Conn Neuroscience in Medicine

3rd Auflage 2008
ISBN: 978-1-60327-455-5
Verlag: Humana Press
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 820 Seiten

Continuing progress has been made in understanding the brain at the molecular, anatomic, and physiological levels in the years following the "Decade of the Brain," with the results providing insight into the underlying basis of many neurological disease processes. In Neuroscience in Medicine, Third Edition, a distinguished panel of basic and clinical investigators, noted for their teaching excellence, provide thoroughly updated and revised chapters to reflect these remarkable advances. Designed specifically for medical students and allied health professionals, this up-to-date edition alternates scientific and clinical chapters that explain the basic science underlying neurological processes and then relate that science to the understanding of neurological disorders and their treatment. These popular and now expanded "clinical correlations" cover, in detail, disorders of the spinal cord, neuronal migration, the autonomic nervous system, the limbic system, ocular motility, and the basal ganglia, as well as demyelinating disorders, stroke, dementia and abnormalities of cognition, congenital chromosomal and genetic abnormalities, Parkinson's disease, nerve trauma, peripheral neuropathy, aphasias, sleep disorders and myasthenia gravis. In addition to concise summaries of the most recent biochemical, physiological, anatomical, and behavioral advances, the chapters summarize current findings on neuronal gene expression and protein synthesis at the molecular level.

Authoritative and comprehensive, Neuroscience in Medicine, Third Edition provides a fully up-to-date and readily accessible guide to brain functions at the cellular and molecular level, as well as clearly demonstrating their emerging diagnostic and therapeutic importance.

Autoren/Hrsg.

