GLORIA

GEOMAR Library Ocean Research Information Access

feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
  • 1
    Online-Ressource
    Online-Ressource
    Cham :Springer International Publishing AG,
    Schlagwort(e): Stress (Psychology). ; Electronic books.
    Materialart: Online-Ressource
    Seiten: 1 online resource (259 pages)
    Ausgabe: 1st ed.
    ISBN: 9783319911168
    DDC: 612.82
    Sprache: Englisch
    Anmerkung: Intro -- Preface -- Acknowledgements -- Contents -- List of Abbreviations -- List of Figures -- List of Tables -- 1: Grey Matter Changes in the Brain Following Stress and Trauma -- 1.1 During Maturity -- 1.1.1 Previous Studies -- 1.1.2 Hippocampal Volume -- 1.1.3 Amygdala Volume -- 1.1.4 Anterior Cingulate Cortex Volume -- 1.1.5 Discussion -- 1.2 During Childhood -- 1.2.1 Hippocampal Volume -- 1.2.2 Amygdala Volume -- 1.2.3 Prefrontal Cortex Volume -- 1.2.4 Discussion -- 1.2.4.1 Age -- 1.2.4.2 Gender -- 1.2.4.3 Diagnosis and Type of Maltreatment -- 1.3 Animal Models -- 1.3.1 Changes in Grey Matter Volume Following Stress -- References -- 2: Synaptic Changes Responsible for Grey Matter Changes in the Brain of Animal Models Following Stress -- 2.1 Changes in MRI-Determined GMV Following Stress -- 2.2 Changes in the Number of Neurons, Astrocytes and Oligodendrocytes Following Stress -- 2.3 Discussion -- 2.3.1 Density of Cell Types in the Cortex Before and After Stress -- 2.3.2 Dendritic Lengths and Spine Densities Before and After Stress -- 2.4 The Relation Between Stress-Induced Decreases in Synapses/Dendrites and Grey Matter Loss -- 2.5 The Relation Between Decreases in Synapses, Dendrites and Grey Matter -- References -- 3: Identification of the Core Neural Network Subserving PTSD in Animal Models and Their Modulation -- 3.1 Animal Models of PTSD -- 3.1.1 PTSD Diagnostic Criteria in the Diagnostic and Statistical Manual of Mental Disorders Version IV (DSM-IV) Applied to Ani... -- 3.1.2 Acquisition and Extinction of Conditioned Fear in PTSD and Animal Models -- 3.1.3 Summary of Parallel Changes in Grey Matter and White Matter in PTSD and Animal Models -- 3.2 Neural Circuitry Subserving Animal Models of PTSD -- 3.2.1 The Core Synaptic Circuit: Amygdala, Medial Prefrontal Cortex and Hippocampus. , 3.2.1.1 The Local Inhibitory Intercalated Neurons, ITC, of the Amygdala -- 3.2.2 Input and Output of the Core Synaptic Circuit: Thalamus, Periaqueductal Grey and Hypothalamus -- 3.2.2.1 The Output Circuitry of the Amygdala -- 3.2.2.2 The Input Circuitry of the Amygdala -- 3.2.3 Modulation of the Core Synaptic Circuit by Basal Ganglia: The Ventral Tegmentum Area (VTA), Raphe Nucleus and Nucleus Ac... -- 3.3 Transmitters and Growth Factors Mediating Modulation of the Core Synaptic Circuit in PTSD Animal Models -- 3.3.1 Dopamine and Serotonin Receptors/Transporters: Action at Synapses and their Nucleotide Polymorphisms in PTSD -- 3.3.2 Brain-Derived Neurotrophic Factor (BDNF): Action on Dopamine Receptors and Their Nucleotide Polymorphisms in PTSD -- 3.4 Conclusion -- References -- 4: Modulation of the Core Neural Network in Stress: The Role of Brain-Derived Neurotrophic Factor and LTP -- 4.1 BDNF Gene Transcription Controlled by Glucocorticoid and Mineralocorticoid Receptors -- 4.1.1 The BDNF Gene -- 4.1.2 Glucocorticoid Receptors, Mineralocorticoid Receptors, Their Chaperones and Co-activators -- 4.1.3 Co-chaperones FKBP5 and FKBP4: Polymorphisms and Stress -- 4.2 Evidence that BDNF Gene Transcription Controlled by Epigenetic Changes -- 4.2.1 Epigenetic Changes in the BDNF Gene -- 4.2.2 Epigenetic Changes in the BDNF Gene Following Different Behavioural Paradigms -- 4.2.2.1 Childhood Stress -- 4.2.2.2 Restraint Stress -- 4.2.2.3 Predator and Social