Neurobiological Substrates of Age-Associated Decline in Neuronal Excitability - Lipid Peroxidation-Dependent Modulation of Transient Potassium Current Inactivation?
Accessioned
2013-01-21T20:40:24ZAvailable
2013-06-15T07:01:45ZIssued
2013-01-21Submitted
2013Classification
NeuroscienceAging
Lymnaea stagnalis
Excitability
Voltage-gated potassium currents
Frequency-dependent spike broadening
Learning and memory
Senescence
Lipid peroxidation
Vitamin E
Subject
Animal PhysiologyNeuroscience
Zoology
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Abstract
Aging is a universal phenomenon that is observed in almost all organisms within the animal kingdom, yet the biological substrates that underlie the onset and progression of aging are not entirely understood. While aging produces dysfunction in all organ systems, aging of the nervous system can result in severe consequences including age-associated cognitive impairment and deficiencies in learning and memory formation. Long term memory formation often involves repetitive, high frequency periods activity and therefore is affected by electrophysiological properties of the nervous system, including neuronal excitability: excitability of the nervous system declines with age and this may contribute to age-associated cognitive dysfunction. This thesis will investigate age-associated intrinsic neuronal excitability decline in the model system Lymnaea stagnalis, investigate the ionic mechanisms underlying this dysfunction with a focus on voltage gated potassium channels, and seek to implicate oxidative stress and lipid peroxidation with the aging process in these neurons.Citation
Nelson, M. A. (2013). Neurobiological Substrates of Age-Associated Decline in Neuronal Excitability - Lipid Peroxidation-Dependent Modulation of Transient Potassium Current Inactivation? (Unpublished master's thesis). University of Calgary, Calgary, AB. doi:10.11575/PRISM/27081Collections
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