Conn, P. Michael

Inhaltsverzeichnis

1;PREFACE;5
2;CONTENTS;6
3;CONTRIBUTORS;9
4;LIST OF COLOR PLATES;11
5;Cytology and Organization of Cell Types: Light and Electron Microscopy;12
5.1;1. NEURONAL RESPONSE TO A CHANGING ENVIRONMENT;12
5.2;2. MECHANISMS OF NEURONAL FUNCTION;15
5.3;3. CYTOSKELETON DETERMINATION OF NEURONAL FORM;21
5.4;4. NEURONAL SYNAPSES;24
5.5;5. GLIAL CELLS;29
6;Anatomy of the Spinal Cord and Brain;35
6.1;1. INTRODUCTION;35
6.2;2. SPINAL CORD EXTERNAL ANATOMY;35
6.3;3. BRAIN;42
6.4;SELECTED READINGS;61
7;Ion Channels, Transporters, and Electrical Signaling;62
7.1;OVERVIEW;63
7.2;1. RESTING MEMBRANE POTENTIALS;63
7.3;2. ELECTRICAL EXCITABILITY OF THE CELL MEMBRANE;69
7.4;3. VOLTAGE-GATED CHANNELS;73
7.5;4. EXTRACELLULAR LIGAND-GATED CHANNELS;85
7.6;5. ENaC/DEGENERIN FAMILY OF CHANNELS;90
7.7;6. INTRACELLULAR AND INTERCELLULAR CHANNELS;91
7.8;7. ACTIVE TRANSPORTERS;94
7.9;8. A CROSS-COMMUNICATION BETWEEN ELECTRICAL AND RECEPTOR- MEDIATED SIGNALING PATHWAYS;97
7.10;SELECTED READINGS;98
8;Demyelinating Disorders;99
8.1;IMPAIRED OR BLOCKED IMPULSE CONDUCTION;99
8.2;DISEASES THAT AFFECT MYELIN;99
8.3;MS HAS A DISTINCT AGE, GENDER, RACE, AND GEOGRAPHIC PROFILE;100
8.4;MS IS CHARACTERIZED BY THE PRESENCE OF NUMEROUS DISCRETE AREAS OF DEMYELINATION THROUGHOUT THE BRAIN AND SPINAL CORD;100
8.5;THE SYMPTOMS OF MS REMIT AND REAPPEAR IN CHARACTERISTIC FASHION;100
8.6;THE DIAGNOSIS OF MS CAN BE AIDED BY IMAGING STUDIES AND LABORATORY TESTS IMMUNOSUPPRESSION IS THE MOST;101
8.7;COMMON FORM OF THERAPY USED IN MS;101
8.8;SELECTED READINGS;102
9;Synaptic Transmission;103
9.1;OVERVIEW;103
9.2;1. PROPERTIES OF CHEMICAL AND ELECTRICAL SYNAPSES;104
9.3;2. A MODEL SYNAPSE: THE NEUROMUSCULAR JUNCTION;109
9.4;3. PRESYNAPTIC EXOCYTOSIS IS CA DEPENDENT;109
9.5;4. NEUROTRANSMITTERS AND THEIR RECEPTORS IN THE MAMMALIAN BRAIN;111
9.6;5. THE INTERPLAY OF EXCITATION AND INHIBITION;112
9.7;6. SYNAPSES ARE HETEROGENEOUS AND CAN BE SPECIALIZED;113
9.8;7. SHORT-TERM AND LONG-TERM SYNAPTIC PLASTICITY;116
9.9;SELECTED READINGS;117
10;Presynaptic and Postsynaptic Receptors;118
10.1;1. RECEPTOR CLASSIFICATION SCHEMES: ANATOMIC, PHARMACOLOGIC, AND STRUCTURAL/ MECHANISTIC;118
10.2;2. RECEPTOR STRUCTURE AND FUNCTION;119
10.3;3. NEUROTRANSMITTERS AND THEIR RECEPTORS;126
10.4;4. CONCLUSION;137
10.5;SUGGESTED READINGS;137
11;Neuroembryology and Neurogenesis;138
11.1;1. INTRODUCTION;138
11.2;2. EMBRYONIC DEVELOPMENT OR THE NERVOUS SYSTEM;139
11.3;3. NEUROGENESIS IN THE EMBRYONIC NERVOUS SYSTEM;147
11.4;4. NEURONAL APOPTOSIS IN THE DEVELOPING NERVOUS SYSTEM;149
11.5;SELECTED READINGS;150
12;Disorders of Neuronal Migration;151
12.1;CORTICAL NEURONS IN NEURONAL MIGRATION DISORDERS;151
12.2;EPILEPSY AS A SYMPTOM OF ABNORMAL CORTICAL NEURONAL MIGRATION;151
12.3;KALLMANN’S SYNDROME AS A PROTOTYPE OF THE HERITABLE DISORDERS OF NEURONAL MIGRATION;152
12.4;SELECTED READINGS;152
13;The Vasculature of the Human Brain;153
13.1;1. INTRODUCTION;153
13.2;2. INTRACRANIAL ARTERIAL SYSTEM ( TABLE 1);155
13.3;3. COLLATERAL CIRCULATION (TABLE 8);164
13.4;4. CAPILLARIES;165
13.5;5. INTRACRANIAL VENOUS SYSTEM ( TABLE 9);167
13.6;SELECTED READINGS;172
14;Stroke;173