Defeat Stress -- 4.2.2.4 Fear Conditioning (Memory) -- 4.2.2.5 Suicide -- 4.3 BDNF Control of Dendritic Spines -- 4.3.1 BDNF/TrkB Changes in ERK-Mediated Control of Dendritic Spines -- 4.3.1.1 Control of Dendritic Spines Through the ERK Pathway -- 4.3.2 BDNF/TrkB Changes in Small GTPase-Mediated Control of Dendritic Spines -- 4.3.2.1 RhoA, Rac1, Cde42 and Vav2/3. , 4.3.3 BDNF/TrkB Changes in mRNA Modulation of ERK-Mediated Control of Dendritic Spines -- 4.3.3.1 microRNA -- 4.3.4 BDNF/TrkB Changes to TRCP3 Channel-Mediated Control of Dendritic Spines -- 4.4 BDNF/TrkB Control of Dendritic Spines Modulated by Glucocorticoid and Mineralocorticoid Receptors -- 4.4.1 Glucocorticoid and Mineralocorticoid Modulation of ERK and GTPase Pathways for Control of Dendritic Spines: The GR-ERK-B... -- 4.5 BDNF/TrkB Control of Dendritic Spines Modulated by Corticotropin-Releasing Factor (Hormone) -- 4.5.1 Corticotropin-Releasing Factor (Hormone) Modulation of Protein Lipase C (PLC)/Small GTPase Pathway for Control of Dendri... -- 4.5.2 Corticotropin-Releasing Factor (Hormone) Modulation of Tissue Plasminogen Activator (tPA) Pathway for Control of Dendrit... -- 4.5.2.1 tpA and Dendritic Spines -- 4.5.2.2 CRF Control of Spine Formation and Regression -- 4.6 Cannabinoid (Receptor CB1) Modulation of BDNF Gene Transcription and BDNF/TrkB Control of Dendritic Spines -- 4.7 Serotonin Transporter (SERT) Modulation of BDNF Gene Transcription and BDNF/TrkB Control of Dendritic Spines -- 4.8 Conclusion -- 4.8.1 Dendritic Spines and BDNF -- 4.8.2 BDNF, Glucocorticoid and Mineralocorticoid Receptors -- 4.8.3 Post-traumatic Stress Disorder -- References -- 5: Modulation of the Core Neural Network in Stress: The Role of Endocannabinoids and LTD -- 5.1 The Role of Endocannabinoids -- 5.1.1 Clinical Observations on Endocannabinoids and Extinction -- 5.1.2 Genetic Observations Implicating Endocannabinoids in Extinction -- 5.1.3 The Core Neural Network in Endocannabinoid-Mediated Extinction -- 5.1.4 The Maintenance of Extinction by Endocannabinoids and BDNF -- 5.2 Functional Amygdala Networks in Acquisition and Extinction -- 5.2.1 Lateral Amygdala (LA) -- 5.2.2 Basal Amygdala (BA) and Infralimbic (IL) Cortex. , 5.3 Classical LTP and LTD in the Functional Networks Mediating Acquisition and Extinction -- 5.3.1 Mechanism of Classical Early LTP and LTD at Synaptic Spines -- 5.3.2 Mechanism of Late Classical LTP and LTD at Synaptic Spines -- 5.3.2.1 Changes in Receptor Distributions -- 5.3.2.2 Changes in Spine Shape -- 5.4 Endocannabinoids in Functioning Networks in the Basolateral Amygdala -- 5.4.1 Evidence that Endocannabinoids Have a Critical Role in Extinction -- 5.4.1.1 Acquisition -- 5.4.1.2 Extinction -- 5.4.2 Mechanisms of Action of Endocannabinoids -- 5.4.3 Endocannabinoid Modulation by Glucocorticoids -- 5.4.4 Endocannabinoid Modulation by BDNF -- 5.5 Functional Amygdala Networks that Mediate Extinction: The Roles of LTDi and Endocannabinoids at Extinction Neurons in the ... -- 5.5.1 Summary of Key Observations -- 5.5.2 A Model of the Amygdala in Extinction -- 5.5.3 Caveats Concerning Postulated Roles for Endocannabinoids and Brain-Derived Neurotrophic Factor in Extinction -- 5.6 Conclusion -- 5.6.1 LTP Occurs Consequent on High-Frequency Stimulation (100-200 Hz for 1 S) -- 5.6.2 LTD Occurs as a Consequence of Low-Frequency Stimulation (1 Hz for 900 s) -- 5.6.3 The Synthesis, Release and Uptake of Endocannabinoids -- 5.6.4 proBDNF Control of Synaptic Spine Regression -- References -- 6: Functioning of the Core Neural Network in Fear and Extinction -- 6.1 Fear -- 6.1.1 Fear Activation -- 6.1.1.1 Principal Pathways -- 6.1.2 Fear Memory -- 6.1.2.1 The LAd Module -- 6.1.2.2 The BAF Module -- 6.2 