Handbook of Psychopharmacology
Kluwer Academic/Plenum Publishers (Verlag)
978-0-306-38933-7 (ISBN)
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Especially gratifying is the sense that, while contributing to an understanding of how the brain functions, psychopharmacology is a discipline whose fruits offer genuine help to the mentally ill with promises of escalating benefits in the future. L. L. 1. S. D. 1. S. H. S. vii CONTENTS CHAPTER 1 Peptides and the Central Nervous System ARTHUR]. PRANGE, ]R. , CHARLES B. NEMEROFF, MORRIS A. LIPTON, GEORGE R. BREESE, and IAN C. WILSON 1. Introduction ...1 2. Hypothalamic Releasing Hormones: Animal Studies...2 2. 1. Thyrotropin-Releasing Hormone (TRH, Thyroliberin) ...
1 Peptides and the Central Nervous System.- 1. Introduction.- 2. Hypothalamic Releasing Hormones: Animal Studies.- 2.1. Thyrotropin-Releasing Hormone (TRH, Thyroliberin).- 2.2. Pro-Leu-Gly-NH2 (PLG, MIF-I).- 2.3. Luteinizing Hormone-Releasing Hormone (LHRH, Gonadoliberin).- 2.4. Somatotropin Release-Inhibiting Factor (SRIF, Somatostatin).- 3. Pituitary Peptide Hormones: Animal Studies.- 3.1. Anterior Pituitary Hormones: Corticotropin-Related Peptides (MSH, ACTH, LPH).- 3.2. Anterior Pituitary Hormones: Glycoprotein Hormones (LH, FSH, TSH, CG).- 3.3. Anterior Pituitary Hormones: Somatomammotropins (GH, PRL, CS).- 3.4. Posterior Pituitary Hormones.- 4. Other Brain Peptides: Animal Studies.- 4.1. Angiotensin II (Angiotensin).- 4.2. Cholecystokinin (CCK, Pancreozymin).- 4.3. Substance P.- 4.4. Bradykinin (Kinin-9).- 4.5. Neurotensin.- 4.6. Sleep-Inducing Peptides.- 4.7. Learning-Related Peptides.- 4.8. Morphine-like Peptides.- 4.9. Dipeptides.- 4.10. Other Peptides.- 5. Hypothalamic Releasing Hormones: Human Studies.- 5.1. Introduction.- 5.2. Thyrotropin-Releasing Hormone.- 5.3. Pro-Leu-Gly-NH2.- 5.4. Luteinizing Hormone-Releasing Hormone.- 6. Pituitary Peptide Hormones: Human Studies.- 6.1. Anterior Pituitary Hormones.- 6.2. Posterior Pituitary Hormones.- 7. Discussion.- 8. References.- 2 The Limbic-Hypothalamic-Pituitary-Adrenal System and Human Behavior.- 1. Introduction.- 2. Description of the Limbic-Hypothalamic-Pituitary-Adrenal System.- 2.1. Brief Outline.- 2.2. Description of LHPA Subunits.- 3. Procedures for Evaluating LHPA Function in Humans.- 3.1. Study of Neuronal Regulatory Mechanisms.- 3.2. Tissue Exposure to ACTH/Cortisol.- 3.3. General Methodologic Issues.- 3.4. Psychotropic Drug Effects on LHPA Function.- 4. Relationship between Mental Phenomena and the LHPA System.- 4.1. Behavioral Abnormalities in Patients with Disorders of the LHPA System.- 4.2. LHPA Function in Psychiatric Disorders.- 5. Summary.- 6. References.- 3 Approaches to Brain Amines in Psychiatric Patients: A Reevaluation of Cerebrospinal Fluid Studies.- 1. Introduction.- 1.1. Purpose.- 1.2. Amine Hypotheses of Affective Illness and Schizophrenia.- 2. Methodological Considerations for Spinal Fluid Studies.- 2.1. Origins of Amine Metabolites.- 2.2. The Probenecid Technique.- 2.3. Clinical Methodology.- 3. CSF Amine Metabolites in Affective Illness.- 4. Amine Metabolism in Schizophrenic Patients.- 5. Pharmacological Approaches: Integration with Amine Metabolite Data.- 5.1. Amine Precursor Strategies.- 5.2. Inhibitors of Amine Synthesis.- 5.3. Newer Amine-Receptor Stimulators and Implications.- 5.4. Amine Alterations Associated with "Routine" Antidepressant Treatments.