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  • 1
    Online Resource
    Online Resource
    Cambridge :MIT Press,
    Keywords: Hypothalamus-Popular works. ; Hypothalamic hormones-Popular works. ; Electronic books.
    Description / Table of Contents: How hormonal signals in one small structure of the brain--the hypothalamus--govern our physiology and behavior.
    Type of Medium: Online Resource
    Pages: 1 online resource (277 pages)
    Edition: 1st ed.
    ISBN: 9780262346993
    DDC: 573.4/59
    Language: English
    Note: Intro -- Contents -- Preface -- 1. Prelude -- 2. The European Brain -- 3. The Classical Neuron -- 4. Enlightenment -- 5. Far from the Madding Crowd -- 6. Pulsatile Secretion -- 7. Dendritic Secretion and Priming -- 8. The GnRH Neuron -- 9. Kisspeptin -- 10. The Bistable Neuron -- 11. Vasopressin -- 12. Numbers -- 13. Whispered Secrets and Public Announcements -- 14. Plasticity -- 15. Rhythms -- 16. Obesity -- 17. The Empty Medicine Cabinet -- 18. Appetite -- 19. The Sweet Hormone -- 20. The Hybrid Neuron -- 21. Behavior -- 22. The Evolved Brain -- 23. Redundancy and Degeneracy -- 24. The Tangled Web -- Notes -- Index.
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  • 2
    Online Resource
    Online Resource
    Newark :John Wiley & Sons, Incorporated,
    Keywords: Gonadotropin-Releasing Hormone - physiology. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (396 pages)
    Edition: 1st ed.
    ISBN: 9781119159452
    Series Statement: Wiley-INF Masterclass in Neuroendocrinology Series
    DDC: 612.8
    Language: English
    Note: Intro -- Title Page -- Copyright -- Table of Contents -- List of Contributors -- Series Preface -- Preface -- About the Companion Website -- Chapter 1: Bridging Between Experiments and Equations: A Tutorial on Modeling Excitability -- 1.1 Introducing excitability -- 1.2 Introducing the Morris-Lecar model -- 1.3 Opening XPP and triggering an action potential -- 1.4 Action potentials in the phase plane -- 1.5 Model response to sustained current injection -- 1.6 Reading a bifurcation diagram -- 1.7 Saddle node on an invariant circle (SNIC) bifurcation -- 1.8 Time-scale separation -- 1.9 Homoclinic bifurcation -- 1.10 Bursting -- 1.11 Eigenvalues and stability -- 1.12 Perspectives -- Acknowledgement -- References -- Chapter 2: Ion Channels and Electrical Activity in Pituitary Cells: A Modeling Perspective -- 2.1 Endocrine pituitary cells are electrically active -- 2.2 Endocrine pituitary cell types -- 2.3 Voltage-gated ion channels -- 2.4 Nonselective cation channels -- 2.5 Ligand-gated ion channels -- 2.6 Spontaneous electrical activity and ca2+ signalling -- 2.7 Modulation of spontaneous electrical activity by GPCRs -- 2.8 The dynamic clamp technique for studying the contributions of ion channels to electrical activity -- 2.9 Perspectives -- Recommended reading -- Chapter 3: Endoplasmic Reticulum- and Plasma-Membrane-Driven Calcium Oscillations -- 3.1 Introduction -- 3.2 Calcium balance equations -- 3.3 ER-driven calcium oscillations -- 3.4 Combining ER and PM oscillators -- 3.5 The road goes ever on -- 3.6 Conclusions -- Acknowledgments -- References -- Chapter 4: A Mathematical Model of Gonadotropin-Releasing Hormone Neurons -- 4.1 Introduction -- 4.2 Previous models of GnRH neurons -- 4.3 A model of GnRH neurons in hypothalamic slices -- 4.4 Model results -- 4.5 Conclusions and future work -- 4.6 Appendix: the model equations and parameters. , References -- Chapter 5: Modeling Spiking and Secretion in the Magnocellular Vasopressin Neuron -- 5.1 Background -- 5.2 Modeling -- 5.3 Bursting in a spiking model -- 5.4 Modeling spike-triggered secretion -- 5.5 Population modeling -- 5.6 Conclusion -- References -- Further Reading -- Chapter 6: Modeling Endocrine Cell Network Topology -- 6.1 Introduction -- 6.2 Networks -- 6.3 Step-by-step experimental and analytical protocol -- 6.4 Worked example -- 6.5 Perspectives -- Further reading -- References -- Chapter 7: Modeling the Milk-Ejection Reflex -- 7.1 The milk-ejection reflex -- 7.2 The Model -- 7.3 Building the model -- 7.4 Model behavior -- 7.5 Discussion -- 7.6 Perspectives -- Bibliography -- Chapter 8: Dynamics of the HPA Axis: A Systems Modeling Approach -- 8.1 Introduction -- 8.2 Mathematically modeling the HPA axis -- 8.3 Unveiling the mechanism of ultradian pulsatility -- 8.4 Exploring model predictions experimentally -- 8.5 Significance of ultradian pulsatility for stress responsiveness -- 8.6 Discussion -- 8.7 Perspectives -- References -- Chapter 9: Modeling the Dynamics of Gonadotropin-Releasing Hormone (GnRH) Secretion in the Course of an Ovarian Cycle -- 9.1 Introduction -- 9.2 A single dynamical framework for the control of the GnRH pulse and surge generator by ovarian steroids -- 9.3 GnRH secretion pattern along an ovarian cycle -- 9.4 Reproducing known effects of ovarian steroids on the surge -- 9.5 Steroid challenges in the pulsatile regime -- 9.6 Conclusion -- References -- Glossary -- Index -- End User License Agreement.