14.1;PATHOLOGIC MECHANISMS OF STROKE;173
14.2;THE NORMAL BLOOD SUPPLY TO THE BRAIN CAN BE DISRUPTED BY SEVERAL MECHANISMS;173
14.3;TRANSIENT ISCHEMIC SYMPTOMS OFTEN PRECEDE CEREBRAL INFARCTION;174
14.4;THE NEUROLOGIC DEFICIT IN ISCHEMIC STROKE DEPENDS ON WHICH BLOOD VESSEL IS INVOLVED;174
14.5;LACUNAR INFARCTIONS DO NOT CONFORM TO THE DISTRIBUTION OF MAJOR CEREBRAL ARTERIES;176
14.6;TREATMENT OF STROKE;176
14.7;SELECTED READINGS;177
15;Choroid Plexus–Cerebrospinal Fluid Circulatory Dynamics: Impact on Brain Growth, Metabolism, and Repair;178
15.1;1. STRUCTURAL AND FUNCTIONAL COMPONENTS OF THE CEREBROSPINAL FLUID;178
15.2;2. DIVERSE ROLES OF CSF IN EFFECTING BRAIN WELL- BEING;179
15.3;3. PIVOTAL MODULATORY FUNCTIONS OF THE CSF IN FETAL BRAIN DEVELOPMENT;182
15.4;4. PHYSICAL DIMENSIONS OF THE ADULT CSF SYSTEM;183
15.5;5. CSF-BORDERING CELLS THAT DEMARCATE THE VENTRICULO- SUBARACHNOID SYSTEM;186
15.6;6. CIRCUMVENTRICULAR ORGANS OUTSIDE BLOOD- BRAIN BARRIER;187
15.7;7. ELABORATION OF CSF;189
15.8;8. INTERACTIVE BLOOD-CSF AND BLOOD- BRAIN INTERFACES IN MILIEU STABILIZATION;193
15.9;9. FLUID IMBALANCES: EFFECTS ON BRAIN AND CSF VOLUMES;195
15.10;10. CIRCULATION OF CSF;195
15.11;11. DRAINAGE OF CSF;196
15.12;12. CSF PRESSURE-VOLUME RELATIONSHIPS;198
15.13;13. CELLULAR COMPOSITION OF CSF;200
15.14;14. CLINICAL USAGE OF CSF;201
15.15;15. NEW OUTLOOKS FOR CSF TRANSLATIONAL RESEARCH AND THERAPY;202
15.16;REFERENCES;203
16;Organization of the Spinal Cord;206
16.1;1. THE SPINAL CORD;206
16.2;2. SPINAL NEURONS ORGANIZED INTO NUCLEI AND INTO LAMINAE;208
16.3;3. ASCENDING AND DESCENDING TRACTS IN WHITE MATTER;208
16.4;4. MOTOR NEURONS;213
16.5;5. REGIONAL SPECIALIZATIONS;214
16.6;6. SPINAL REFLEXES;215
16.7;7. SPINAL LESIONS;218
16.8;8. STRATEGIES TO REPAIR INJURED SPINAL CORD;219
16.9;SELECTED READINGS;220
17;Disorders of the Spinal Cord;221
17.1;CAUSES OF SPINAL CORD DISORDERS;221
17.2;LOCALIZATION OF THE CAUSATIVE LESION;221
17.3;SPARING OF SACRAL SENSATION MAY HELP DIFFERENTIATE A LESION IN THE CENTER OF THE SPINAL CORD FROM ONE ON ITS CIRCUMFERENCE;222
17.4;LESIONS INVOLVING HALF THE SPINAL CORD PRODUCE A DISTINCT CLINICAL SYNDROME;222
17.5;A CAPE-LIKE SENSORY LOSS MAY ALSO BE A CLUE TO THE LOCALIZATION OF A SPINAL- CORD LESION;222
17.6;THE ANTERIOR PORTION OF THE SPINAL CORD CAN BE PREFERENTIALLY INVOLVED IN ISCHEMIC LESIONS;222
17.7;PATHOLOGY BELOW THE L1 THROUGH L2 VERTEBRAL LEVEL AFFECTS THE CAUDA EQUINA BUT NOT THE SPINAL CORD;223
17.8;DIAGNOSTIC NEUROIMAGING PROCEDURES AND ELECTROPHYSIOLOGIC TESTS;223
17.9;TREATMENT OF SPINAL CORD INJURY;223
17.10;SELECTED READINGS;224
18;The Cerebellum;225
18.1;1. OVERVIEW;225
18.2;2. THE GENERAL ORGANIZATION OF THE CEREBELLUM;226
18.3;3. THE CYTOARCHITECTURE OF THE CEREBELLAR CORTEX IS CONSPICUOUSLY UNIFORM;233
18.4;4. THE INPUT AND OUTPUT SYSTEMS OF THE CEREBELLUM;237
18.5;5. THE CEREBELLUM AND MOTOR LEARNING;242
18.6;6. CEREBELLAR DYSFUNCTION;244
18.7;7. SUMMARY;247
18.8;REFERENCES;248
19;The Brain Stem and Cranial Nerves;250
19.1;1. INTRODUCTION;250
19.2;2. EXTERNAL ANATOMY OF THE BRAIN STEM;250
19.3;3. VENTRICULAR SYSTEM OF THE BRAIN STEM;254
19.4;4. INTERNAL STRUCTURE OF THE BRAIN STEM;257