- 5.5. Neuroleptic Treatments: Implications for the Dopamine Hypothesis.- 5.6. Psychotogenic Agents.- 6. Theoretical Overview: The Question of Specificity.- 6.1. Relationship of Metabolite Data to Amine Theories.- 6.2. Implications of Parkinson's Disease Model.- 6.3. Drug-Metabolite Interactions: Contributions to Amine Theories.- 7. A Model for Defects in Compensatory and Regulatory Mechanisms.- 8. References.- 4 Amine Hypotheses of Affective Disorders.- 1. Introduction.- 2. Classification of Depressions.- 2.1. Multidimensional Diagnosis of Depressions.- 2.2. Syndromal Points of View.- 2.3. Etiological Points of View.- 2.4. Classification According to Course.- 2.5. Pathogenetic Points of View.- 2.6. Other Diagnostic Classifications.- 2.7. Conclusions.- 3. Serotonin Metabolism in Affective Disorders: Study of Peripheral Indicators.- 3.1. Urinary Excretion of Indoleamines.- 3.2. 5-HT Synthesis.- 3.3. Availability of Tryptophan.- 3.4. Conclusions.- 4. Metabolism of Catecholamines in Affective Disorders: Study of Peripheral Indicators.- 4.1. Catecholamines and Some of Their Metabolites in Urine and Blood.- 4.2. Urinary MHPG Excretion: A Peripheral Indicator of Central Noradrenaline Activity?.- 4.3. Tyrosine in Blood.- 4.4. Enzyme Studies.- 4.5. Neuroendocrine Factors as "Markers"1 Peptides and the Central Nervous System.- 1. Introduction.- 2. Hypothalamic Releasing Hormones: Animal Studies.- 2.1. Thyrotropin-Releasing Hormone (TRH, Thyroliberin).- 2.2. Pro-Leu-Gly-NH2 (PLG, MIF-I).- 2.3. Luteinizing Hormone-Releasing Hormone (LHRH, Gonadoliberin).- 2.4. Somatotropin Release-Inhibiting Factor (SRIF, Somatostatin).- 3. Pituitary Peptide Hormones: Animal Studies.- 3.1. Anterior Pituitary Hormones: Corticotropin-Related Peptides (MSH, ACTH, LPH).- 3.2. Anterior Pituitary Hormones: Glycoprotein Hormones (LH, FSH, TSH, CG).- 3.3. Anterior Pituitary Hormones: Somatomammotropins (GH, PRL, CS).- 3.4. Posterior Pituitary Hormones.- 4. Other Brain Peptides: Animal Studies.- 4.1. Angiotensin II (Angiotensin).- 4.2. Cholecystokinin (CCK, Pancreozymin).- 4.3. Substance P.- 4.4. Bradykinin (Kinin-9).- 4.5. Neurotensin.- 4.6. Sleep-Inducing Peptides.- 4.7. Learning-Related Peptides.- 4.8. Morphine-like Peptides.- 4.9. Dipeptides.- 4.10. Other Peptides.- 5. Hypothalamic Releasing Hormones: Human Studies.- 5.1. Introduction.- 5.2. Thyrotropin-Releasing Hormone.- 5.3. Pro-Leu-Gly-NH2.- 5.4. Luteinizing Hormone-Releasing Hormone.- 6. Pituitary Peptide Hormones: Human Studies.- 6.1. Anterior Pituitary Hormones.- 6.2. Posterior Pituitary Hormones.- 7. Discussion.- 8. References.- 2 The Limbic-Hypothalamic-Pituitary-Adrenal System and Human Behavior.- 1. Introduction.- 2. Description of the Limbic-Hypothalamic-Pituitary-Adrenal System.- 2.1. Brief Outline.- 2.2. Description of LHPA Subunits.- 3. Procedures for Evaluating LHPA Function in Humans.- 3.1. Study of Neuronal Regulatory Mechanisms.- 3.2. Tissue Exposure to ACTH/Cortisol.- 3.3. General Methodologic Issues.- 3.4. Psychotropic Drug Effects on LHPA Function.- 4. Relationship between Mental Phenomena and the LHPA System.- 4.1. Behavioral Abnormalities in Patients with Disorders of the LHPA System.- 4.2. LHPA Function in Psychiatric Disorders.- 5. Summary.- 6. References.- 3 Approaches to Brain Amines in Psychiatric Patients: A Reevaluation of Cerebrospinal Fluid Studies.