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The effect of structural changes in perineuronal nets and deep cooling on synaptic plasticity and memory of tauopathy mice
Šafránková, Kristýna ; Růžička, Jiří (advisor) ; Telenský, Petr (referee)
Tauopathy is accompanied by both loss of neurons and synapses. The neuronal loss is irreversible with very low chance of functional replacement therapy. However, lost synapses could be restored with proper stimuli. Perineuronal nets (PNNs) are serving as a protecting barrier for neurons, on the other hand they are significantly decreasing the synaptic plasticity. Temporary disintegration of the PNNs by enzymatic therapy might lead to rewiring and accelerate processes of memory and learning. Model of Cold Induced plasticity leads to the withdrawal of significant number of synapses across the brain. The recovery of these could be followed in healthy and diseased animals. Moreover, it can stimulate Cold shock protein dependent neuroprotective mechanisms. This master thesis is focused on these two forms of synaptic plasticity models; forced remodeling of PNNs and model of cold induced synaptic plasticity. Both will serve as a tool to modulate processes of memory and learning in the P301S tauopathy, in mice. In detail, the work will follow changes in the number of synapses at the region of CA1 of hippocampus and synaptic protein levels at level of whole hippocampus and behavioral recovery of pre-trained long-term memory task dependent on dorsal hippocampus. Key words: Perineuronal nets, aggrecan,...
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The effect of structural changes in perineuronal nets and deep cooling on synaptic plasticity and memory of tauopathy mice
Šafránková, Kristýna ; Růžička, Jiří (advisor) ; Telenský, Petr (referee)
Tauopathy is accompanied by both loss of neurons and synapses. The neuronal loss is irreversible with very low chance of functional replacement therapy. However, lost synapses could be restored with proper stimuli. Perineuronal nets (PNNs) are serving as a protecting barrier for neurons, on the other hand they are significantly decreasing the synaptic plasticity. Temporary disintegration of the PNNs by enzymatic therapy might lead to rewiring and accelerate processes of memory and learning. Model of Cold Induced plasticity leads to the withdrawal of significant number of synapses across the brain. The recovery of these could be followed in healthy and diseased animals. Moreover, it can stimulate Cold shock protein dependent neuroprotective mechanisms. This master thesis is focused on these two forms of synaptic plasticity models; forced remodeling of PNNs and model of cold induced synaptic plasticity. Both will serve as a tool to modulate processes of memory and learning in the P301S tauopathy, in mice. In detail, the work will follow changes in the number of synapses at the region of CA1 of hippocampus and synaptic protein levels at level of whole hippocampus and behavioral recovery of pre-trained long-term memory task dependent on dorsal hippocampus. Key words: Perineuronal nets, aggrecan,...
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Central nervous system plasticity in adulthood and after injury.
Procházková, Natálie ; Jendelová, Pavla (advisor) ; Chmelová, Martina (referee)
Perineural nets are a structure of extracellular matrix, enwrapping several subpopulations of neurons in the central nervous system. Their formation is linked to the closure of critical period and significant plasticity restriction. In a healthy organism, they are important for stabilisation of mature nervous system, support of highly active neurons, and neuroprotection. However, they are one of the factors that restrict tissue regeneration during pathological conditions by participating in the formation of glial scar and upregulating molecules that have inhibitory impact on neuron sprouting. Digestion of perineuronal nets, which is mostly achieved enzymatically, leads to re-opening of critical period and renewal of plasticity, potentiating neuronal sprouting and growth and overall regeneration of central nervous system after mechanical damage, such as spinal cord injury, or during neurodegenerative diseases, as is Alzheimer's disease. Perineural nets play a similar role in Alzheimer's disease and aging, where they participate in memory loss. Renewal of plasticity in these conditions leads to facilitation of synaptic transmission and therefore eliminating the memory deficit. Key words: neurodegenerative diseases, CNS injury, Alzheimer's disease, perineural nets, chondroitinsulfate proteoglycans
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The role of link proteins in the stabilization of the brain extracellular matrix and in formation and maintaining of the perineuronal nets
Suchá, Petra ; Vargová, Lýdia (advisor) ; Jendelová, Pavla (referee)
The brain extracellular space (ECS) contains specified macromolecules forming the extracellular matrix (ECM), containing a high amount of negative charges that could bind water or other soluble ions and molecules diffusing within the ECS. In specific brain areas, the ECM molecules form a condensed, reticular-like structure of perineuronal nets (PNNs). It has been found that PNNs appear at the end of the critical period, when they stabilize the synapses and terminate their plasticity and may have also neuroprotective function. To study the role of brain link protein 2 (Bral2) in stabilizing the ECM complexes, we employed the real-time iontophoretic method and immunohistochemical analysis to show the difference in the ECS diffusion parameters and level of expression of the ECM molecules between the wild type and Bral2-deficient mice. We also compared changes in the ECS diffusion parameters induced by Bral2 deficiency with those appeared after enzymatic destruction of the ECM by the chondroitinase ABC (chABC). In the Bral2-deficient mice, we discovered significantly decreased values of tortuosity in the trapezoid body. This difference was age related and did not manifest itself in young mice. Immunohistochemical analysis showed that inferior colliculus does not contain Bral2-brevican based...
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