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  • 1
    Online Resource
    Online Resource
    Newark :John Wiley & Sons, Incorporated,
    Keywords: Hormones. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (405 pages)
    Edition: 2nd ed.
    ISBN: 9783527633845
    DDC: 612.8
    Language: English
    Note: Intro -- Hormones in Neurodegeneration, Neuroprotection, and Neurogenesis -- Contents -- List of Contributors -- Part I Estrogens, Progestins, Allopregnanolone and Neuroprotection -- 1 Interactions of Estradiol and Insulin-like Growth Factor-I in Neuroprotection: Implications for Brain Aging and Neurodegeneration -- 1.1 Introduction: Hormones, Brain Aging, and Neurodegeneration -- 1.2 Estradiol, IGF-I, Brain Aging, and Neuroprotection -- 1.3 Molecular Interactions of Estrogen Receptors and IGF-I Receptor in the Brain -- 1.4 Regulation of IGF-I Receptor Signaling by Estradiol in the Brain -- 1.5 Regulation of Estrogen Receptor Transcriptional Activity by IGF-I in Neural Cells -- 1.6 Implications of the Cross Talk between Estrogen Receptors and IGF-I Receptors for Brain Aging, and Neurodegeneration -- Acknowledgment -- References -- 2 Structure-Nongenomic Neuroprotection Relationship of Estrogens and Estrogen-Derived Compounds -- 2.1 Introduction -- 2.2 In vitro Assessments of Structure-Neuroprotective Activity Relationships -- 2.2.1 Estradiol and Other Known Estratrienes -- 2.2.2 A-Ring Derivatives -- 2.2.3 B- and C-Ring Derivatives -- 2.2.4 D-Ring Derivatives -- 2.2.5 Correlation between Inhibition of TBARs and Protection against Glutamate and IAA -- 2.2.6 Estrogen Receptor Binding -- 2.2.7 Correlation between Inhibition of TBARs or Neuroprotection and ER Binding -- 2.2.8 Interpretation of In vitro Findings -- 2.3 In vivo Assessment of Structure-Neuroprotective Activity Relationships -- 2.4 In vitro Assessment of Structure-Cell Signaling Relationships -- 2.5 Summary -- Acknowledgment -- References -- 3 Progestins and Neuroprotection: Why the Choice of Progestin Matters -- 3.1 Introduction -- 3.2 The Biology of Progesterone -- 3.3 Membrane-Associated Progesterone Receptors -- 3.4 Progesterone-Induced Protection. , 3.5 Mechanisms Underlying Progesterone's Protective Effects -- 3.6 Medroxyprogesterone Acetate -- Acknowledgments -- References -- 4 Endogenous and Synthetic Neurosteroids in the Treatment of Niemann-Pick Type C Disease -- 4.1 Introduction -- 4.2 Niemann-Pick Type C Disease as a Model of Disrupted Neurosteroidogenesis -- 4.3 Steroidogenesis and Neurosteroidogenesis in NP-C -- 4.4 Treatment of NP-C Mice with Allopregnanolone -- 4.5 Mechanism of Allopregnanolone Action: GABAA Receptor -- 4.6 Mechanism of Allopregnanolone Action: Pregnane-X Receptor -- 4.7 Mechanism of Allopregnanolone Action: Reduction of Cellular Oxidative Stress -- 4.8 Conclusions - Mechanisms of Allopregnanolone Action in Treatment of NP-C and Other Neurodegenerative Diseases -- Acknowledgments -- References -- Part II Glucocorticoids, Dehydroepiandrosterone, Neuroprotection and Neuropathy -- 5 Glucocorticoids, Developmental ''Programming,'' and the Risk of Affective Dysfunction -- 5.1 Introduction to Programming -- 5.2 Programming -- 5.2.1 Epidemiology -- 5.2.2 Birth