"Neuronal Plasticity" - Books

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Select item 14410041.

Neural Plasticity and Memory: From Genes to Brain Imaging.

Bermúdez-Rattoni F, editor.

Boca Raton (FL): CRC Press/Taylor & Francis; 2007.

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Select item 13699922.

The Dynamic Synapse: Molecular Methods in Ionotropic Receptor Biology.

Kittler JT, Moss SJ, editors.

Boca Raton (FL): CRC Press/Taylor & Francis; 2006.

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Select item 23871563.

Jasper's Basic Mechanisms of the Epilepsies [Internet]. 4th edition.

Noebels JL, Avoli M, Rogawski MA, et al., editors.

Bethesda (MD): National Center for Biotechnology Information (US); 2012.

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Select item 14152804.

Madame Curie Bioscience Database [Internet].

Austin (TX): Landes Bioscience; 2000-2013.

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Select item 44036685.

StatPearls [Internet].

Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Select item 49719686.

Brain Health Across the Life Span: Proceedings of a Workshop.

National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Population Health and Public Health Practice; Nicholson A, editor.

Washington (DC): National Academies Press (US); 2020 Mar 31.

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Select item 18813827.

Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition.

Siegel GJ, Agranoff BW, Albers RW, et al., editors.

Philadelphia: Lippincott-Raven; 1999.

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Select item 18602428.

WormBook: The Online Review of C. elegans Biology [Internet].

Pasadena (CA): WormBook; 2005-2018.

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Select item 41031749.

Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects.

Kobeissy FH, editor.

Boca Raton (FL): CRC Press/Taylor & Francis; 2015.

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Select item 139691010.

Biology of the NMDA Receptor.

Van Dongen AM, editor.

Boca Raton (FL): CRC Press/Taylor & Francis; 2009.

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Select item 187145811.

In Vivo Optical Imaging of Brain Function. 2nd edition.

Frostig RD, editor.

Boca Raton (FL): CRC Press/Taylor & Francis; 2009.

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Select item 145259412.

Brain Aging: Models, Methods, and Mechanisms.

Riddle DR, editor.

Boca Raton (FL): CRC Press/Taylor & Francis; 2007.

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Select item 165096213.

Webvision: The Organization of the Retina and Visual System [Internet].

Kolb H, Fernandez E, Nelson R, editors.

Salt Lake City (UT): University of Utah Health Sciences Center; 1995-.

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Select item 162585214.

Neuroscience. 2nd edition.

Purves D, Augustine GJ, Fitzpatrick D, et al., editors.

Sunderland (MA): Sinauer Associates; 2001.

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Select item 255392415.

Neuroproteomics.

Alzate O, editor.

Boca Raton (FL): CRC Press/Taylor & Francis; 2010.

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Select item 413791816.

Translational Research in Traumatic Brain Injury.

Laskowitz D, Grant G, editors.

Boca Raton (FL): CRC Press/Taylor and Francis Group; 2016.

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Select item 340129417.

Endotext [Internet].

Feingold KR, Anawalt B, Blackman MR, et al., editors.

South Dartmouth (MA): MDText.com, Inc.; 2000-.

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Select item 226089018.

The Aging Mind: Opportunities in Cognitive Research.

National Research Council (US) Committee on Future Directions for Cognitive Research on Aging; Stern PC, Carstensen LL, editors.

Washington (DC): National Academies Press (US); 2000.

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Select item 255463619.

The Neurobiology of Olfaction.

Menini A, editor.

Boca Raton (FL): CRC Press/Taylor & Francis; 2010.

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Select item 145328820.

Methods for Neural Ensemble Recordings. 2nd edition.

Nicolelis MAL, editor.

Boca Raton (FL): CRC Press/Taylor & Francis; 2008.

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Supplemental Content

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Figure 29-5

Simplified mechanism by which growth factors may regulate neuronal plasticity following injury to the CNS. Primed by the original insult, microglia, astroglia and neurons interact with each other by releasing growth factors to the extracellular space. The actions of growth factors are organized in molecular cascades in which one growth factor affects the release or action of another growth factor. This generally results in increased cell survival and/or sprouting. IL-1, interleukin-1; TGF-β1, transforming growth factor β1; FGF-2, basic fibroblast growth factor 2; NGF, nerve growth factor; CNTF, ciliary neurotrophic factor; BDNF, brain-derived neurotrophic factor; NCAM, neural cell adhesion molecule.

Axon Sprouting and Reactive Synaptogenesis.

