GLORIA

GEOMAR Library Ocean Research Information Access

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Nervous system--Degeneration--Congresses. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (551 pages)
    Edition: 1st ed.
    ISBN: 9780080862422
    Series Statement: Issn Series
    Language: English
    Note: Front Cover -- NEURONAL DEGENERATION AND REGENERATION: FROM BASIC MECHANISMS TO PROSPECTS FOR THERAPY -- Copyright Page -- Contents -- List of contributors -- Preface -- Acknowledgements -- Section I: Mechanisms of nerve cell death and nerve cell survival -- Chapter 1. Neuronal cell death: an updated view -- Chapter 2. Corticosteroid hormones and neuronal vulnerability: towards identification of candidate vulnerability genes -- Chapter 3. Ubiquitin and its role in neurodegeneration -- Chapter 4. Studying signal transduction in neuronal cells: the Trk/NGF system -- Chapter 5. Developmental changes in the neurotrophic factor survival requirements of peripheral nervous system neurons -- Chapter 6. Regulation of brain-derived neurotrophic factor mRNA levels in hippocampus by neuronal activity -- Chapter 7. Instructive roles of neurotrophins in synaptic plasticity -- Chapter 8. Neurotrophin receptors in Alzheimer's disease -- Section II: Biological factors that determine neuronal differentiation, axonal growth, guidance and target recognition -- Chapter 9. Discrete clusters of axonin-1 and NgCAM at neuronal contact sites: facts and speculations on the regulation of axonal fasciculation -- Chapter 10. Molecular mechanisms of commissural axon pathfinding -- Chapter 11. Semaphorin-mediated neuronal growth cone guidance -- Chapter 12. Semaphorin III: role in neuronal development and structural plasticity -- Chapter 13. Role for semaphorin III and its receptor neuropilin-1 in neuronal regeneration and scar formation? -- Chapter 14. EPH receptors and ligands in axon pathway choice, target recognition, and synaptogenesis -- Section III: The role of glial cells in neurodegeneration and regeneration -- Chapter 15. Boundary molecules during brain development, injury, and persistent neurogenesis - in vivo and in vitro studies. , Chapter 16. Cellular activation in neuroregeneration -- Chapter 17. Cellular and molecular correlates of the regeneration of adult mammalian CNS axons into peripheral nerve grafts -- Chapter 18. Oligodendrocyte regeneration in the adult rodent CNS and the failure of this process in multiple sclerosis -- Chapter 19. Genetic basis of peripheral neuropathies -- Section IV: Critical events in neurodegenerative diseases, prion diseases and multiple sclerosis -- Chapter 20. Neuropathological hallmarks of Alzheimer's and Parkinson's diseases -- Chapter 21. Neurofibrillary pathology of Alzheimer's disease and other tauopathies -- Chapter 22. A new approach to the genetic analysis of nervous system diseases: retrospective genotyping of archival brains -- Chapter 23. Alzheimer's disease: identification of genes and genetic risk factors -- Chapter 24. Neurodegenerative Alzheimer-like pathology in PDAPP 717V → F transgenic mice -- Chapter 25. Strain dependent and invariant features of transgenic mice expressing Alzheimer amyloid precursor proteins -- Chapter 26. Reduced neuronal activity and reactivation in Alzheimer's disease -- Chapter 27. Dinucleotide deletions in neuronal transcripts: a novel type of mutation in non-familial Alzheimer's disease and Down syndrome patients -- Chapter 28. Pathogenesis of neurodegenerative diseases associated with expanded glutamine repeats: new answers, new questions -- Chapter 29. Molecular studies of prion diseases -- Chapter 30. The small heat shock protein αB-crystallin as kem autoantigen in multiple sclerosis -- Section V: Strategies to promote regeneration of injured neurons: direct intervention and neural replacement -- Chapter 31. Spinal cord injury: bridging the lesion and the role of neurotrophic factors in repair -- Chapter 32. Neurotrophin gene therapy in CNS models of trauma and degeneration. , Chapter 33. Gene therapy for inherited neurological disorders: towards therapeutic intervention in the Lesch-Nyhan syndrome -- Chapter 34. Towards gene therapy of neurodegenerative disease -- Chapter 35. Prospectives for cell and gene therapy in Huntington's disease -- Index.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Neuroplasticity -- Congresses. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (497 pages)
    Edition: 1st ed.