Weight and Neuropsychiatric Disorders -- 5.3 Glucocorticoids and Fetal Development -- 5.4 Glucocorticoids: the Endocrine Programming Factor -- 5.4.1 Placental 11β-HSD2: a Barrier to Maternal Glucocorticoids -- 5.4.2 Glucocorticoid Programming -- 5.4.3 Transgenerational Effects -- 5.4.4 The Placenta -- 5.4.5 A Common Mechanism? -- 5.5 Fetal Tissue Glucocorticoid Sensitivity -- 5.6 Stress and Glucocorticoids: Key Programmers of the Brain -- 5.6.1 Programming the HPA Axis -- 5.6.2 Sex-Specific Effects -- 5.6.3 Programming Behavior -- 5.7 CNS Programming Mechanisms -- 5.7.1 The GR Gene: a Common Programming Target? -- 5.7.2 Epigenetics -- 5.8 Glucocorticoid Programming in Humans -- 5.8.1 Clinical Use of Prenatal Glucocorticoid Therapy -- 5.8.2 Consequences of Human Fetal Glucocorticoid Overexposure. , 5.8.3 Programming and Posttraumatic Stress Disorder (PTSD) -- 5.8.4 Programming Other Glucocorticoid Metabolizing Enzymes -- 5.9 Future Perspectives and Therapeutic Opportunities -- 5.10 Overview -- References -- 6 Regulation of Structural Plasticity and Neurogenesis during Stress and Diabetes -- Protective Effects of Glucocorticoid Receptor Antagonists -- 6.1 The Stress Response -- 6.2 HPA Axis and Glucocorticoids -- 6.3 Glucocorticoid Actions -- 6.4 Feedback Regulation -- 6.5 Stress and Depression -- 6.6 Stress-Induced Viability Changes in the Hippocampus: Effect on Function, Volume, Cell Number, and Apoptosis -- 6.7 Effects of Stress on Dendritic Atrophy, Spine, and Synaptic Changes -- 6.8 Adult Hippocampal Neurogenesis -- 6.9 Effect of Stress on Adult Hippocampal Neurogenesis -- 6.10 Normalization of the Effects of Stress on the Hippocampus by Means of GR Blockade -- 6.11 Normalization of Hippocampal Alterations during Diabetes Mellitus Using the GR Antagonist Mifepristone -- 6.12 Concluding Remarks -- Acknowledgments -- Disclosure -- References -- 7 Neuroactive Steroids and Peripheral Neuropathy -- 7.1 Introduction -- 7.2 Regulation of Neuroactive Steroid Responsiveness in Peripheral Nerves -- 7.2.1 Synthesis and Metabolism of Neuroactive Steroids -- 7.2.2 Classical and Nonclassical Steroid Receptors are Expressed in Peripheral Nerves -- 7.3 Schwann Cell Responses to Neuroactive Steroids -- 7.4 Sexually Dimorphic Changes of Neuroactive Steroid Levels Induced by Pathology in Peripheral Nerves -- 7.5 Neuroactive Steroids as Protective Agents in PNS -- 7.5.1 Aging Process -- 7.5.2 Physical Injury -- 7.5.3 Diabetic Neuropathy -- 7.6 Chemotherapy-Induced Peripheral Neuropathy -- 7.7 Concluding Remarks -- Acknowledgments -- References -- 8 Neuroprotective and Neurogenic Properties of Dehydroepiandrosterone and its Synthetic Analogs -- 8.1 Introduction. , 8.2 Neuroprotective and Neurogenic Effects of DHEA in Hippocampal Neurons -- 8.3 Neuroprotective Effects of DHEA in Nigrostriatal Dopaminergic Neurons -- 8.4 Neuroprotective Effects of DHEA in Autoimmune Neurodegenerative Processes -- 8.5 Neuroprotective Effects of DHEA against Brain Ischemia and Trauma -- 8.6 Signaling Pathways Involved in the Effects of DHEA on Neuronal Cell Fate -- 8.7 Therapeutic Perspectives of DHEA and its Synthetic Analogs in Neurodegenerative Diseases -- References -- 9 Neurosteroids and Pain