Siegel GJ, Agranoff BW, Albers RW, et al., editors. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition. Philadelphia: Lippincott-Raven; 1999.
Figure 3

Fibrotic scar deposition by reactive neurovascular unit cells. Glial scar formation entails the deposition of fibrotic molecules at the injury core to prevent the infiltration of peripheral leukocytes and inflammatory signaling into the healthy tissue. A, Mural PDGFRβ⁺ cells give rise to scar-forming fibroblasts that migrate to the injury core and become a major source of fibrotic molecules. B, At the injury site, microglia respond to multiple signaling, including TGF-β and TnC to modulate the recruitment of peripheral immune cells and astrocyte activation. C, In turn, reactive astrocytes constitute the primary reservoirs of scar-forming TnC as well as CSPGs, which exert immunoregulatory roles and facilitate tissue replacement. Due to its high ligand capacity, TnC allows determining the action of distinct ECM molecules at the fibrotic scar. D, The abundant deposition of fibrotic proteins, including collagen, laminin, and fibronectin by fibroblast-like cells deriving from PDGFRβ⁺ cells that invade the lesion core, determines tissue elasticity and stiffness, and thus control neuronal plasticity inhibition or promotion balance.

Neurovascular Reactivity in Tissue Scarring Following Cerebral Ischemia.

Pluta R, editor. Cerebral Ischemia [Internet]. Brisbane (AU): Exon Publications; 2021 Nov 6.
FIGURE 43.1

Illustration of extradural CS following an experimental model of ischemic damage and resulting brain plasticity. (a) Illustration of a rat brain demonstrating the relative location of the extradural electrode and ischemic lesion/damage of the SMC. (b) Image of a rat reaching through a small window to retrieve a pellet in the single-pellet reaching task. When CS is delivered via implanted electrode (purple arrow) concurrent with the impaired forelimb (red asterisk) practice on a skilled reaching task, animals significantly improve their reaching performance compared with animals undergoing training without CS. (c) Example of ischemic damage (red starburst) to the SMC shown in a coronal Nissl-stained section. The black box represents the sampling area within the remaining motor cortex, where CS plus training effects on neuronal plasticity are found. (d) Photomicrograph representative image of microtubule-2 immunoreactive (MAP2-IR) dendritic processes in layer V of the lesion hemisphere’s remaining motor cortex. Three weeks of subdural 50-Hz bipolar CS concurrent with impaired limb reach training significantly increased the density of MAP2-IR processes compared to training alone (Adkins-Muir and Jones, 2003). (e) Electron microscopy photomicrograph of layer V of remaining motor cortex following unilateral ischemic lesion. Cathodal 100HZ CS combined with reach training significantly increased the density of synapses (orange arrows) compared with reach training alone (Adkins et al., 2008).

Cortical Stimulation-Induced Structural Plasticity and Functional Recovery after Brain Damage.

Kobeissy FH, editor. Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects. Boca Raton (FL): CRC Press/Taylor & Francis; 2015.
FIGURE 8.1

Adaptive changes in serotonergic neurons in 5-HT receptor knock-out mice. BO: olfactory bulb, CX: cortex, GP: globus pallidus, LC: locus coeruleus, SN: substantia nigra. (From 1. Ase, A.R. et al., J Neurochem 75(6), 2415–26, 2000; 2. Ase, A. R. et al., J Neurochem, 78(3), 619–630; 3. Bortolozzi, A. et al., J Neurochem, 88(6), 1373–1379, 2004; 4. Clifton, P.G. et al., Eur J Neurosci, 17(1), 185–190, 2003; 5. Compan, unpublished; 6. Conductier, G., et al., Eur J Neurosci, 24(4), 1053–1062, 2006; 8. Evrard, A. et al., Eur J Neurosci, 11(11), 3823–3831, 1999; 9. Lee, M. D. et al., Psychopharmacology 176(1), 39–49,2004; 10. Ramboz, S. et al., Proc Natl Acad Sci USA, 95(24), 14476–14481, 1998; Richer, M. et al., Eur J Pharmacol, 435(2–3), 195–203, 2002. With permission.)

Do Limits of Neuronal Plasticity Represent an Opportunity for Mental Diseases, Such as Addiction to Food and Illegal Drugs? Use and Utilities of Serotonin Receptor Knock-Out Mice.

Chattopadhyay A, editor. Serotonin Receptors in Neurobiology. Boca Raton (FL): CRC Press/Taylor & Francis; 2007.