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Title: Gene expression underlying experience dependent plasticity in the mouse barrel cortex
Author: Abraham, Richard
Awarding Body: Cardiff University
Current Institution: Cardiff University
Date of Award: 2005
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Throughout the life of an organism the synaptic connections that link neurons are in a constant state of flux, being strengthened and weakened in response to external stimuli. This plasticity provides the central nervous system with a means of adaptability, allowing it to respond to changes in the external environment and is believed to underlie the processes of learning and memory (Lynch, 2004). Neuronal plasticity can be studied using the paradigm of vibrissal deprivation in rodents (Fox, 2002). The mystacial vibrissae are represented in layer IV of the somatosensory cortex by clusters of neurons, termed barrels, in which the majority of neurons are responsive to stimulation of only the corresponding vibrissae (Woolsey and Van der Loos, 1970). The deprivation of the vibrissae results in a shift in responsiveness of neurons in deprived barrels to stimulation of surrounding spared vibrissae, and potentiation of responses of neurons in spared barrels to stimulation of the corresponding (principal) vibrissae ie experience dependent plasticity (Fox, 1992, Simons and Land, 1987). It had previously been shown that, like other plasticity paradigms, gene transcription, mediated by the cyclic AMP Response Element Binding Protein (CREB), is associated with experience-dependent plasticity in the mouse barrel cortex (Barth et al., 2000). The finding that upregulation of a reporter gene, under the transcriptional control of CREB, following vibrissal deprivation conditions that induce plasticity, has been complementated with studies showing that deletion of CREB impairs plasticity in the barrel cortex (Glazewski et al., 1999). Using microarray technology, this study analysed the changes in expression of endogenous genes to vibrissal deprivation patterns that induce neuronal plasticity. It was found that significant upregulation of a sub-set of plasticity related genes (PRGs) occurs, as in CRE reporter gene studies, early in the time course of deprivation that leads to plasticity. Real-Time PCR has confirmed the upregulation of a number of these genes. Functional analysis has identified a significant over-representation of genes involved in protein synthesis from the group of PRGs. Further to this three of the PRGs have been identified as candidate plasticity genes in a number of paradigms. The products of these genes are key components of the extracellular matrix. This suggests that modifications to this fundamental part of the central nervous system may be the mechanism that results in experience dependent plasticity in the mouse barrel cortex.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available