- 1. Introduction.- 1.1. Purpose.- 1.2. Amine Hypotheses of Affective Illness and Schizophrenia.- 2. Methodological Considerations for Spinal Fluid Studies.- 2.1. Origins of Amine Metabolites.- 2.2. The Probenecid Technique.- 2.3. Clinical Methodology.- 3. CSF Amine Metabolites in Affective Illness.- 4. Amine Metabolism in Schizophrenic Patients.- 5. Pharmacological Approaches: Integration with Amine Metabolite Data.- 5.1. Amine Precursor Strategies.- 5.2. Inhibitors of Amine Synthesis.- 5.3. Newer Amine-Receptor Stimulators and Implications.- 5.4. Amine Alterations Associated with "Routine" Antidepressant Treatments.- 5.5. Neuroleptic Treatments: Implications for the Dopamine Hypothesis.- 5.6. Psychotogenic Agents.- 6. Theoretical Overview: The Question of Specificity.- 6.1. Relationship of Metabolite Data to Amine Theories.- 6.2. Implications of Parkinson's Disease Model.- 6.3. Drug-Metabolite Interactions: Contributions to Amine Theories.- 7. A Model for Defects in Compensatory and Regulatory Mechanisms.- 8. References.- 4 Amine Hypotheses of Affective Disorders.- 1. Introduction.- 2. Classification of Depressions.- 2.1. Multidimensional Diagnosis of Depressions.- 2.2. Syndromal Points of View.- 2.3. Etiological Points of View.- 2.4. Classification According to Course.- 2.5. Pathogenetic Points of View.- 2.6. Other Diagnostic Classifications.- 2.7. Conclusions.- 3. Serotonin Metabolism in Affective Disorders: Study of Peripheral Indicators.- 3.1. Urinary Excretion of Indoleamines.- 3.2. 5-HT Synthesis.- 3.3. Availability of Tryptophan.- 3.4. Conclusions.- 4. Metabolism of Catecholamines in Affective Disorders: Study of Peripheral Indicators.- 4.1. Catecholamines and Some of Their Metabolites in Urine and Blood.- 4.2. Urinary MHPG Excretion: A Peripheral Indicator of Central Noradrenaline Activity?.- 4.3. Tyrosine in Blood.- 4.4. Enzyme Studies.- 4.5. Neuroendocrine Factors as "Markers" of Catecholaminergic Activity.- 4.6. Cyclic AMP and Central Catecholaminergic Activity.- 4.7. Conclusions.- 5. Postmortem Study of Central Monoamine Metabolism in Depressions.- 5.1. Introduction.- 5.2. Indoleamines.- 5.3. Catecholamines.- 5.4. Monoamine Oxidase.- 5.5. Significance of Postmortem Findings.- 5.6. Conclusions.- 6. Central Monoamine Metabolism in Affective Disorders: CSF Studies Without Probenecid.- 6.1. Monoamine Metabolites in CSF: Do They Reflect Central Monoamine Metabolism?.- 6.2. Monoamine Metabolites in Lumbar CSF: Do They Reflect Cerebral or Spinal Monoamine Metabolism?..- 6.3. Shortcomings of the CSF Strategy.- 6.4. Monoamine Metabolites in the CSF in Affective Disorders.- 6.5. Causes of the Variability of the Results of CSF Studies.- 6.6. Are the CSF Changes Syndrome-Dependent or Syndrome-Independent?.- 6.7. Specificity of CSF Findings.- 6.8. Ability of the CNS to Synthesize Monoamines.- 6.9. Conclusions.- 7. Central Monoamine Metabolism in Affective Disorders: CSF Studies After Probenecid Loading.- 7.1. Principles of the Probenecid Technique.- 7.2. Advantages of the Probenecid Technique over "Plain" CSF Determination.- 7.3. Procedure of the Probenecid Test.- 7.4. Does the Probenecid Technique Afford Information on Human Dopamine and 5-HT Turnover?.- 7.5. Shortcomings of the Probenecid Technique.- 7.6. Central 5-HT Turnover in Depressions.- 7.7. Central Dopamine Turnover in Depressions.