19.5;5. PERIPHERAL DISTRIBUTIONS OF THE CRANIAL NERVES;262
19.6;6. NUCLEAR COMPONENTS OF THE CRANIAL NERVES AND THEIR FUNCTIONS;264
19.7;7. CEREBELLUM;270
19.8;8. OTHER PROMINENT BRAIN STEM STRUCTURES;270
19.9;SUGGESTED READINGS;272
20;Disorders of the Autonomic Nervous System;273
20.1;PERIPHERAL-NERVE DYSFUNCTION;273
20.2;CENTRAL NERVOUS SYSTEM DISORDERS;273
20.3;ABNORMALITIES OF NEUROTRANSMITTER METABOLISM;274
20.4;CLINICAL TESTS USEFUL IN DOCUMENTING AUTONOMIC DYSFUNCTION;274
20.5;SELECTED READINGS;275
21;The Brain Stem Reticular Formation;276
21.1;1. INTRODUCTION;276
21.2;2. ANATOMIC CHARACTERISTICS OF RETICULAR FORMATION NEURONS;277
21.3;3. RETICULAR FORMATION PATHWAYS;280
21.4;4. OTHERS RELATED BRAIN STEM NUCLEI;283
21.5;5. RETICULAR FORMATION FUNCTIONS AND INTERACTIONS;284
21.6;SELECTED READINGS;288
22;The Trigeminal System;290
22.1;1. INTRODUCTION;290
22.2;2. PERIPHERIAL DISTRIBUTION OF THE TRIGEMINAL NERVE;290
22.3;3. CENTRAL CONNECTIONS OF THE TRIGEMINAL SYSTEM;294
22.4;4. ASCENDING TRIGEMINAL PATHWAYS;298
22.5;5. FUNCTIONS OF THE TRIGEMINAL SYSTEM;299
22.6;6. TRIGEMINAL SYSTEM LESIONS;300
22.7;SELECTED READINGS;301
23;The Hypothalamus;303
23.1;1. INTRODUCTION;303
23.2;2. ANATOMY OF THE HYPOTHALAMUS;306
23.3;3. TECHNIQUES FOR STUDYING HYPOTHALAMIC FUNCTION;331
23.4;4. PHYSIOLOGIC PROCESSES CONTROLLED BY THE HYPOTHALAMUS;342
23.5;5. CONCLUSION;360
23.6;SELECTED READING;360
24;The Cerebral Cortex;361
24.1;1. INTRODUCTION;361
24.2;2. SURFACE FEATURES OF THE CEREBRAL CORTEX;361
24.3;3. CORTICAL CYTOLOGY;363
24.4;4. STRUCTURE AND DISTRIBUTION OF CORTICAL AREAS;367
24.5;5. FUNCTIONAL SUBDIVISIONS OF THE CEREBRAL CORTEX;370
24.6;6. CORTICAL CONNECTIVITY;373
24.7;7. SUMMARY OF THE ORGANIZATION OF THE CEREBRAL CORTEX;377
24.8;SELECTED READING;378
25;Dementia and Abnormalities of Cognition;379
25.1;REGIONAL BRAIN PATHOLOGY ALZHEIMER’S DISEASE;379
25.2;SUDDEN ABNORMALITIES OF MEMORY AND COGNITION;380
25.3;SELECTED READINGS;380
26;The Limbic System;381
26.1;1. HISTORY OF THE NEUROANATOMY OF THE LIMBIC SYSTEM;381
26.2;2. NEUROANATOMY OF THE LIMBIC SYSTEM;383
26.3;3. MAJOR CONNECTIONS OF THE LIMBIC SYSTEM;389
26.4;4. FUNCTIONAL CONSIDERATIONS;394
26.5;5. LIMBIC SYSTEM OVERVIEW;398
26.6;SUGGESTED READINGS;398
27;Disorders of the Limbic System;399
27.1;THE LIMBIC SYSTEM PLAYS A ROLE IN EPILEPSY;399
27.2;THE LIMBIC SYSTEM ALSO PLAYS A ROLE IN ALZHEIMER’S DISEASE;399
27.3;THE LIMBIC SYSTEM PLAYS A ROLE IN WERNICKE- KORSAKOFF’S SYNDROME;400
27.4;SELECTED READINGS;401
28;The Basal Ganglia;402
28.1;1. INTRODUCTION;402
28.2;2. ANATOMY OF THE BASAL GANGLIA;403
28.3;3. INTRINSIC CIRCUITS OF THE BASAL GANGLIA;406
28.4;4. BASAL GANGLIA–THALAMOCORTICAL CIRCUITS;408
28.5;5. FUNCTION AND PHYSIOLOGY OF THE BASAL GANGLIA;410
28.6;6. PHARMACOLOGY OF THE BASAL GANGLIA;412
28.7;SELECTED READINGS;414
29;Disorders of the Basal Ganglia;416
29.1;CHOREA;416
29.2;DYSTONIA;417
29.3;TICS;417
29.4;BASAL GANGLIA DISORDERS CAUSING MULTIPLE FORMS OF ABNORMAL MOVEMENT;418
29.5;SELECTED READINGS;418
30;The Thalamus;419
30.1;1. INTRODUCTION;419
30.2;2. HISTORY;420
30.3;3. NUCLEAR SUBDIVISIONS OF THE THALAMUS;421
30.4;4. CELL TYPES OF THE THALAMUS;422
