Browsing by Subject "hippocampus"
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(2023)Temporal lobe epilepsy (TLE), a condition defined by unprovoked and recurrent seizures originating from the temporal lobe, is among the most ubiquitous of the various forms of epilepsy. Despite being chronic and highly prevalent, the available treatment options concerning the same remains a critical issue. Since the current therapeutic condition of epilepsy requires more development, renewed focus studying its molecular mechanisms and therapies is imminent. One of the longstanding theories trying to decode the molecular perturbations in TLE has been deficits in GABAergic inhibition resulting in abnormal neuronal activation. K+ - Cl- co-transporter (KCC2) activity is vital for maintaining a hyperpolarizing GABA response. The past decades have intimately and causally linked the prognosis of the seizures observed in TLE with deficits in KCC2 functioning. However, the precise mechanisms relevant to the disruption of KCC2 activity are still blurry. Here we show how KCC2 de-stabilization/localization in the neuronal bilayer is a characteristic of epileptic animal tissue. With the help of co-immunoprecipitation assays, western blot, and mass spectrometry, we found that in normal healthy brain tissue, GM1 ganglioside present in the membrane has specific and direct interactions with the KCC2 cotransporter. However, in the pilocarpine model of TLE, the interaction of this complex was significantly disturbed, primarily in the hippocampus and to some extent in the cortex. Our results act as an extension to previous research which stated that the structural association of the KCC2 clusters with neuronal lipid rafts is crucial for the functionality of the KCC2 cotransporter. Having learned about the unique nature of the pathophysiology of TLE, it is imminent to note that additional research in the direction of studying its biochemical pathways is required. The findings of this experimental study support the claim that KCC2 and GM1 as a complex are closely associated in the epileptic conditions and hence, this research paves the way to further explore the role of KCC2 and GM1 as a consequential complex in the pathophysiology of TLE.
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(2024)Faculty: Faculty of Biological and Environmental Sciences Degree programme: Master’s Programme in Neuroscience Study track: Neuroscience track Author: Ariel Olivia Vasques Ojeda Title: The effects of sleep disruption on sleep architecture and microglial morphology Level: Master’s thesis Month and year: May 2024 Number of pages: 50 pages Keywords: Sleep disruption, microglia, frontal cortex, adolescents, older mice, EEG, microglial morphology, hippocampus Supervisor or supervisors: Birgitte Rahbek Kornum, Christine Egebjerg Jensen Where deposited: University of Helsinki library Additional information: Abstract: Although sleep is an essential biological need for all beings, we have yet to understand why exactly it is a crucial aspect of our lives. The loss of sleep is seen as a natural occurrence that increases as we begin to age. The consequences of sleep deprivation are not yet fully understood but have been associated with a range of detrimental effects on comorbid conditions, including reduced quality of life, cognitive impairments, immune suppression, and various other adverse outcomes. The role of microglia in response to sleep deprivation is a discussion that is also yet to be understood, but that can be a pivotal point for future understanding. This master's thesis investigates the impact of sleep deprivation on sleep architecture in aged mice and microglial activation in adolescents. The study aims to understand how sleep disruption affects these age groups, focusing on microglial morphology and overall sleep patterns. Using EEG/EMG recordings, sleep disruption was induced by introducing novel objects for four hours daily at ZT 2-6 over seven days. The study found that older mice experienced a shift in their sleep patterns, with significant changes in NREM and REM sleep occurring during the dark phase, highlighting the influence of the circadian rhythm. In adolescent mice, sleep disruption led to increased morphological changes, suggesting a reduction in microglial activity or an intermediary state of activation. The results underscore the importance of sleep in maintaining neural homeostasis and highlight age-dependent differences in the response to sleep loss. The study discusses the implications of these findings for understanding the neurobiological mechanisms underlying sleep and its disruption, particularly in relation to microglial function and brain health.
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