- 7.8. Central 5-HT and Dopamine Turnover in Mania.- 7.9. Selectivity of the Probenecid Findings.- 7.10. Are the Disorders of 5-HT and Dopamine Metabolism Syndrome-Dependent or Syndrome-Independent?.- 7.11.Conclusions.- 8. Verification of the Monoamine Hypothesis with the Aid of Drugs: I. Monoamine Precursors and Synthesis Inhibitors.- 8.1. Justification of the Strategy.- 8.2. Studies with Drugs Which Increase 5-HT Synthesis.- 8.3. Studies with Drugs Which Increase Catecholamine Synthesis.- 8.4. Imperfections of the Precursor Strategy.- 8.5. Studies with Drugs Which Inhibit Monoamine Synthesis.- 8.6. Conclusions.- 9. Verification of the Monoamine Hypothesis with the Aid of Drugs and Other Methods of Antidepressant Therapy: II. Direct Influencing of the Transmission Process.- 9.1. Disorders in Central Monoamine Metabolism and Therapeutic Efficacy of Antidepressants.- 9.2. Tricyclic Antidepressants Combined with MAOIs.- 9.3. MAOIs Combined with Reserpine.- 9.4. Tricyclic Antidepressants and Central Stimulants.- 9.5. Tricyclic Antidepressants Combined with Reserpine..- 9.6. Enhancement of Central 5-HT Activity with the Aid of Chloramphetamines.- 9.7. Thyrotropin-Releasing Hormone.- 9.8. Neuroleptics and ?-Blockers.- 9.9. Methysergide.- 9.10. Lithium.- 9.11. Electroconvulsive Therapy.- 9.12. Conclusions.- 10. Theories to Explain the Monoamine Deficiency in Depressions.- 10.1. Possible Causes of the Monoamine Deficiency.- 10.2. Precursor Deficiency.- 10.3. Diminished Synthetic Capacity.- 10.4. Postsynaptic Defects.- 10.5. Conclusions.- 11. Preliminaries to Expansion of the Monoamine Hypothesis 270 11.1 Acetylcholine.- 11.2. Phenylethylamine.- 11.3. Conclusions.- 12. General Conclusions.- 13. References.- 5 Clinical Pharmacokinetics of Selected Psychotropic Drugs.- 1. Introduction.- 2. Tricyclic Antidepressants.- 2.1. Absorption.- 2.2. Steady-State Plasma Levels.- 2.3. Distribution.- 2.4. Volume of Distribution.- 2.5. Plasma Protein Binding.- 2.6. Biotransformation.- 2.7. Pharmacokinetics and Therapeutic Response.- 3. Lithium.- 3.1. Absorption, Doses, and Plasma Levels.- 3.2. Distribution.- 3.3. RBC/Plasma Lithium Ratio.- 3.4. Excretion.- 3.5. General Considerations.- 4. Benzodiazepines.- 4.1. Diazepam.- 4.2. Chlordiazepoxide.- 5. CNS Stimulants (Amphetamine).- 5.1. Absorption.- 5.2. Distribution.- 5.3. Metabolism and Excretion.- 5.4. Pharmacokinetics and Drug Response.- 6. Chlorpromazine.- 6.1. Absorption.- 6.2. Distribution.- 6.3. Metabolism and Excretion.- 6.4. Plasma Levels of Chlorpromazine and Metabolites.- 6.5. Plasma Levels and Clinical Correlates.- 7. Conclusion.- 8. References.- 6 Behavioral Pharmacology of Antianxiety Drugs.- 1. Introduction.- 2. Anticonflict Properties of Antianxiety Agents.- 2.1. Validity of Conflict Methodology.- 2.2. Separation between Effective and Ineffective Agents..- 2.3. Exceptions to Anticonflict Generalizations.- 2.4. Species Generality of Conflict Methodology.- 2.5. Studies with Drug-Nai1 Peptides and the Central Nervous System.- 1. Introduction.- 2. Hypothalamic Releasing Hormones: Animal Studies.- 2.1. Thyrotropin-Releasing Hormone (TRH, Thyroliberin).- 2.2. Pro-Leu-Gly-NH2 (PLG, MIF-I).- 2.3. Luteinizing Hormone-Releasing Hormone (LHRH, Gonadoliberin).- 2.4. Somatotropin Release-Inhibiting Factor (SRIF, Somatostatin).- 3. Pituitary Peptide Hormones: Animal Studies.