30.5;5. BASIC SYNAPTIC ORGANIZATION OF THE DORSAL THALAMUS;424
30.6;6. SYNAPTIC CONNECTIVITY OF THE RETICULAR NUCLEUS;425
30.7;7. NEUROTRANSMITTERS IN THE THALAMUS;426
30.8;8. SPECIFIC CONNECTIONS OF THALAMIC NUCLEAR GROUPS;429
30.9;9. THE CORTICOTHALAMIC SYSTEM;437
30.10;10. THE THALAMOSTRIATAL SYSTEMS;438
30.11;11. SYMPTOMS AFTER THALAMIC LESIONS;440
30.12;12. THALAMOTOMY AND THALAMIC DEEP BRAIN STIMULATION FOR BRAIN DISEASES;441
30.13;13. CONCLUDING REMARKS;441
30.14;SELECTED READINGS;442
31;Spinal Mechanisms for Control of Muscle Length and Force;443
31.1;1. A BRIEF REVIEW OF MUSCLE FUNCTION;443
31.2;2. MECHANICAL PROPERTIES OF WHOLE MUSCLE;447
31.3;3. MUSCLE RECEPTORS;450
31.4;4. AFFERENT PATHWAYS TO THE SPINAL CORD;458
31.5;5. MOTONEURONS AND MOTOR UNITS;464
31.6;6. NEUROMODULATION OF SPINAL CIRCUITS;472
31.7;7. SPINAL REGULATION OF MOVEMENT;474
31.8;SELECTED READINGS;478
32;Chemical Messenger Systems;479
32.1;1. NEUROTRANSMITTERS, NEUROHORMONES, AND NEUROMODULATORS;479
32.2;2. NEUROTRANSMITTERS ARE SMALL ORGANIC MOLECULES THAT CARRY A CHEMICAL MESSAGE FROM A NEURONAL AXON OR DENDRITE TO ANOTHER CELL OR NERVE;479
32.3;3. NEUROHORMONES ARE CHEMICAL MESSENGERS THAT ARE SECRETED BY THE BRAIN INTO THE CIRCULATORY SYSTEM AND ALTER CELLULAR FUNCTION AT A DISTANCE;480
32.4;4. NEUROMODULATORS ARE TRANSMITTERS OR NEUROPEPTIDES THAT ALTER THE ENDOGENOUS ACTIVITY OF THE TARGET CELL;480
32.5;5. THE RESPONSE TO TRANSMITTERS CAN BE EITHER FAST OR SLOW;482
32.6;6. NERVE ACTIVITY CAN BE MEASURED BY DETERMINING THE FIRING RATE OR RATE OF NEUROTRANSMITTER RELEASE OR TURNOVER;482
32.7;7. SMALL-MOLECULAR-WEIGHT NEUROTRANSMITTERS;483
32.8;8. AMINO ACID NEUROTRANSMITTERS: GABA, GLUTAMATE, AND GLYCINE;497
32.9;9. ENDOCANNABINOIDS;501
32.10;10. NITRIC OXIDE;502
32.11;11. NEUROACTIVE PEPTIDES;502
32.12;12. CONCLUSION;506
32.13;REFERENCES;506
32.14;SELECTED READINGS;507
33;Parkinson’s Disease;508
33.1;PARKINSON’S DISEASE SYMPTOMS;508
33.2;AGE-RELATED INCIDENCE OF PARKINSON’S DISEASE;509
33.3;THE LEWY BODY IS THE PATHOLOGIC HALLMARK OF PARKINSON’S DISEASE;510
33.4;ETIOLOGY AND TREATMENT;510
33.5;SELECTED READINGS;512
34;Pain;513
34.1;1. PAIN IS A COMPLEX SENSORY EVENT;513
34.2;2. SOMATOSENSORY PRIMARY AFFERENTS TRANSDUCE STIMULUS ENERGY AND TRANSMIT INFORMATION FROM THE PERIPHERAL TISSUES INTO THE CENTRAL NERVOUS SYSTEM;514
34.3;3. NOCICEPTIVE SENSORY NEURONS PROJECT TO THE DORSAL HORN;517
34.4;4. PARALLEL ASCENDING PATHWAYS UNDERLIE DISTRIBUTED PROCESSING OF NOCICEPTIVE INFORMATION;518
34.5;5. VISCERAL NOCICEPTION;520
34.6;6. PAIN PROCESSES IN INJURED OR INFLAMED TISSUE;521
34.7;7. REGULATORY MECHANISMS: GATE CONTROL AND DESCENDING MODULATION;522
34.8;8. PAIN DUE TO INJURY TO PERIPHERAL OR CENTRAL NERVOUS SYSTEM;523
34.9;SELECTED READINGS;525
35;Physical Trauma to Nerves;526
35.1;NERVE SEVERANCE RESULTS IN A PREDICTABLE SEQUENCE OF CHANGES IN THE NERVE AND MUSCLE NERVE- CONDUCTION TESTING IS USEFUL IN DETERMINING THE EXTENT;526
35.2;AND LOCATION OF NERVE DAMAGE;526
35.3;CHRONIC COMPRESSION AND ENTRAPMENT ARE AMONG THE MOST COMMON FORMS OF NERVE INJURY;527
35.4;RECOVERY AFTER NERVE TRAUMA MAY DEPEND ON NERVE REGENERATION;527
