Abstract
In this work, we introduce the kinetic framework for modelling synaptic transmission in an existing neural mass model of the thalamocortical circuitry to study Electroencephalogram (EEG) slowing within the alpha frequency band (8–13 Hz), a hallmark of Alzheimer’s disease (AD). Ligand-gated excitatory and inhibitory synapses mediated by AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and GABAA (gamma-amino-butyric acid) receptors respectively are modelled. Our results show that the concentration of the GABA neurotransmitteracts as a bifurcation parameter, causing the model to switch from a limit cycle mode to a steady state. Further, the retino-geniculate pathway connectivity plays a significant role in modulating the power within the alpha band, thus conforming to research proposing ocular biomarkersin AD. Overall, kinetic modelling of synaptic transmission in neural mass models has enabled a more detailed investigation into the neural correlates underlying abnormal EEG in AD.
Original language | English |
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Title of host publication | Unknown Host Publication |
Publisher | Springer |
Pages | 645-652 |
Number of pages | 8 |
Publication status | Published (in print/issue) - 2012 |
Event | International Conference on Artificial Neural Networks (ICANN) - Duration: 1 Jan 2012 → … |
Conference
Conference | International Conference on Artificial Neural Networks (ICANN) |
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Period | 1/01/12 → … |
Keywords
- neural modelling
- alzheimer's disease
- alpha rhythm
- synaptic function