Wildering, WicNelson, Mark A.2013-01-212013-06-152013-01-212013http://hdl.handle.net/11023/440Aging 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.engUniversity of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.Animal PhysiologyNeuroscienceZoologyNeuroscienceAgingLymnaea stagnalisExcitabilityVoltage-gated potassium currentsFrequency-dependent spike broadeningLearning and memorySenescenceLipid peroxidationVitamin Emaster thesis10.11575/PRISM/27081