35.5;SELECTED READING;527
36;Peripheral Neuropathy;528
36.1;AXONAL DEGENERATION CAN TAKE SEVERAL FORMS;528
36.2;DEMYELINATION OF PERIPHERAL NERVES MAY BE PRIMARY OR SECONDARY;528
36.3;THE TYPICAL SYMPTOMS OF PERIPHERAL NEUROPATHY INCLUDE POSITIVE AND NEGATIVE PHENOMENA;529
36.4;NERVE-CONDUCTION TESTING IS USEFUL IN ANALYZING PERIPHERAL NEUROPATHIES;529
36.5;PERIPHERAL NEUROPATHY MAY DEVELOP ACUTELY OR CHRONICALLY;530
36.6;THERAPY FOR NEUROPATHIES CAN BE DIRECTED AT THE SYMPTOMS AND THE CAUSE;530
36.7;SELECTED READING;530
37;Vision;531
37.1;1. INTRODUCTION;531
37.2;2. REFRACTION;532
37.3;3. THE RETINA;533
37.4;4. PHOTOTRANSDUCTION;534
37.5;5. THE OPTIC PATHWAYS;537
37.6;6. CRITICAL PERIODS IN VISUAL SYSTEM DEVELOPMENT;541
37.7;7. ADULT ORGANIZATION OF THE VISUAL PATHWAY FROM RETINA TO CORTEX;542
37.8;8. ACTIVITY-INDEPENDENT DEVELOPMENT OF ORDER IN THE VISUAL SYSTEM;542
37.9;9. ACTIVITY-DEPENDENT DEVELOPMENT OF ORDER IN THE VISUAL SYSTEM;544
37.10;10. DEFINITION OF THE OCULOMOTOR SYSTEM;555
37.11;11. TYPES OF EYE MOVEMENTS;555
37.12;12. EXTRAOCULAR MUSCLES;556
37.13;13. EXTRAOCULAR MOTOR NUCLEI;556
37.14;14. PRE-OCULOMOTOR NUCLEI;559
37.15;15. ROLE OF THE CEREBRAL CORTEX AND CEREBELLUM IN EYE MOVEMENT;562
37.16;16. ROLE OF THE BASAL GANGLIA IN EYE MOVEMENT;565
37.17;17. CONTROL OF VERGENCE EYE MOVEMENTS;565
37.18;18. BASIS OF DISEASE STATES;565
37.19;19. DISORDERS OF OCULAR MOTILITY;568
37.20;SELECTED READINGS;571
38;Disorders of Ocular Motility;572
38.1;SEVERAL SUPRANUCLEAR SYSTEMS GUIDE EYE MOVEMENT;572
38.2;ABNORMALITIES OF CONJUGATE GAZE IMPLY BRAIN- STEM PATHOLOGY;573
38.3;DISTINCT PATTERNS OF IMPAIRED OCULAR MOTILITY RESULT FROM LESIONS OF INDIVIDUAL CRANIAL NERVES;573
38.4;DISORDERS OF MUSCLE OR NEUROMUSCULAR TRANSMISSION CAN AFFECT OCULAR MOTILITY;573
38.5;NYSTAGMUS IS AN ABNORMAL PATTERN OF REPETITIVE EYE MOVEMENTS;574
38.6;SELECTED READINGS;574
39;Audition;575
39.1;1. INTRODUCTION;575
39.2;2. THE PHYSICAL NATURE OF SOUND;575
39.3;3. THE PERIPHERAL AUDITORY SYSTEM;576
39.4;4. FREQUENCY TUNING AND TEMPORAL INFORMATION ARE TRANSMITTED BY AUDITORY NERVE FIBERS;581
39.5;5. CENTRAL AUDITORY SYSTEM;582
39.6;SELECTED READINGS;589
40;The Vestibular System;590
40.1;1. INTRODUCTION;590
40.2;2. VESTIBULAR REFLEXES;590
40.3;3. THE VESTIBULAR RECEPTORS;591
40.4;4. CENTRAL VESTIBULAR CONNECTIONS AND PATHWAYS ARE RELATED TO THE CONTROL OF EYE MOVEMENTS, BALANCE, AND POSTURE;594
40.5;5. NYSTAGMUS;597
40.6;6. VESTIBULAR ASSESSMENT;599
40.7;SELECTED READINGS;599
41;The Gustatory System;600
41.1;1. INTRODUCTION;600
41.2;2. PERIPHERAL TASTE SYSTEM;602
41.3;3. CENTRAL TASTE SYSTEM;606
41.4;SELECTED READINGS;609
42;The Olfactory System;610
42.1;1. INTRODUCTION;610
42.2;2. THE OLFACTORY EPITHELIUM;610
42.3;3. THE MAIN OLFACTORY BULB;613
42.4;4. THE PRIMARY OLFACTORY CORTEX ( FIG. 4);617
42.5;5. THE ACCESSORY OLFACTORY SYSTEM;620
42.6;6. OLFACTION AND BEHAVIOR;620
43;Sleep, Dreams, and States of Consciousness;622
43.1;1. INTRODUCTION AND ORGANIZATION OF SLEEP- WAKEFULNESS;622
43.2;2. SLEEP HAS DISTINCTIVE ONTOGENETIC AND PHYLOGENETIC FEATURES;626
43.3;3. SLEEP ONSET AND SLEEPINESS IS DETERMINED BY CIRCADIAN TIME OF DAY AND BY PRIOR WAKEFULNESS;626