Christine Patte-Mensah, Laurence Meyer, V´eronique Schaeffer, Cherkaouia -- 9.1 Introduction -- 9.2 General Background on Neurosteroids -- 9.3 Overview on Pain -- 9.4 Involvement of Endogenous Neurosteroids in the Control of Pain -- 9.4.1 Evidence for the Local Production of Neurosteroids in the Spinal Circuit -- 9.4.2 Endogenous Neurosteroids and Pain Modulation -- 9.5 Conclusion -- Acknowledgments -- References -- Part III Polypeptide Hormones and Neuroprotection -- 10 The Insulin/IGF-1 System in Neurodegeneration and Neurovascular Disease -- 10.1 Introduction -- 10.2 Insulin and Insulin Growth Factors -- 10.3 Local versus Systemic Actions -- 10.4 Insulin/IGF Signaling Pathway -- 10.5 The Insulin/IGF Axis in the Brain -- 10.6 Insulin/IGF and Neuroprotection -- 10.7 Alzheimer's Disease -- 10.8 Parkinson's Disease -- 10.9 Vascular Dementia -- 10.10 Neurovascular Degeneration -- 10.11 Conclusion -- References -- 11 Leptin Neuroprotection in the Central Nervous System -- 11.1 Introduction -- 11.1.1 Origin, Source, and Structure of Leptin -- 11.1.2 Functions of Leptin -- 11.1.3 Leptin Receptors -- 11.1.4 Leptin Transport across the Blood-Brain Barrier -- 11.2 Mutation of Leptin or Leptin Receptors -- 11.3 Neurotrophic Role of Leptin -- 11.4 Leptin Neuroprotection against Disorders of the Central Nervous System. , 11.4.1 Acute Neurological Disorders -- 11.4.2 Neurodegenerative Diseases and Other Disorders -- 11.4.3 Leptin Neuroprotective Mechanisms -- 11.5 Significance -- References -- 12 Somatostatin and Neuroprotection in Retina -- 12.1 Introduction -- 12.2 Somatostatin and Related Peptides -- 12.3 Somatostatin Receptors and Signaling -- 12.4 Somatostatin and its Receptors in Retina -- 12.5 Localization of Somatostatin Receptors in Retinal Neurons -- 12.5.1 Sst1 -- 12.5.2 Sst2 -- 12.5.3 Sst3 -- 12.5.4 Sst4 -- 12.5.5 Sst5 -- 12.6 Somatostatin Receptor Function in Retinal Circuitry -- 12.6.1 Effects on Glutamate Release -- 12.6.2 Effects on Dopamine Release -- 12.6.3 Effects on Nitric Oxide/GMP -- 12.6.4 Effects on Somatostatin Release -- 12.7 Neuroprotection by Somatostatin Analogs -- 12.7.1 Retinal Ischemia and Excitotoxicity -- 12.7.2 Anti-Ischemic Actions of SRIF -- 12.7.2.1 Ex vivo Studies -- 12.7.2.2 In vivo Studies -- 12.8 Mechanisms of SRIF's Neuroprotection -- 12.8.1 Involvement of NO/cGMP -- 12.8.2 NO/cGMP Mediates SRIF's Neuroprotective Effects -- 12.9 Therapeutic Potential of Somatostatin Agents -- 12.10 Conclusions -- Acknowledgments -- Abbreviations -- References -- 13 Neurotrophic Effects of PACAP in the Cerebellar Cortex -- 13.1 Expression of PACAP and its Receptors in the Developing Cerebellum -- 13.2 Effects of PACAP on Granule Cell Proliferation -- 13.3 Effects of PACAP on Granule Cell Migration -- 13.4 Effects of PACAP on Granule Cell Survival -- 13.5 Effects of PACAP on Granule Cell Differentiation -- 13.6 Functional Relevance -- Acknowledgments -- References -- 14 The Corticotropin-Releasing Hormone in Neuroprotection -- 14.1 Introduction -- 14.2 The CRH Family of Proteins and Molecular Signal Transduction -- 14.3 From the Physiology to the Pathophysiology of CRH -- 14.4 CRH and Neurodegenerative Conditions. , 14.5 Protective Activities of CRH.
