Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.778865
Title: An exploration into the link between brain rhythms and synaptic plasticity in health and infectious disease
Author: Hartnell, Iain
ISNI:       0000 0004 7964 5900
Awarding Body: University of York
Current Institution: University of York
Date of Award: 2018
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Abstract:
During wakefulness, synapses are strengthened to enable memory formation. Whereas, during sleep, weaker connections are 'pruned' to help consolidate memories. These synaptic alterations are related to cortical oscillations, which are generally faster during wakefulness (30-80Hz, gamma), and slower during deep sleep (1-4Hz, delta). Synaptic strength is thought to decrease during delta rhythms (compared to gamma rhythms). Neuroinflammation can disturb these brain rhythms and lead to a decline in cognitive function, which may result from aberrations in synaptic plasticity. To test the laminar and cellular changes in synaptic plasticity during sleep- and wake-related oscillations, in vitro electrophysiology and immunofluorescence were employed using acute rat neocortical slices. To examine the effect of neuroinflammation on these brain states, systemic infection was induced using synthetic analogues of pathogenic bacterial and viral material, and a biological parasitic disease model. The expression of an immediate early gene (IEG) marker of neuronal plasticity (Arc) was higher during delta oscillations compared to gamma oscillations and was concentrated to mid-apical dendrite bundles from layer V intrinsically bursting cells. These bundles represented cortical microcolumns which are known to exhibit synchronous activity, allowing parallel processing of information. Increased Arc expression in these columns during delta oscillations may promote synaptic rescaling and highlights the role of cortical microcolumns in memory consolidation. A balance of pro- and anti-inflammatory cytokines was found after short term systemic infection which gave way to a predominately pro-inflammatory state when the infection was longer term. The oscillatory activity also changed, with a continued decline in gamma power. However, delta power increased short term but decreased with a longer infection. The systemic infection had no effect on cortical plasticity. These results were corroborated in a mouse model of Leishmaniasis and show that systemic infection alters neuronal communication by changes to oscillatory activity, but does not change synaptic plasticity levels.
Supervisor: Whittington, Miles ; Chawla, Sangeeta ; Randall, Fiona Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.778865  DOI: Not available
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