43.4;4. SLOW-WAVE SLEEP FACTORS;628
43.5;5. CONTROL OF EEG SYNCHRONIZATION AND DESYNCHRONIZATION;632
43.6;6. REM SLEEP PHYSIOLOGY AND RELEVANT BRAIN ANATOMY;633
43.7;7. OREXIN, NARCOLEPSY, AND THE CONTROL OF SLEEP AND WAKEFULNESS;640
43.8;8. MOLECULAR BIOLOGY OF SLEEP;641
43.9;9. THE FORM OF DREAMS AND THE BIOLOGY OF REM SLEEP;642
43.10;10. FUNCTION(S) OF NON-REM AND REM SLEEP;643
44;Disorders of Sleep;646
45;Higher Brain Functions;649
45.1;1. INTRODUCTION;649
45.2;2. BRAIN AND BEHAVIOR ASSOCIATIONS;650
45.3;3. THE OCCIPITAL LOBES;654
45.4;4. THE TEMPORAL LOBES;655
45.5;5. THE PARIETAL LOBES;658
45.6;6. THE FRONTAL LOBES;659
45.7;7. SUBCORTICAL STRUCTURES;662
45.8;8. CLOSING REMARKS SELECTED READINGS;663
46;The Aphasias and Other Disorders of Language;665
47;Neuroimmunology: An Overview;668
47.1;1. INTRODUCTION;668
47.2;2. INNERVATION OF LYMPHOID ORGANS;668
47.3;3. CYTOKINES IN THE NERVOUS SYSTEM;670
47.4;4. PRESENCE OF NEUROENDOCRINE PEPTIDES IN IMMUNE CELLS;671
47.5;5. NEUROIMMUNOMODULATION BY NEUROENDOCRINE PEPTIDES;672
47.6;6. AUTOIMMUNITY AND NEUROIMMUNOLOGY;672
47.7;SELECTED READINGS;672
48;Nervous System–Immune System Interactions;673
48.1;1. INTRODUCTION;673
48.2;2. INTERACTIONS OF THE NERVOUS AND IMMUNE SYSTEMS IN THE PERIPHERY;673
48.3;3. IMMUNE INTERACTIONS WITHIN THE CNS;676
48.4;4. INFLAMMATORY RESPONSES IN THE CNS DURING TRAUMA OR DISEASE;679
48.5;5. CONCLUSION;682
48.6;SELECTED READINGS;683
49;Myasthenia Gravis;684
50;Degeneration, Regeneration, and Plasticity in the Nervous System;687
50.1;1. INTRODUCTION;687
50.2;2. BASIC CELLULAR RESPONSES IN THE PNS AND CNS TO AXONAL DAMAGE: GENERAL PRINCIPLES;688
50.3;3. NEURONAL RESPONSES TO AXONAL INJURY IN THE PERIPHERAL NERVOUS SYSTEM;696
50.4;4. NEURONAL RESPONSES TO INJURY OR DISEASE IN THE CENTRAL NERVOUS SYSTEM;701
50.5;5. CNS NEURONS CAN EXPRESS CONSIDERABLE INTRINSIC GROWTH CAPACITIES UNDER CERTAIN CONDITIONS;705
50.6;6. A BALANCE BETWEEN INTRINSIC AND EXTRINSIC FACTORS GOVERNING AXONAL REGENERATION IN THE CNS;706
50.7;7. THE INJURED CNS HAS SOME INTRINSIC POTENTIAL FOR SELF- REPAIR: CONCEPT OF NEUROPLASTICITY;710
50.8;8. POTENTIAL INTERVENTIONS TO PROMOTE CNS REPAIR ARE BASED ON CELLULAR RESPONSES TO INJURY AND DISEASE;714
50.9;9. CAN CELLS THAT DIE BECAUSE OF NECROSIS OR APOPTOSIS BE REPLACED?;717
50.10;10. ARE CNS CIRCUITS AND PATHWAYS RIGIDLY WIRED?;721
50.11;11. SUMMARY;722
50.12;SELECTED READINGS;723
51;Congenital Chromosomal and Genetic Abnormalities;724
52;The Biology of Drug Addiction;727
52.1;1. INTRODUCTION;727
52.2;2. TECHNIQUES USED TO STUDY ADDICTION;729
52.3;3. SEX DIFFERENCES AND THE NEUROENDOCRINE SYSTEM IN ADDICTION;730
52.4;4. CIRCADIAN RHYTHMS AND ADDICTION;732
52.5;5. MECHANISMS OF ACTION FOR SPECIFIC ADDICTIVE DRUGS;734
52.6;6. GENERAL MOLECULAR AND CELLULAR MECHANISMS OF ADDICTION;740
52.7;SELECTED READINGS;743
53;The Neuropathology of Disease;744
53.1;1. INTRODUCTION;744
53.2;2. VASCULAR-RELATED PATHOLOGY;744
53.3;3. TUMORS;755
53.4;4. INFECTIONS;758
53.5;5. PERINATAL ABNORMALITIES: HYDROCEPHALUS;760
53.6;6. CONGENITAL MALFORMATIONS;761
53.7;7. OTHER COMMON PATHOLOGIES;766
53.8;SELECTED READINGS;769
54;INDEX;770