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 734 (1994), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0730-2312
    Keywords: dexamethasone ; actin ; polymerization ; Ishikawa cells ; cAMP ; actinomycin D ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Glucocorticoids, in addition to their well characterized effects on the genome, may affect cell function in a manner not involving genomic pathways. The mechanisms by which the latter is achieved are not yet clear. A possible means for this action may involve the actin cytoskeleton, since the dynamic equilibrium of actin polymerization changes rapidly following exposure to several stimuli, including hormones. The aim of the present work was to find out if glucocorticoids exert rapid, nongenomic effects on actin polymerization in Ishikawa human endometrial cells, which represent a well characterized in vitro cell model expressing functional glucocorticoid receptors. Short term exposure of the cells to the synthetic glucocorticoid dexamethasone resulted in an overall decrease of the G/total-actin ratio in a time- and dose-dependent manner. Specifically, in untreated Ishikawa cells the G/total-actin ratio was 0.48 ± 0.01 (n = 26). It became 0.35 ± 0.01 (n = 13, P 〈 0.01) following exposure to 10-7 M dexamethasone for 15 min. This was induced by a significant decrease of the cellular G-actin level, without affecting the total actin content, indicating a rapid actin polymerization. This conclusion was fully confirmed by direct fluorimetry measurements, that showed a significant increase of the F-actin content by 44% (n = 6, P 〈 0.001) in cells treated with dexamethasone (10-7 M, 15 min). The rapid dexamethasone-induced alterations of the state of actin polymerization were further supported by fluorescence microscopy. The latter studies showed that the microfilaments of cells pretreated with 10-7 M dexamethasone for 15 min were more resistant to various concentrations of the antimicrofilament drug cytochalasin B, compared to untreated cells, implying microfilament stabilization. The action of dexamethasone on actin polymerization seems to be mediated via specific glucocorticoid binding sites, since the addition of the glucocorticoid antagonist RU486 completely abolished its effect. Moreover, it appears to act via non-transcriptional pathways, since actinomycin D did not block the dexamethasone-induced actin polymerization. In addition, cell treatment with 10-7 M dexamethasone for 15 min fully reversed the forskolin-, but not the 8-bromo-cAMP-induced actin depolymerization. In line with these findings, the cAMP content of Ishikawa cells was decreased by 29.2% after a 15 min treatment with 10-7 M dexamethasone (n = 4, P 〈 0.01). In conclusion, our results showed that dexamethasone induces rapid, time-, and dose-dependent changes in actin polymerization dynamics in Ishikawa cells. This action seems to be mediated via cAMP, involving probably nongenomic pathways. The above findings offer new perspectives for the understanding of the early cellular responses to glucocorticoids. © 1996 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0730-2312
    Keywords: dexamethasone ; nongenomic effect ; actin assembly ; signal transduction ; confocal microscopy ; total actin ; actin transcript ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Dexamethasone exerts a stimulatory effect of rapid-onset on the polymerization of actin. This has been documented in human endometrial adenocarcinoma Ishikawa cells, resulting in an acute, dose-dependent decrease in the G/total-actin ratio. In the present study we completely characterized this fast and apparently nongenomic effect of dexamethasone on actin assembly. We followed the morphological alterations of actin cytoskeleton and measured the time-dependent dynamics of actin polymerization both by ruling out any changes of total actin in the cells and by measuring its transcript. Rapid changes in actin polymerization were accurately measured using a highly sensitive and quantitative rhodamine-phalloidin fluorimetric assay. Ishikawa cells, exposed to 0.1 μM dexamethasone for various time periods up to 24 h, showed a highly significant, rapid, and transient increase in the polymerization of actin starting within 15 min of dexamethasone exposure and lasting 2 h. Treated cells showed a significant (1.79-fold) enhancement of the fluorescent signal compared to untreated cells at 15 min. This value decreased continuously in a time-dependent manner, reaching control levels after 120 min and remained so for the next 24 h. Confocal laser scanning microscopy studies confirmed these findings. Intensive coloration of microfilaments over several scanning sections suggested an enhanced degree of actin polymerization in cells preincubated for 15 min with 0.1 μM dexamethasone. Moreover, actin filaments were more resistant to cytochalasin B. Additionally, quantitative immunoblot analysis showed that the content of total cellular actin remained the same during this period, suggesting that the biosynthesis of actin was unaffected. Northern blot analysis showed that the concentration of the actin transcript was also unaffected. Our data suggest that glucocorticoids induce a fast and self-limited polymerization of actin in human endometrial cells without affecting its synthesis. These findings strengthen the hypothesis that glucocorticoids exert rapid, nongenomic cellular effects and that the actin-based cytoskeleton is an integral part of this pathway, playing an essential role in receiving and mediating steroid signals for the modulation of cellular responses. J. Cell. Biochem. 65:492-500. © 1997 Wiley-Liss Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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