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 6 (1994), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In rats, the release of growth hormone (GH) is inhibited during electrical stimulation of the periventricular nucleus but after the end of stimulation, there is a rebound ‘hypersecretion’ of GH. We examined the responses of arcuate neurones in pentobarbitone-anaesthetized male rats, following electrical stimulation of the periventricular nucleus to test the hypothesis that the effects of periventricular nucleus stimulation on GH secretion are mediated via effects upon GH-releasing hormone (GRF) neurones in the arcuate nucleus. The electrical activity of 2 groups of arcuate neurones were analysed before, during and after periventricular nucleus stimulation (10 Hz, 5 min, 0.5 mA biphasic, 0.5/1.0 ms): a) putative neurosecretory cells which were antidromically identified (AD) as projecting to the median eminence (n = 53) and b) non-neurosecretory cells, identified by their spontaneous ‘bursting’ pattern of activity (n = 29). During stimulation predominantly inhibitory responses were observed in both AD and bursting cell groups. Of the 39 AD cells which were spontaneously active, 25 were inhibited during the periventricular nucleus stimulation, and 10 of these showed a rebound hyperactivation following the end of stimulation. Fifteen bursting cells were inhibited during stimulation and 4 of these displayed a rebound hyperactivation following the end of stimulation. Additional evidence was sought for the identity of these cells by testing their response to electrical stimulation of the basolateral amygdala (which has previously been shown to increase plasma GH concentration without influencing the release of other pituitary hormones). Six of the 10 AD cells which displayed the inhibition/rebound response to periventricular nucleus stimulation were also excited following electrical stimulation of the basolateral amygdala. We conclude that 1) electrical stimulation of the periventricular nucleus and the basolateral amygdala exert predominantly inhibitory and excitatory effects respectively upon the activity of arcuate neurones but for neither site were the effects of stimulation exclusively upon GRF neurones, and 2) the rebound hypersecretion of GH following PeN stimulation is likely to involve the rebound activation of arcuate neurones.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 15 (2003), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 16 (2004), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 15 (2003), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 14 (2002), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 14 (2002), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 12 (2000), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 9 (1997), S. 0 
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To examine the role of endogenous vasopressin on the electrical activity of vasopressin neurons within the supraoptic nucleus of the rat brain in vivo, we have developed a novel technical approach for administering neuroactive drugs directly into the extracellular environment of the neuronal dendrites. A microdialysis probe was used for controlled local drug administration into the dendritic area of the nucleus during extracellular recording of single neurons in vivo. Vasopressin or selective V1 receptor antagonists were administered for between 10 and 30 min via a U-shaped microdialysis probe placed flat on the surface of the supraoptic nucleus after transpharyngeal exposure of the nucleus in urethane-anaesthetized rats. Microdialysis administration (retrodialysis) of vasopressin inhibited vasopressin neurons by reducing their firing rate, sometimes to total inactivity. Retrodialysis of V1-receptor antagonists partially reversed the effect of vasopressin, and a subsequent vasopressin administration was not effective in reducing the activity of these neurons, suggesting a receptor-mediated action of endogenous vasopressin. In addition, the duration of the periods of activity and the mean frequency during the active phase were increased in vasopressin neurons after retrodialysis of V1-receptor antagonist, indicating a physiological role of endogenous vasopressin. Neither vasopressin nor the antagonists altered the activity of continuously firing oxytocin neurons. Thus, vasopressin released within the supraoptic nucleus may act via V1 receptors located specifically on vasopressin neurons to regulate their phasic activity by an auto-inhibitory action. Since vasopressin release from the dendrites of vasopressin neurons is increased and prolonged after various forms of stimulation, it is proposed that this mechanism will act to limit excitation of vasopressin neurons, and hence secretion from the neurohypophysis. In addition, combined in vivo retrodialysis/ single cell recording allows controlled introduction of neuroactive substances into the extracellular fluid in the immediate vicinity of recorded neurons. This is shown to provide a novel approach to study neurotransmitter actions on supraoptic neurons in vivo.
    Type of Medium: Electronic Resource
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