Extinction -- 6.2.1 Extinction Activation -- 6.2.1.1 Principal Pathways -- 6.2.2 Extinction Memory -- 6.2.2.1 The BAE Module -- 6.2.2.2 The ITC Module -- 6.3 Synaptic Plasticity -- 6.3.1 Conditions for Plasticity -- 6.3.2 Neuromodulators -- 6.3.3 Theta and Gamma Oscillations -- 6.3.4 Excitability -- 6.4 Models of the Amygdala in Fear and Extinction. , 6.4.1 Fear Engram -- 6.4.2 Context -- 6.4.3 Endocannabinoids -- 6.4.4 Hebbian Plasticity -- 6.5 A New Model of the Amygdala in Extinction -- 6.5.1 Incorporating Local Inhibitory Mechanisms for LAd, BAF and BAE Neurons in the Model -- 6.5.2 Control of the CeM Output Neurons in the Model -- 6.6 Considerations of the Model -- References -- 7: Modulation of the Core Synaptic Network in Extinction: The Role of Brain-Derived Neurotrophic Factor -- 7.1 BDNF Function at Synapses in the Core Neural Network for Extinction -- 7.1.1 BDNF-Mediated Synaptic Interactions Between the BLA, IL and HPC in Extinction -- 7.1.2 BDNF Autoregulatory Loops -- 7.1.3 BDNF Support for Long Periods of Long-Term Potentiation (lLTP) -- 7.2 The Role of the MeCP2 Complex in Extinction -- 7.2.1 MeCP2 Phosphorylation and Neural Activity -- 7.2.2 MeCP2S421 Activity -- 7.2.3 MeCP2S421/S424 Activity -- 7.2.4 MeCP2S80 Activity -- 7.2.5 MeCP2 Residues at S80, S421 and S424 -- 7.2.6 The MeCP2 Hypothesis for Activity-Dependent Transcription of BDNF -- 7.3 Hypotheses Concerning Mechanisms for Extending Periods of Extinction -- 7.3.1 Spine Loss and the Need to Block Glucocorticoids -- 7.3.2 Maintaining lLTP Through Enhanced Basal Levels of BDNF -- 7.3.3 Enhancing Basal Levels of BDNF Through Phosphorylation of MeCP2 Residues -- References -- Appendix A: F-Actin Determination of Dendritic Spine Integrity -- A.1 Introduction -- A.2 Treadmilling Model -- A.2.1 Polymerization and Depolymerization -- A.2.2 Density of Minus Ends -- A.2.3 Steady-State Solutions -- A.2.4 Monte Carlo Simulation -- A.2.5 Parameter Values -- A.2.6 Results for Treadmilling Model -- A.3 Recycling of F-actin -- A.3.1 Inclusion of NMDA -- A.3.2 NMDA and Profilin -- A.3.3 Steps in the Calculation -- A.3.4 NMDA and Cofilin -- A.3.5 Results for Recycling Model -- A.4 Discussion -- Appendix B: Regulation of NMDA Receptors. , B.1 NMDA Receptor Control of Dendritic Spine Formation and Regression.
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 2
    Online-Ressource
    Online-Ressource
    New York :Columbia University Press,
    Schlagwort(e): Bennett, M. R. -- Philosophical foundations of neuroscience. ; Cognitive neuroscience -- Philosophy. ; Electronic books.
    Beschreibung / Inhaltsverzeichnis: Neuroscience and Philosophy begins with an excerpt from Philosophical Foundations of Neuroscience, in which Maxwell Bennett and Peter Hacker question the conceptual commitments of cognitive neuroscientists. Daniel Dennett and John Searle then criticize their position, and Bennett and Hacker respond. Their impassioned exchange encompasses a wide range of central themes: the nature of consciousness, the bearer and location of psychological attributes, the intelligibility of so-called brain maps and representations, the notion of qualia, and the relationships between mind, brain, and body. Pulling all of these strands together, Daniel Robinson then explains why this confrontation is so crucial to the understanding of neuroscientific research. Clearly argued and thoroughly engaging, the authors present fundamentally different conceptions of philosophical method, cognitive-neuroscientific explanation, and human nature, and their debate will appeal to anyone interested in the relation of mind to brain, of psychology to neuroscience, of causal to rational explanation, and of consciousness to self-consciousness.
