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dc.contributor.authorKuo, Min-Chingen
dc.date2010-04-29 14:02:30.742
dc.date.accessioned2010-04-29T19:18:57Z
dc.date.available2010-04-29T19:18:57Z
dc.date.issued2010-04-29T19:18:57Z
dc.identifier.urihttp://hdl.handle.net/1974/5620
dc.descriptionThesis (Ph.D, Psychology) -- Queen's University, 2010-04-29 14:02:30.742en
dc.description.abstractRecent evidence indicates that the mature neocortex retains a higher degree of plasticity than traditionally assumed. Up- and down-regulation of synaptic strength, long-term potentiation (LTP) and long-term depression (LTD), is thought to be the primary mechanism mediating experience-dependent plasticity of cortical networks. The present thesis investigate factors that regulate adult cortical plasticity, focusing on the role of neuromodulators, recent sensory experience, and different anatomical divisions of the cortex in influencing synaptic strength. First, I investigated the role of the neuromodulator histamine in gating plasticity in the primary visual cortex (V1) of urethane anesthetized adult rats. Histamine applied locally in V1 produced an enhancement of LTP elicited by theta burst stimulation (TBS) of dorsal lateral geniculate nucleus (dLGN) and allowed a sub-threshold TBS to produce stable LTP. Second, the impact of visual deprivation on LTP in V1 was assessed. Animals that received 2 and 5 hr dark exposure showed greater potentiation of field potentials when stimulated though retinal light flashes or weak TBS of the dLGN, which failed to induce LTP in control animals kept in continuous light. Third, I performed a detailed characterization of LTP induced by different TBS protocols, recording in either the monocular or binocular segment of both V1 hemispheres (i.e., ipsi- and contralateral to the stimulated dLGN). Stronger, NMDA receptor-independent LTP was found in the contralateral V1. Interestingly, weak TBS induced LTD that was NMDA receptor-dependent in the ipsilateral V1. Furthermore, a lower LTP induction threshold was observed in the binocular than the monocular segment of ipsilateral V1. Lastly, I investigated cholinergic modulation of sensory-induced activity in the barrel cortex. Basal forebrain stimulation enhanced multi-unit activity elicited by whisker deflection, an effect that was more pronounced for weaker response driven by a secondary whisker than principal whisker deflection. This thesis demonstrates that neocortical plasticity consists of multiple forms of synaptic modification. Adult cortical plasticity is greatly influenced by preceding activity of the synapse by various neuromodulator systems, and by anatomical subdivisions within primary sensory cortex fields. Together, these mechanisms may facilitate the detection, amplification, and storage of inputs to primary sensory fields of the neocortex.en
dc.language.isoengen
dc.relation.ispartofseriesCanadian thesesen
dc.rightsThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.en
dc.subjectAdult neocortical plasticityen
dc.subjectLong term potentiationen
dc.subjectLong term depressionen
dc.subjectVisual cortexen
dc.subjectBarrel Cortexen
dc.subjectNMDA receptoren
dc.subjectNeurotransmitteren
dc.subjectHistamineen
dc.subjectAcetylcholineen
dc.subjectSensory deprivationen
dc.titleRegulators of Sensory Cortical Plasticity by Neuromodulators and Sensory Experienceen
dc.typethesisen
dc.description.degreePhDen
dc.contributor.supervisorDringenberg, Hans C.en
dc.contributor.departmentPsychologyen
dc.degree.grantorQueen's University at Kingstonen


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