- 3.1. Anterior Pituitary Hormones: Corticotropin-Related Peptides (MSH, ACTH, LPH).- 3.2. Anterior Pituitary Hormones: Glycoprotein Hormones (LH, FSH, TSH, CG).- 3.3. Anterior Pituitary Hormones: Somatomammotropins (GH, PRL, CS).- 3.4. Posterior Pituitary Hormones.- 4. Other Brain Peptides: Animal Studies.- 4.1. Angiotensin II (Angiotensin).- 4.2. Cholecystokinin (CCK, Pancreozymin).- 4.3. Substance P.- 4.4. Bradykinin (Kinin-9).- 4.5. Neurotensin.- 4.6. Sleep-Inducing Peptides.- 4.7. Learning-Related Peptides.- 4.8. Morphine-like Peptides.- 4.9. Dipeptides.- 4.10. Other Peptides.- 5. Hypothalamic Releasing Hormones: Human Studies.- 5.1. Introduction.- 5.2. Thyrotropin-Releasing Hormone.- 5.3. Pro-Leu-Gly-NH2.- 5.4. Luteinizing Hormone-Releasing Hormone.- 6. Pituitary Peptide Hormones: Human Studies.- 6.1. Anterior Pituitary Hormones.- 6.2. Posterior Pituitary Hormones.- 7. Discussion.- 8. References.- 2 The Limbic-Hypothalamic-Pituitary-Adrenal System and Human Behavior.- 1. Introduction.- 2. Description of the Limbic-Hypothalamic-Pituitary-Adrenal System.- 2.1. Brief Outline.- 2.2. Description of LHPA Subunits.- 3. Procedures for Evaluating LHPA Function in Humans.- 3.1. Study of Neuronal Regulatory Mechanisms.- 3.2. Tissue Exposure to ACTH/Cortisol.- 3.3. General Methodologic Issues.- 3.4. Psychotropic Drug Effects on LHPA Function.- 4. Relationship between Mental Phenomena and the LHPA System.- 4.1. Behavioral Abnormalities in Patients with Disorders of the LHPA System.- 4.2. LHPA Function in Psychiatric Disorders.- 5. Summary.- 6. References.- 3 Approaches to Brain Amines in Psychiatric Patients: A Reevaluation of Cerebrospinal Fluid Studies.- 1. Introduction.- 1.1. Purpose.- 1.2. Amine Hypotheses of Affective Illness and Schizophrenia.- 2. Methodological Considerations for Spinal Fluid Studies.- 2.1. Origins of Amine Metabolites.- 2.2. The Probenecid Technique.- 2.3. Clinical Methodology.- 3. CSF Amine Metabolites in Affective Illness.- 4. Amine Metabolism in Schizophrenic Patients.- 5. Pharmacological Approaches: Integration with Amine Metabolite Data.- 5.1. Amine Precursor Strategies.- 5.2. Inhibitors of Amine Synthesis.- 5.3. Newer Amine-Receptor Stimulators and Implications.- 5.4. Amine Alterations Associated with "Routine" Antidepressant Treatments.- 5.5. Neuroleptic Treatments: Implications for the Dopamine Hypothesis.- 5.6. Psychotogenic Agents.- 6. Theoretical Overview: The Question of Specificity.- 6.1. Relationship of Metabolite Data to Amine Theories.- 6.2. Implications of Parkinson's Disease Model.- 6.3. Drug-Metabolite Interactions: Contributions to Amine Theories.- 7. A Model for Defects in Compensatory and Regulatory Mechanisms.- 8. References.- 4 Amine Hypotheses of Affective Disorders.- 1. Introduction.- 2. Classification of Depressions.- 2.1. Multidimensional Diagnosis of Depressions.- 2.2. Syndromal Points of View.- 2.3. Etiological Points of View.- 2.4. Classification According to Course.- 2.5. Pathogenetic Points of View.- 2.6. Other Diagnostic Classifications.- 2.7. Conclusions.- 3. Serotonin Metabolism in Affective Disorders: Study of Peripheral Indicators.- 3.1. Urinary Excretion of Indoleamines.- 3.2. 5-HT Synthesis.- 3.3. Availability of Tryptophan.- 3.4. Conclusions.- 4. Metabolism of Catecholamines in Affective Disorders: Study of Peripheral Indicators.- 4.1. Catecholamines and Some of Their Metabolites in Urine and Blood.