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Differences in behaviour and in forelimb cortical neurons of two rat strains following reach-trainingMcVagh, John R. 14 September 2006 (has links)
The brain undergoes structural changes in response to new experiences like learning a new skill. Skilled motor movements depend greatly on the primary motor cortex for their execution. Recent studies describe rat strain differences in motor performance related to differential synaptic efficacy in the motor cortex of rats. Previous studies identified differences in motor performance related to differential dendritic morphology and strain related differences in synaptic function in the motor cortex. Strain differences are one way of investigating anatomical organization and behaviour of the motor system. The object of this research was to examine strain related differences in dendritic morphology in layer II / III pyramidal cells of the forelimb area of the sensory motor cortex in both Long-Evans and Fischer 344 rats after reach training. This research also examined whether changes in reaching behaviour could be attributed to changes in dendritic morphology. Rats were trained once a day for 30 days to reach for a food pellet through a slot in a reaching box. Pyramidal cells in the motor sensory forelimb (MSF) cortex were stained with the Golgi Cox method. Subsequent analysis of Sholl and branch order data of cell drawings determined that there were no significant differences in any measure of dendritic length or dendritic length at branch order 3, 4, 5 of pyramidal cells in layer II/III of the MSF cortex between the Long Evans and Fischer 344 rat strain. The only significant strain related difference was that the Fischer 344 strain exhibited fewer reaches for each food pellet obtained, demonstrating greater reaching proficiency than similarly trained Long-Evans rats. These findings suggest that further research examining strain comparisons is required to understand the neural mechanisms underlying the differences in motor behaviour observed in these rat strains.
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Endocannabinoid Function in Hippocampal Synaptic Plasticity and Spatial Working MemoryBlaskovits, Farriss 12 September 2013 (has links)
Cannabis has been used medicinally for millennia, but the cannabinoid (CB) field exploded with the identification of its endogenous receptors and endocannabinoids (eCBs). In vitro experimentation established that eCBs alter synaptic plasticity at presynaptic nerve terminals; however, the characterization of the eCB system (ECS) in vivo remains incomplete. This study aimed to determine the mechanism of in vivo eCB-mediated hippocampal synaptic plasticity and
to analyze the effects this plasticity had on spatial working memory (SWM). With in vivo
recordings of field excitatory postsynaptic potentials (fEPSPs) in anesthetized mice and rats as well as pharmacological manipulation of the ECS and glutamate receptor antagonism, it was found that eCBs, both anandamide (AEA) and 2-arachnidonyl glycerol (2-AG), caused LTD at hippocampal CA3-CA1 synapses. Induction of eCB-LTD occurs via a sequential activation of
cannabinoid type-1 receptor (CB1R) and NR2B-containing NMDA receptor (NR2BR) and is
expressed through the endocytosis of AMPA receptors (AMPARs). Increased eCB tone also
caused an impairment of SWM for over 24 hours in the Delayed Non-Match-To-Sample (DNMTS) T-maze. This study provides the first evidence that an acute administration of eCB degradative enzyme inhibitors not only produces an in vivo LTD at hippocampal CA3-CA1
synapses that requires CB1R, NR2BR, and AMPAR, but also impairs SWM, a phenomenon also
caused by an acute injection of exogenous CBs.
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Activation of Sigma-1 Receptors Increases Expression, Trafficking, and Surface Levels of NMDA ReceptorsPabba, Mohan 16 April 2014 (has links)
Sigma-1 receptors (σ-1Rs) are chaperone-like proteins that are broadly distributed throughout the central nervous system and in other tissues. They have been implicated in several physiological and pathological processes, primarily by their ability to modulate certain voltage- and ligand-gated ion channels. Growing evidence suggests that σ-1Rs regulate the functions of ion channels, such as voltage-gated K+ 1.2 (Kv 1.2) and the human Ether-à-go-go-Related Gene (hERG) ion channels, by modulating their expression, trafficking, and targeting.
While it is well documented that σ-1Rs enhance the function of N-methyl-D-aspartate receptors (NMDARs), the mechanisms of this enhancement remain poorly understood. Using biochemical methods, we show that 90 minutes after intraperitoneal (i.p.) injection of σ-1R agonists such as (+)-SKF 10,047 (SKF) or (+)-Pentazocine (PTZ) (2 mg/kg), there is an increase in the expression of GluN2 subunits of NMDARs and postsynaptic density protein-95 (PSD-95) in the rat hippocampus. Following activation of σ-1Rs, co-immunoprecipitation (Co-IP) experiments reveal an increased interaction between σ-1Rs and NMDAR subunits; sucrose gradient centrifugation demonstrates an increase in the protein levels of GluN2 subunits in vesicular compartment; and biotinylation shows an increase in the surface levels of GluN2A-containing NMDARs.