Leseproben

OVERVIEW

The nervous system is composed of specialized cellular circuits that allow an animal to perform tasks essential for survival. Neurons are organized to form these circuits, and they transmit electrical and chemical signals among themselves to process sensory input, initiate behavioral responses, and regulate an animal’s internal physiology. The critical link between neurons that permits communication and establishes the foundation for neuronal circuitry is called the synapse, and this chapter will discuss fundamental synaptic properties.

Synapses are sites of close cellular contact where fast, highly localized transmission of chemical and electrical signals can occur. The human brain has approximately 1011neurons that form about 1015 synapses. By comparison, the simple nematode worm C. elegans has exactly 320 neurons with only about 7600 synapses. The capacity of the human brain to form such an astronomical number of synapses has surely contributed to the success of our species and its vast repertoire of behaviors. In order to understand how synapses confer such complexity of neuronal circuitry, it is important to explore the details of information transfer at the synapse.

The process of communication between neurons, termed synaptic transmission, is also key to developing better medical treatments of neurologic conditions for several reasons. The causes of severalmental disorders and neuromuscular diseases can be traced to dysfunctional synapses. Synapses are also the locus of action for several neurotoxins and psychoactive drugs (some of which can cause debilitating and life-long addictions).

Finally, determining how synapses transmit signals and how neuronal circuits are remodeled and modulated at the synaptic level will eventually allow us to understand the basis of neuronal learning and memory.

Synapses vary widely in shape, size, and functional capability. Presumably, such architectural and functional diversities are tailored for the specialized information transfer and processing needs of individual neurons and circuits. For example, many synapses function as high-fidelity relay stations. The connection between motor neurons and muscle fibers (termed the neuromuscular junction), the giant synapses in the mammalian and aviary auditory systems involved in sound localization, and the squid giant synapse, which allows a rapid escape behavior, are all examples of high-fidelity relays. These are synapses where reliability is at a premium, and the synaptic architecture is designed as a fail-safe mechanism for information transfer.

Other synapses, such as the bouton-type synapses of the cortex and hippocampus, often fail to transmit signals and are thus considered comparatively unreliable. These bouton synapses, however, have the capacity to become more fail-safe with repetitive use. This type of change in synaptic strength is an example of plasticity and is thought to underlie the long-lasting storage of information acquired through repetitive use of an associated neuronal circuit. In other words, the specific strengthening of a particular set of synaptic connections may form the basis for some types of learning and memory. Equally important may be the weakening of synaptic connections, a process that could either cause the loss of certain synaptic memory or endow the freedom for retasking a particular neuronal circuit. Thus, synapses must be considered as highly dynamic and plastic structures that can adapt their output to match the demands imposed by their current information processing needs.