- 4.2. Urinary MHPG Excretion: A Peripheral Indicator of Central Noradrenaline Activity?.- 4.3. Tyrosine in Blood.- 4.4. Enzyme Studies.- 4.5. Neuroendocrine Factors as "Markers" of Catecholaminergic Activity.- 4.6. Cyclic AMP and Central Catecholaminergic Activity.- 4.7. Conclusions.- 5. Postmortem Study of Central Monoamine Metabolism in Depressions.- 5.1. Introduction.- 5.2. Indoleamines.- 5.3. Catecholamines.- 5.4. Monoamine Oxidase.- 5.5. Significance of Postmortem Findings.- 5.6. Conclusions.- 6. Central Monoamine Metabolism in Affective Disorders: CSF Studies Without Probenecid.- 6.1. Monoamine Metabolites in CSF: Do They Reflect Central Monoamine Metabolism?.- 6.2. Monoamine Metabolites in Lumbar CSF: Do They Reflect Cerebral or Spinal Monoamine Metabolism?..- 6.3. Shortcomings of the CSF Strategy.- 6.4. Monoamine Metabolites in the CSF in Affective Disorders.- 6.5. Causes of the Variability of the Results of CSF Studies.- 6.6. Are the CSF Changes Syndrome-Dependent or Syndrome-Independent?.- 6.7. Specificity of CSF Findings.- 6.8. Ability of the CNS to Synthesize Monoamines.- 6.9. Conclusions.- 7. Central Monoamine Metabolism in Affective Disorders: CSF Studies After Probenecid Loading.- 7.1. Principles of the Probenecid Technique.- 7.2. Advantages of the Probenecid Technique over "Plain" CSF Determination.- 7.3. Procedure of the Probenecid Test.- 7.4. Does the Probenecid Technique Afford Information on Human Dopamine and 5-HT Turnover?.- 7.5. Shortcomings of the Probenecid Technique.- 7.6. Central 5-HT Turnover in Depressions.- 7.7. Central Dopamine Turnover in Depressions.- 7.8. Central 5-HT and Dopamine Turnover in Mania.- 7.9. Selectivity of the Probenecid Findings.- 7.10. Are the Disorders of 5-HT and Dopamine Metabolism Syndrome-Dependent or Syndrome-Independent?.- 7.11.Conclusions.- 8. Verification of the Monoamine Hypothesis with the Aid of Drugs: I. Monoamine Precursors and Synthesis Inhibitors.- 8.1. Justification of the Strategy.- 8.2. Studies with Drugs Which Increase 5-HT Synthesis.- 8.3. Studies with Drugs Which Increase Catecholamine Synthesis.- 8.4. Imperfections of the Precursor Strategy.- 8.5. Studies with Drugs Which Inhibit Monoamine Synthesis.- 8.6. Conclusions.- 9. Verification of the Monoamine Hypothesis with the Aid of Drugs and Other Methods of Antidepressant Therapy: II. Direct Influencing of the Transmission Process.- 9.1. Disorders in Central Monoamine Metabolism and Therapeutic Efficacy of Antidepressants.- 9.2. Tricyclic Antidepressants Combined with MAOIs.- 9.3. MAOIs Combined with Reserpine.- 9.4. Tricyclic Antidepressants and Central Stimulants.- 9.5. Tricyclic Antidepressants Combined with Reserpine..- 9.6. Enhancement of Central 5-HT Activity with the Aid of Chloramphetamines.- 9.7. Thyrotropin-Releasing Hormone.- 9.8. Neuroleptics and ?-Blockers.- 9.9. Methysergide.- 9.10. Lithium.- 9.11. Electroconvulsive Therapy.- 9.12. Conclusions.- 10. Theories to Explain the Monoamine Deficiency in Depressions.- 10.1. Possible Causes of the Monoamine Deficiency.- 10.2. Precursor Deficiency.- 10.3. Diminished Synthetic Capacity.- 10.4. Postsynaptic Defects.- 10.5. Conclusions.- 11. Preliminaries to Expansion of the Monoamine Hypothesis 270 11.1 Acetylcholine.- 11.2. Phenylethylamine.- 11.3. Conclusions.- 12. General Conclusions.- 13. References.- 5 Clinical Pharmacokinetics of Selected Psychotropic Drugs.