Assessing the Effect of Neuronal Calcium Dyshomeostasis on Sleep Using a Transgenic Mouse Model
Sleep is an important of our daily routine; in fact, humans spend 1/3 of their day sleeping. Indeed, sleep is pivotal for neuronal survival and function, including learning and memory, by mediating the conversion of newly acquired information during wakefulness into long-term memory. In mammals, there are two states of sleep; the dream-occurring rapid eye-movement (REM) sleep, and the deep-sleep state, namely non-rapid eye-movement (NREM) sleep. These two states cyclically alternate during sleep, creating a distinct pattern. Notably, it is thought that the interaction of neuronal calcium (Ca2+) and potassium (K+) currents in the thalamus gives rise to the oscillations that generate the sleep spindles that promote NREM sleep. Considering that a constellation of intricate molecular pathways is involved in sleep regulation, disruption in any of these processes could elicit sleep deficits, which are typically observed in different neuropsychiatric disorders, including ADHD, schizophrenia, and autistic spectrum disorders. Despite the vast investigation on sleep architecture and its components, the neurobiology of sleep is not completely defined yet, and it remains a hot topic for debate among neuroscientists. Our group has identified a novel Ca2+-regulating protein expressed in the brain and we are demonstrating for the first time its implication in regulating sleep, using a gentically modified mouse strain. In the context of this presentation we will demonstrate overwhelming data derived from state-of-the-art electroencephalography (EEG)-based polysomnography, to support the pivotal role of this novel protein in the neurobiology of sleep.
Primary Advisor's Department
Stander Symposium Posters, College of Arts and Sciences
United Nations Sustainable Development Goals
Good Health and Well-Being
"Assessing the Effect of Neuronal Calcium Dyshomeostasis on Sleep Using a Transgenic Mouse Model" (2020). Stander Symposium Projects. 1882.