    ISBN: 9780080497730
    Series Statement: Issn Series
    Language: English
    Note: Front Cover -- PLASTICITY IN THE ADULT BRAIN: FROM GENES TO NEUROTHERAPY -- Copyright Page -- Contents -- List of Contributors -- Preface -- Acknowledgements -- Section I: Neurogenesis in adulthood: New neurons in old brains -- Chapter 1. Neurogenesis in adult primates -- Section II: Brain plasticity: From molecule to neural network -- Chapter 2. Semaphorins: contributors to structural stability of hippocampal networks? -- Chapter 3. Neurotrophins and visual cortical plasticity -- Chapter 4. Dendritic spines: elementary structural units of neuronal plasticity -- Chapter 5. Abnormal plastic changes in a rat model for mesial temporal lobe epilepsy: a short review -- Chapter 6. Cortical map plasticity in animals and humans -- Section III: Learning and memory -- Chapter 7. A brain adaptation view of plasticity: is synaptic plasticity an overly limited concept? -- Chapter 8. Environmental enrichment and the brain -- Chapter 9. Sex hormones, neuroprotection and cognition -- Chapter 10. Memory reactivation and consolidation during sleep: from cellular mechanisms to human performance -- Chapter 11. Sensory loss and cortical reorganization in mature primates -- Chapter 12. Human brain plasticity: evidence from sensory deprivation and altered language experience -- Section IV: Circadian and seasonal plasticity -- Chapter 13. Modes of plasticity within the mammalian circadian system -- Chapter 14. Functional plasticity of the circadian timing system in old age: light exposure -- Chapter 15. What is the adaptive role of neurogenesis in adult birds? -- Chapter 16. A brain for all seasons: cellular and molecular mechanisms of photoperiodic plasticity -- Section V: Neural plasticity in aging and neuropathology -- 17. Regulation of synaptic plasticity in memory and memory decline with aging -- 18. Synaptic plasticity in the diabetic brain: advanced aging?. , 19. Adult neurogenesis: implications for psychiatry -- 20. Brain aging and Alzheimer's disease -- use it or lose it -- 21. Functional genomics and psychiatric illness -- Section VI: Cell implantation and gene therapy -- Chapter 22. The fifteenth C.U. Ariëns Kappers Lecture (An introduction) -- Chapter 23. New strategies in neural repair -- Chapter 24. Regulation of dopamine cell type and transmitter function in fetal and stem cell transplantation for Parkinson's disease -- Chapter 25. Neuroprotection for Parkinson's disease using viral vector-mediated delivery of GDNF -- Section VII: Stem cells: Their role in brain repair -- Chapter 26. Glial stem-like cells: implications for ontogeny, phylogeny, and CNS regeneration -- Chapter 27. Induced neurogenesis by endogenous progenitor cells in the adult mammalian brain -- Chapter 28. The use of human embryonic stem cells for research: an ethical evaluation -- Subject Index.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2014-09-02
    Description: Long-term synaptic potentiation (LTP) is thought to be a key process in cortical synaptic network plasticity and memory formation. Hebbian forms of LTP depend on strong postsynaptic depolarization, which in many models is generated by action potentials that propagate back from the soma into dendrites. However, local dendritic depolarization has been shown to mediate these forms of LTP as well. As pyramidal cells in supragranular layers of the somatosensory cortex spike infrequently, it is unclear which of the two mechanisms prevails for those cells in vivo. Using whole-cell recordings in the mouse somatosensory cortex in vivo, we demonstrate that rhythmic sensory whisker stimulation efficiently induces synaptic LTP in layer 2/3 (L2/3) pyramidal cells in the absence of somatic spikes. The induction of LTP depended on the occurrence of NMDAR (N-methyl-d-aspartate receptor)-mediated long-lasting depolarizations, which bear similarities to dendritic plateau potentials. In addition, we show that whisker stimuli recruit synaptic networks that originate from the posteromedial complex of the thalamus (POm). Photostimulation of channelrhodopsin-2 expressing POm neurons generated NMDAR-mediated plateau potentials, whereas the inhibition of POm activity during rhythmic whisker stimulation suppressed the generation of those potentials and prevented whisker-evoked LTP. Taken together, our data provide evidence for sensory-driven synaptic LTP in vivo, in the absence of somatic spiking. Instead, LTP is mediated by plateau potentials that are generated through the cooperative activity of lemniscal and paralemniscal synaptic circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gambino, Frederic -- Pages, Stephane -- Kehayas, Vassilis -- Baptista, Daniela -- Tatti, Roberta -- Carleton, Alan -- Holtmaat, Anthony -- England -- Nature. 