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Full-Text Articles in Neuroscience and Neurobiology
Circadian Rhythmicity And Neurodevelopment Of Disco And Grim Mutations In Drosophila Melanogaster, John Patrick Story
Circadian Rhythmicity And Neurodevelopment Of Disco And Grim Mutations In Drosophila Melanogaster, John Patrick Story
EURēCA: Exhibition of Undergraduate Research and Creative Achievement
The death gene grim and its pathway for apoptosis has been studied extensively in Drosophila Melanogaster. The effects of grim mutations on circadian neurodevelopment and locomotor assays have yet to be investigated. Mutations in the gene disconnected (disco) has been shown to disrupt the normal development of the circadian circuitry, specifically the small ventro-lateral neurons (s-LNv’s). Which has shown to severely decrease rhythmicity during free-running periods. Alternatively, we have observed an increase in rhythmicity during free-running periods in grim mutations. Our goal is to investigate the neurodevelopment of the circadian circuitry and their associated locomotor activities in these Drosophila mutations.
Acute Social Defeat-Induced Neuroinflammation In The Vmpfc Of Syrian Hamsters Via Microglial Activation, Thomas Clarity
Acute Social Defeat-Induced Neuroinflammation In The Vmpfc Of Syrian Hamsters Via Microglial Activation, Thomas Clarity
EURēCA: Exhibition of Undergraduate Research and Creative Achievement
Research suggests causal relationships between neuroinflammation and stress-related psychopathologies. Exposure to moderate or chronic psychological stress in rodents leads to increased activation of microglia, the brain’s resident immune cells. The ventral medial prefrontal cortex (vmPFC) is a key limbic region involved in top-down regulation of psychological stress and mediates the deleterious effects of microglial activity following prolonged restraint stress. While there is a growing body of literature indicating that chronic social defeat increases microglial activity in the vmPFC, there has been little research investigating the effects of acute social defeat stress. Here, we used an acute social defeat paradigm in …
The Neural Circuitry Of Sweaty Palms: A Neuroimaging Meta-Analysis, Sydnie Colette Toler, Derek C. Wenger
The Neural Circuitry Of Sweaty Palms: A Neuroimaging Meta-Analysis, Sydnie Colette Toler, Derek C. Wenger
EURēCA: Exhibition of Undergraduate Research and Creative Achievement
Emotion and cognitive processes often cause autonomic nervous system responses. A common example is when the palms of your hands become sweaty before giving a speech or when a police officer is driving behind you. Increased sweat on the palms is a marker of sympathetic nervous system (SNS) activity. The aim of this study was to identify networks of brain activity that make our palms sweat. We compiled a list of neuroimaging studies that report brain activity associated with palm sweat. Our search resulted in sixteen studies, comprised of 251 participants. We used activation likelihood estimation analysis to determine nonrandom …
Acute Social Defeat Stress Induces Microglial Activation In Key Limbic Regions, Thomas Clarity
Acute Social Defeat Stress Induces Microglial Activation In Key Limbic Regions, Thomas Clarity
EURēCA: Exhibition of Undergraduate Research and Creative Achievement
Research suggests a causal relationship between neuroinflammation and stress-related psychopathologies. Exposure to moderate psychological stress in rodent models leads to elevated markers of immune activity in the brain, for example, microglia. Research has shown that tail shock stress can prime the subsequent, immune-challenged activation of microglia, which can lead to a degradative, proinflammatory response. Although social defeat is an ethologically relevant model of acute stress, there has been little research investigating the effects of acute social defeat stress on immune activity. Here, we used an acute social defeat paradigm in Syrian hamsters consisting of three, 5-minute aggressive encounters in the …
Circadian Rhythmic Localization Of Tpa And Pai-1 In The Scn 2.2 Cell Culture May Provide Evidence For Determining The Mechanism Of Gating Photic Phase Shifts, Grayson T Hunley
Circadian Rhythmic Localization Of Tpa And Pai-1 In The Scn 2.2 Cell Culture May Provide Evidence For Determining The Mechanism Of Gating Photic Phase Shifts, Grayson T Hunley
EURēCA: Exhibition of Undergraduate Research and Creative Achievement
Mammalian circadian rhythms are controlled by a central pacemaker located in the suprachiasmatic nucleus (SCN) of the brain. The SCN exhibits endogenous rhythms in neuronal activity and entrains to external stimuli, particularly light. Interestingly, phase shifts in response to light only occur at night and the mechanisms gating phase shifting are not well characterized. Our lab demonstrated that the extracellular protease, tissue-type plasminogen activator (tPA) and its inhibitor, plasminogen activator inhibitor (PAI-1), help gate phase shifting. Total tPA and PAI-1 expression are rhythmic in mouse SCN. These proteins mediate different functions depending on their exact subcellular localization. Therefore, knowing where …