Taken together, our results suggest σ-1Rs may enhance NMDARs function by increasing their expression, trafficking, and surface levels. This σ-1R-mediated increase in NMDAR expression and surface levels might be involved in several physiological processes such as learning and memory. Our findings also suggest that σ-1Rs could form a potential target for designing novel antipsychotics.
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The Nucleus of the Solitary Tract is Necessary for Apnea-induced Respiratory PlasticityTorontali, Zoltan 23 July 2012 (has links)
The respiratory system is attentive, adaptive, learns and has memory. The respiratory system remembers repeated respiratory challenges to fine tune its motor activity by modulating neuronal synaptic strength. This phenomenon, respiratory long term facilitation (LTF), functions to strengthen the ability of respiratory motor neurons to enhance contraction of breathing muscles. LTF could serve as a protective mechanism against obstructive sleep apnea, a disease characterized by the collapse of upper airways, by restoring upper airway patency. LTF can be induced through modulation of vagal afferent feedback via repeated apneas. Here, we used reverse microdialysis, electrophysiology, neuropharmacology, and histology to determine if the nucleus of the solitary tract (NTS), a brain region exclusively receiving vagal afferents, is the origin of the neural circuit responsible for apnea-induced plasticity. My work shows bilateral injection of 5% lidocaine into the NTS prevented LTF. We conclude the NTS is required for triggering apnea-induced LTF.
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The Nucleus of the Solitary Tract is Necessary for Apnea-induced Respiratory PlasticityTorontali, Zoltan 23 July 2012 (has links)
The respiratory system is attentive, adaptive, learns and has memory. The respiratory system remembers repeated respiratory challenges to fine tune its motor activity by modulating neuronal synaptic strength. This phenomenon, respiratory long term facilitation (LTF), functions to strengthen the ability of respiratory motor neurons to enhance contraction of breathing muscles. LTF could serve as a protective mechanism against obstructive sleep apnea, a disease characterized by the collapse of upper airways, by restoring upper airway patency. LTF can be induced through modulation of vagal afferent feedback via repeated apneas. Here, we used reverse microdialysis, electrophysiology, neuropharmacology, and histology to determine if the nucleus of the solitary tract (NTS), a brain region exclusively receiving vagal afferents, is the origin of the neural circuit responsible for apnea-induced plasticity. My work shows bilateral injection of 5% lidocaine into the NTS prevented LTF. We conclude the NTS is required for triggering apnea-induced LTF.
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Lateral buckling of beams with web holesLam, Cheuk-wing. January 1984 (has links)
No description available.
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Evolutionary consequences of growth-from plasticity in a red seaweed.Monro, Keyne, School of Biological, Earth & Environmental Sciences, UNSW January 2007 (has links)
Evolutionary processes in any population depend upon patterns of phenotypic variation available to selection and their underlying heritability. In this thesis, I used the filamentous red seaweed Asparagopsis armata, with particular focus on its modularity, to test several key questions underlying its growth-form evolution in heterogeneous environments. I established that experimental manipulations of light quantity and quality mimicking variation in underwater light due to shading or depth induce growthform plasticity in A. armata that may be evolutionarily significant given its variability among clones. Current patterns of plasticity displayed by A. armata appear adaptive, moreover, given that a reciprocal transplant of phenotypes between light environments found densely-branched (phalanx-like) phenotypes to have higher relative growth rates than sparsely-branched (guerrilla-like) phenotypes in well-lit patches, but lower relative growth rates than the latter in shaded patches. Using the capacity for rapid growth as a proxy for fitness, multivariate selection analyses identified environment-dependent patterns of directional selection on single traits coupled with linear and nonlinear selection on multi-trait combinations that shape growth-form variation within patches of differing light intensity, thereby reinforcing plasticity across light environments. Quantitative genetic analyses, however, suggest that the modular iteration of genes in morphogenesis may limit further growth-form evolution in A. armata populations exposed to spatial heterogeneity in light by constraining thallus responses to environment-dependent selection. Last, heritable responses to artificial selection on growth-form variation among clonal cell-lineages revealed the surprising capacity for A.armata to circumvent genetic constraints inherent to its development by adapting to environmental change in the absence of sexually-generated variance among clones.
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Exploring the functional plasticity of human glutathione transferases : allelic variants, novel isoenzyme and enzyme redesign /Johansson, Ann-Sofie. January 2002 (has links)
Diss. (sammanfattning) Uppsala : Univ., 2002. / Härtill 6 uppsatser.
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Modulation of neural plasticity by the ADAMTSs (a disintegrin and metalloproteinase with thrombospondin motifs) /Hamel, Michelle Grace. January 2006 (has links)
Dissertation (Ph.D.)--University of South Florida, 2006. / Includes bibliographical references (leaves 126-136). Also available online.
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A homogenization based continuum plasticity-damage model for ductile fracture of materials containing heterogeneitiesBai, Jie, January 2008 (has links)
Thesis (Ph. D.)--Ohio State University, 2008. / Title from first page of PDF file. Includes bibliographical references (p. 132-138).
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