.2.5 Anatomy and Innervation of the Monkey Hand.- 7.2.6 Anaesthetics and the Representation of the Hand.- 7.2.7 Injury and Subsequent Regeneration of Peripheral Nerves.- 7.2.8 Section and Ligation of Peripheral Nerves.- 7.2.9 Effects of Repeated Stimulation on Cortical Representations.- 7.2.10 Cortical Damage.- 7.3 Plasticity in the Cortex of Adult and Developing Cats.- 7.3.1 Somatotopic Organization, Cytoarchitectonics and Neuronal Responses.- 7.3.2 Thalamic Input and Ineffective Thalamocortical Connections.- 7.3.3 Effects of Anaesthetics and Other Drugs.- 7.3.4 Cordotomy and Section of Ascending Tracts.- 7.3.5 Blockage of Primary Afferent Input in Specific Dorsal Roots.- 7.3.6 Damage to Peripheral Nerves and Effects of Usage on Cortical Representation.- 7.3.7 Cortical Damage.- 7.4 Plasticity in the Cortex of Adult and Infant Raccoons.- 7.4.1 Somatotopic Organization and Cytoarchitectonics.- 7.4.2 Neuronal Responses in SI Cortex and the Effects of Anaesthetics.- 7.4.3 Ineffective Afferent Connections.- 7.4.4 Effects of Amputation on Cortical Somatotopy..- 7.5 Plasticity in the Cortex of Adult and Developing Rodents.- 7.5.1 Somatotopic Organization and Cytoarchitectonics.- 7.5.2 Section and Ligation of Peripheral Nerves in the Adult.- 7.5.3 Effects of Perinatal Nerve Section or Limb Amputation.- 7.5.4 Pharmacological Mechanisms Underlying Somatotopic Reorganization.- 7.5.5 Cortical Damage.- 7.6 Major Conclusions.- 8 Concluding Remarks.- 8.1 Plasticity During Development.- 8.1.1 Disruption of a Growing System and the Influence of the Periphery.- 8.1.2 The Influence of Afferent Axons and the Target Tissue.- 8.2 Evaluation of Experimentally Induced Plasticity in Adult Animals.- 8.2.1 Plasticity in the Peripheral Nervous System.- 8.2.2 Somatotopic Organization in Intact Animals as a Baseline for Assessing Altered Connections.- 8.2.3 Somatotopic-Artifacts in Regions Deprived of Their Normal Input.- 8.2.4 Plasticity and the Level of the Neuraxis.- 8.3 The Case for Ineffective Connections.- 8.3.1 Elucidation of Sub-Threshold Inputs.- 8.3.2 Somatotopically Inappropriate Projections of Afferent Axons.- 8.4 Spatial Extent of Immediate and Long-Term Changes in Somatotopic Organization.- 8.4.1 Distance Limits of Somatotopic Reorganization.- 8.4.2 Sprouting and Synaptogenesis in the Mature System.- 8.4.3 Recovery of Function.- 8.5 Normal Physiological Mechanisms and Plasticity.- 8.5.1 Inhibitory Receptive Fields and Partial Deafferentation.- 8.5.2 Neurotransmitters and Neural Systems That Regulate Sensory Input.- 8.6 Role of Plasticity in the Mature Somatosensory System.- References.

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