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  • 1
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Neurobiology. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (455 pages)
    Edition: 1st ed.
    ISBN: 9780080857701
    Series Statement: Issn Series
    DDC: 573.8
    Language: English
    Note: Front Cover -- International Review of Neurobiology, Volume 36 -- Copyright Page -- Contents -- Chapter 1. Ca2+, N-Methyl-D-aspartate Receptors, and AIDS-Related Neuronal Injury -- I. Introduction -- II. Neuronal Loss in the CNS of AIDS Patients -- III. gpl20-Induced Neuronal Injury Is Ameliorated by Calcium Channel Anotagonists -- IV. Involvement of the NMDA Receptor in gpl20-Induced Neuronal Injury -- V. Indirect Neuronal Injury Mediated by HIV-Infected or gp120-Stimulated Monocytic Cells -- VI. Possible Involvement of Astrocytes, Oligodendrocytes, and Other HIV-1 Proteins in Neuronal Injury -- VII. Overstimulation of NMDA Receptors, a Final Common Pathway -- VIII. Development of Clinically Tolerated NMDA Antagonists for HIV-Related Neuronal Injury -- IX. Excitatory Amino Acid Antagonist Treatments on the Horizon -- X. Conclusion -- References -- Chapter 2. Processing of Alzheimer Aβ-Amyloid Precursor Protein: Cell Biology, Regulation, and Role in Alzheimer Disease -- I. Introduction -- II. Alzheimer Disease Is Associated with an Intracranial Amyloidosis -- III. APP Structure Gives Clues to Some of Its Functions -- IV. APP Is Processed via Several Distinct Enzymatic and Subcellular Pathways -- V. "Alternative" Pathways of APP Metabolism Provide Clues to the Source of Aβ-Amyloid -- VI. Aβ-Amyloid Is a Normal Constituent of Body Fluids and the Conditioned Medium of Cultured Cells -- VII. Evidence Suggests the Existence of an Enzyme, β-Secretase, That Cleaves APP at the Amino Terminus of the Aβ-Amyloid Domain -- VIII. APP Mutations in Familial Cerebral Amyloidoses Occur within or near the Aβ-Amyloid Domain, Segregate with Disease in Affected Kindreds, and Yield APP Molecules That Display Some Proamyloidogenic Properties -- IX. Signal Transduction via Protein Phosphorylation Regulates the Relative Utilization of APP Processing Pathways. , X. Beyond Aβ-Amyloid: Other Molecular Factors in Amyloidogenesis and Factors Differentiating Aging-Related Cerebral Amyloidosis from Alzheimer Disease -- References -- Chapter 3. Molecular Neurobiology of the GABAA Receptor -- I. Introduction -- II. Pharmacology of the GABAA Receptor -- III. Biochemistry -- IV. Molecular Cloning of Receptor Subunits -- V. Characterization of the Receptor Family -- VI. The Future -- Reference -- Chapter 4. The Pharmacology and Function of Central GABAB Receptors -- I. Introduction -- II. Pharmacology of GABAB Receptors -- III. Properties of GABAB Receptors -- IV. Function of GABAB Receptors -- V. Summary and Conclusions -- References -- Chapter 5.The Role of the Amygdala in Emotional Learning -- I. Introduction -- II. Morphology -- III. Electrophysiology -- IV. Anatomical Connections between the Amygdala and Brain Areas Involved in Fear and Anxiety -- V. Elicitation of Fear by Electrical or Chemical Stimulation of the Amygdagdala -- VI. Effects of Amygdala Lesions on Conditioned Fear -- VII. Effects of Amygdala Lesions on Unconditioned Fear -- VIII. Effects of Local Infusion of Drugs into the Amygdala on Measures of Fear and Anxiety -- IX. The Role of the Amygdala in Attention -- X. The Amygdala Is Critical for the Fear-Potentiated Startle Effect -- XI. Are Aversive Memories Actually Stored in the Amygdala? -- XII. Is the Amygdala Absolutely Essential for Fear-Potentiated Startle? -- XIII. Can Initial Fear Conditioning Occur without the Amygdala? -- XIV. The Role of Excitatory Amino Acid Receptors in the Amygdala in Fear Conditioning -- XV. Conclusions -- References -- Chapter 6. Excitotoxicity and Neurological Disorders: Involvement of Membrane Phospholipids -- I. Introduction -- II. Classification of Excitatory Amino Acid Receptors. , III. Excitatory Amino Acid Receptors and Neural Membrane Phospholipid Metabolism . . . -- IV. Role of Enhanced Excitatory Amino Acid-Mediated Phospolipid Metabolism in Developing Brain -- V. Possible Mechanism of Cell Injury Caused by Excitatory Amino Acids -- VI. Excitatory Amino Acid Receptors, Phospholipid Metabolism, and Neurological Disorders -- VII. Excitatory Amino Acid Receptor Antagonists and the Treatment of Neurological Disorders -- VIII. Conclusion -- IX. Summary -- References -- Chapter 7. Injury-Related Behavior and Neuronal Plasticity: An Evolutionary Perspective on Sensitization, Hyperalgesia, and Analgesia -- I. Introduction -- II. Evolutionary Considerations -- III. Adaptive Behavioral Reactions to Injury -- IV. Classes of Injury-Related Behavioral Modifiability -- V. Injury Signals -- VI. Mechanisms of Rapid Nociceptive Sensitization -- VII. Mechanisms of Long-Term Nociceptive Sensitization -- VIII. Conclusions -- References -- Index -- Contents of Recent Volumes.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of applied physiology 63 (1991), S. 129-134 
    ISSN: 1439-6327
    Keywords: Metabolic alkalosis ; Exercise ; Muscle fatigue
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Six thoroughbred horses exercised on a motorised treadmill on two separate occasions at a speed of 11 or 12 m· s−1 for up to 2 min. 4 h prior to exercise each horse was given a 21 test solution of sodium bicarbonate (NaHC03; 0.6 g·kg−1 body mass) or a control solution of water by nasogastric intubation, the order of administration of the two solutions was randomised. Blood samples (n=15) were obtained before and during the 4 h after intubation, during exercise and for 30 min after exercise. (NaHC03; ingestion resulted in changes in pre-exercise acid-base status. The changes in blood lactate and base excess with exercise were greater after (NaHC03; administration; after 1 min of exercise in the case of lactate (P〈0.05) and immediately after exercise in the case of base excess (P〈0.05). Plasma ammonia levels were lower during (P〈0.05) and immediately after (P〈0.05) exercise following (NaHC03; ingestion. The peak change in plasma ammonia with exercise was also lower after (NaHC03; ingestion (P〈0.05). Following exercise after (NaHC03; ingestion, five horses demonstrated lower muscle adenosine 5-triphosphate loss (P〈0.05) and inosine 5-monophosphate formation (P=0.05) and higher glycerol 3-phosphate formation (P〈0.05). There is evidence to suggest that metabolic alkalosis may delay the onset of fatigue by decreasing the extent of adenine nucleotide loss during high-intensity exercise.
    Type of Medium: Electronic Resource
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