2014 Nov 6;515(7525):116-9. doi: 10.1038/nature13664. Epub 2014 Aug 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Basic Neurosciences and the Center for Neuroscience, CMU, University of Geneva, 1 rue Michel Servet, 1211 Geneva, Switzerland [2] [3] Institute for Interdisciplinary Neuroscience (IINS), UMR 5297 CNRS and University of Bordeaux, 146 rue Leo-Saignat, 33077 Bordeaux, France. ; 1] Department of Basic Neurosciences and the Center for Neuroscience, CMU, University of Geneva, 1 rue Michel Servet, 1211 Geneva, Switzerland [2]. ; 1] Department of Basic Neurosciences and the Center for Neuroscience, CMU, University of Geneva, 1 rue Michel Servet, 1211 Geneva, Switzerland [2] Lemanic Neuroscience Doctoral School, 1 rue Michel Servet, 1211 Geneva, Switzerland. ; Department of Basic Neurosciences and the Center for Neuroscience, CMU, University of Geneva, 1 rue Michel Servet, 1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25174710" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Dendrites/*physiology ; *Long-Term Potentiation ; Male ; Mice ; Mice, Inbred C57BL ; Physical Stimulation ; Receptors, N-Methyl-D-Aspartate/metabolism ; Rhodopsin/metabolism ; Somatosensory Cortex/*cytology/*physiology ; Thalamus/cytology/physiology ; Vibrissae/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2014-05-16
    Description: During development, thalamocortical (TC) input has a critical role in the spatial delineation and patterning of cortical areas, yet the underlying cellular and molecular mechanisms that drive cortical neuron differentiation are poorly understood. In the primary (S1) and secondary (S2) somatosensory cortex, layer 4 (L4) neurons receive mutually exclusive input originating from two thalamic nuclei: the ventrobasalis (VB), which conveys tactile input, and the posterior nucleus (Po), which conveys modulatory and nociceptive input. Recently, we have shown that L4 neuron identity is not fully committed postnatally, implying a capacity for TC input to influence differentiation during cortical circuit assembly. Here we investigate whether the cell-type-specific molecular and functional identity of L4 neurons is instructed by the origin of their TC input. Genetic ablation of the VB at birth resulted in an anatomical and functional rewiring of Po projections onto L4 neurons in S1. This induced acquisition of Po input led to a respecification of postsynaptic L4 neurons, which developed functional molecular features of Po-target neurons while repressing VB-target traits. Respecified L4 neurons were able to respond both to touch and to noxious stimuli, in sharp contrast to the normal segregation of these sensory modalities in distinct cortical circuits. These findings reveal a behaviourally relevant TC-input-type-specific control over the molecular and functional differentiation of postsynaptic L4 neurons and cognate intracortical circuits, which instructs the development of modality-specific neuronal and circuit properties during corticogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pouchelon, Gabrielle -- Gambino, Frederic -- Bellone, Camilla -- Telley, Ludovic -- Vitali, Ilaria -- Luscher, Christian -- Holtmaat, Anthony -- Jabaudon, Denis -- England -- Nature. 2014 Jul 24;511(7510):471-4. doi: 10.1038/nature13390. Epub 2014 May 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland. ; 1] Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland [2] Interdisciplinary Institute for NeuroScience, CNRS UMR 5297, 33077 Bordeaux, France. ; 1] Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland [2] Clinic of Neurology, Department of Clinical Neurosciences, Geneva University Hospital, CH-1211 Geneva, Switzerland [3] Institute of Genetics & Genomics in Geneva (iGE3), University of Geneva, CH-1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24828045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/drug effects/physiology ; Capsaicin/pharmacology ; *Cell Differentiation/drug effects ; Female ; Male ; Mice, Inbred C57BL ; Neural Pathways/drug effects/*physiology ; Neurons/*cytology/drug effects/*physiology ; Noxae/pharmacology ; Optogenetics ; Post-Synaptic Density/drug effects/*physiology ; Somatosensory Cortex/cytology/drug effects/*physiology ; Synaptic Potentials/drug effects ; Thalamic Nuclei/cytology/drug effects/*physiology ; Touch/physiology ; Vibrissae/drug effects/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-06-30
    Keywords: Neuroscience
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...