    Materialart: Online-Ressource
    Seiten: 1 online resource (233 pages)
    Ausgabe: 1st ed.
    ISBN: 9780231511940
    DDC: 128.2
    Sprache: Englisch
    Anmerkung: Intro -- CONTENTS -- Introduction by Daniel Robinson vii -- THE ARGUMENT -- Philosophical Foundations of Neuroscience: The Introduction, M. R. Bennett and P.M.S. Hacker -- Philosophical Foundations of Neuroscience: An Excerpt from Chapter 3, M. R. Bennett and P.M.S. Hacker -- Philosophical Foundations of Neuroscience: An Excerpt from Chapter 10, M. R. Bennett and P.M.S. Hacker -- Philosophical Foundations of Neuroscience: An Excerpt from Chapter 14: The Concluding Remarks, M. R. Bennett and P.M.S. Hacker -- Neuroscience and Philosophy Maxwell Bennett -- THE REBUTTALS -- Philosophy as Naive Anthropology: Comment on Bennett and Hacker, Daniel Dennett -- Putting Consciousness Back in the Brain: Reply to Bennett and Hacker, Philosophical Foundations of Neuroscience, John Searle -- REPLY TO THE REBUTTALS -- The Conceptual Presuppositions of Cognitive Neuroscience: A Reply to Critics Maxwell Bennett and Peter Hacker -- Epilogue: Maxwell Bennett -- Still Looking: Science and Philosophy in Pursuit of Prince Reason, Daniel Robinson -- NOTES.
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 3
    Online-Ressource
    Online-Ressource
    Cham : Springer International Publishing
    Schlagwort(e): Neurosciences ; Neurobiology ; Neurology ; Neurobiology ; Neurology ; Neurosciences
    Beschreibung / Inhaltsverzeichnis: This book provides detailed insights into the cellular and molecular alterations that occur in the brain following stress and trauma. The changes to the grey matter in certain areas of the brain are similar in stressed humans and animals, with the most likely basis for these changes being the degeneration of synaptic connections. In the book’s initial sections, the reader will learn about the core network of synaptic connections that are affected by stress and trauma disorders. These connections are chiefly modulated by dopamine, serotonin and Brain Derived Neurotrophic Factor (BDNF). In subsequent chapters, the NMDA-receptor-mediated plasticity of these synapses is discussed, with particular attention paid to how glucocorticoids can interfere with the function of BDNF and thereby affect the synapse’s physical stability. The book concludes by integrating the observations made in the previous sections so as to present plausible hypotheses regarding the identity of the networks, synapses and molecular pathways that promote fear and extinction. Providing an up-to-date overview of the mechanisms of synaptic plasticity and physiological changes in the stressed and traumatized brain, this book will appeal to researchers, clinicians and students in the neurosciences
    Materialart: Online-Ressource
    Seiten: Online-Ressource (XXXIII, 231 p. 47 illus., 18 illus. in color, online resource)
    Ausgabe: Springer eBook Collection. Biomedical and Life Sciences
    ISBN: 9783319911168 , 9783319911168
    Serie: SpringerLink
    Sprache: Englisch
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 4
    ISSN: 0173-0835
    Schlagwort(e): Cardiomyocytes ; P2X receptors ; Autonomic control of the heart ; Heart failure ; Dilated cardiomyopathy ; Chemistry ; Biochemistry and Biotechnology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Chemie und Pharmazie
    Notizen: This is the first report of the analysis of the ATP-specific P2X1 receptor subunit in human hearts. We have examined homogenate samples of human left atria for the presence of P2X1 receptors using Western blots. Anti-P2X1 immunoreactivity was detected in populations of nondiseased atria as well as in atria from explanted hearts from patients with terminally failing heart conditions such as dilated cardiomyopathy. At least three groups of P2X1 immunoreactive proteins were detected in the Western blots with approximate molecular mass values of 50, 70, and 160 kDa. We report changes in expression of their 50 and 70 kDa components. These changes may be related to the type of deficit in these hearts since the changes have been observed in hearts with decreased ejection fractions characteristic of dilated cardiomyopathy.
    Zusätzliches Material: 2 Ill.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...