- 1. Introduction.- 2. Tricyclic Antidepressants.- 2.1. Absorption.- 2.2. Steady-State Plasma Levels.- 2.3. Distribution.- 2.4. Volume of Distribution.- 2.5. Plasma Protein Binding.- 2.6. Biotransformation.- 2.7. Pharmacokinetics and Therapeutic Response.- 3. Lithium.- 3.1. Absorption, Doses, and Plasma Levels.- 3.2. Distribution.- 3.3. RBC/Plasma Lithium Ratio.- 3.4. Excretion.- 3.5. General Considerations.- 4. Benzodiazepines.- 4.1. Diazepam.- 4.2. Chlordiazepoxide.- 5. CNS Stimulants (Amphetamine).- 5.1. Absorption.- 5.2. Distribution.- 5.3. Metabolism and Excretion.- 5.4. Pharmacokinetics and Drug Response.- 6. Chlorpromazine.- 6.1. Absorption.- 6.2. Distribution.- 6.3. Metabolism and Excretion.- 6.4. Plasma Levels of Chlorpromazine and Metabolites.- 6.5. Plasma Levels and Clinical Correlates.- 7. Conclusion.- 8. References.- 6 Behavioral Pharmacology of Antianxiety Drugs.- 1. Introduction.- 2. Anticonflict Properties of Antianxiety Agents.- 2.1. Validity of Conflict Methodology.- 2.2. Separation between Effective and Ineffective Agents..- 2.3. Exceptions to Anticonflict Generalizations.- 2.4. Species Generality of Conflict Methodology.- 2.5. Studies with Drug-Naive Animals.- 2.6. Biochemical Hypotheses of the Mechanisms of Action of Antianxiety Agents.- 2.7. Anxiety and ?-Blockade.- 3. Properties of Antianxiety Agents in Miscellaneous Operant Conditioning Situations.- 4. Properties of Antianxiety Agents in Additional Behavioral Procedures.- 4.1. Unpunished Consummatory Behavior: Appetite-Enhancing Effects.- 4.2. Punished Consummatory Behavior.- 4.3 Unpunished Exploratory and Locomotor Behavior.- 4.4. Punished Exploratory and Locomotor Behavior.- 4.5. Protection Against the Effects of Stress.- 5. Concluding Remarks.- 6. References.- 7 Antianxiety Drugs: Clinical Use in Psychiatry.- 1. Introduction.- 2. Using Drugs to Treat Anxiety.- 2.1. What Is Anxiety?.- 2.2. How Drugs May Be Used to Alleviate Anxiety.- 2.3. Pharmacological Actions of Antianxiety Drugs.- 2.4. Drugs Used in the Treatment of Anxiety.- 2.5. Side Effects of Antianxiety Agents.- 2.6. Tolerance, Habituation, and Addiction with Antianxiety Agents.- 2.7. Minor Tranquilizers and Barbiturates.- 2.8. Diazepam vs. Chlordiazepoxide.- 2.9. Why Physicians Should Employ the Most Effective Antianxiety Agents.- 3. Improving Specific Symptom Profiles of Anxious Patients.- 3.1. Presenting Symptomatology.- 3.2. Improvement Levels Observed in Drug-Treated Anxious Patients.- 3.3. Effect of Antianxiety Agents on Specific Symptoms.- 3.4. Initial Symptom Severity, Duration of Illness, and Clinical Improvement.- 3.5. Implications of Present Findings for Appropriate Use of Antianxiety Agents.- 4. Predicting Improvement in Anxious Patients.- 4.1. Nonspecific Factors Affecting Improvement.- 4.2. Predicting Improvement with the Benzodiazepines.- 4.3. Physician's Prognosis for Antianxiety Drug-Treatment Response.- 5. Conclusion.- 6. References.
Zusatzinfo | biography |
---|---|
Sprache | englisch |
Themenwelt | Geisteswissenschaften ► Psychologie |
Medizin / Pharmazie ► Medizinische Fachgebiete ► Pharmakologie / Pharmakotherapie | |
Medizin / Pharmazie ► Medizinische Fachgebiete ► Psychiatrie / Psychotherapie | |
ISBN-10 | 0-306-38933-9 / 0306389339 |
ISBN-13 | 978-0-306-38933-7 / 9780306389337 |
Zustand | Neuware |
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