Matching Items (40)

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A Review of Podcast Impact and Implications for Education and Beyond

Description

The world of podcasting has exploded in popularity in recent years. This medium is being used in education as well as in the public sector to share ideas, news, and

The world of podcasting has exploded in popularity in recent years. This medium is being used in education as well as in the public sector to share ideas, news, and stories. This paper reviews the research behind podcast success as a news form and in the educational sector and the implications of these findings for the future. Podcast listeners tend to listen to podcasts for entertainment and, notably, to diversify their time while completing other tasks. New ways to directly stream media from portable devices and advances in the internet have helped bolster the popularity of this media form. Podcasting proved to be successful in higher education as students tended to perform better when given access to podcasts. However, they were only successful when using podcasts as classroom adjuncts. This implies that educational podcasts must be produced differently than ones intended for the public. By reviewing the neuroscience behind language, emotion and memory, it was found that narrative formats that also evoked emotions had a positive ability in enhancing the listeners learning and memory. Keeping this in mind, the developed podcast aimed to bridge educational material to the general public by utilizing narrative as a vessel in which to deliver complex information about medicine, science and neuroscience. The accessibility and virtually non-existent barriers to the podcasting world offer a breadth of knowledge and opinions that have numerous factors of social influence. The impact of podcasting on the modern world deserves more research in sociology and psychology as it continues to grow in popularity.

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Date Created
  • 2019-05

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Hyperactive ERK/MAPK Regulates Cortical GABAergic Neuron Development

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Aberrant signaling through the canonical RAS/RAF/MEK/ERK (ERK/MAPK) pathway leads to the pathology of a group of neurodevelopmental disorders called RASopathies. RASopathies are caused by germline mutations in the ERK/MAPK pathway

Aberrant signaling through the canonical RAS/RAF/MEK/ERK (ERK/MAPK) pathway leads to the pathology of a group of neurodevelopmental disorders called RASopathies. RASopathies are caused by germline mutations in the ERK/MAPK pathway and have an incidence of approximately 1:2000 births. The majority of RASopathies stem from mutations that cause gain-of-function in the ERK/MAPK pathway. In this study, we have begun to unravel the roles that GABAergic interneurons play in the pathology of RASopathies. Our data demonstrate that gain-of-function ERK/MAPK signaling expressed in a GABAergic interneuron-specific fashion leads to forebrain hyperexcitability in mutant mice. Further, some GABAergic interneurons experience activated-caspase 3 mediated apoptosis in the embryonic subpallium, leading to a loss of PV-expressing interneurons in the somatosensory cortex. We found that pharmaceutical intervention during embryogenesis using a MEK1 inhibitor may be effective in preventing apoptosis of these neurons. Future work is still needed to understand the mechanism of the death of GABAergic interneurons and to further pursue therapeutic approaches. Taken together, this study suggests potential roles of cortical GABAergic interneurons in ERK/MAPK-linked pathologies and indicates possible approaches to provide therapy for these conditions.

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Date Created
  • 2019-05

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Elucidating the Effects of PRAS40 on Learning and Memory

Description

The mammalian target of rapamycin (mTOR) is integral in regulating cell growth as it maintains a homeostatic balance of proteins by modulating their synthesis and degradation. In the brain, mTOR

The mammalian target of rapamycin (mTOR) is integral in regulating cell growth as it maintains a homeostatic balance of proteins by modulating their synthesis and degradation. In the brain, mTOR regulates protein-driven neuroplastic changes that modulate learning and memory. Nevertheless, upregulation of mTOR can cause detrimental effect in spatial memory and synaptic plasticity. The proline-rich Akt-substrate 40 kDa (PRAS40) is a key negative regulator of mTOR, as it binds mTOR and directly reduces its activity. To investigate the role of PRAS40 on learning and memory, we generated a transgenic mouse model in which we used the tetracycline-off system to regulate the expression of PRAS40 specifically in neurons of the hippocampus. After induction, we found that mice overexpressing PRAS40 performed better than control mice in the Morris Water Maze behavioral test. We further show that the improvement in memory was associated with a decrease in mTOR signaling, an increase in dendritic spines in hippocampal pyramidal neurons, and an increase in the levels of brain-derived neurotrophic factor (BDNF), a neurotrophin necessary for learning and memory. This is the first evidence that shows that increasing PRAS40 in the mouse brain enhances learning and memory deficits.

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  • 2018-05

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Stress and Biological Pathways of Schizophrenia: EGR3 Dependent HTR2A Expression in Response to Sleep Deprivation

Description

Environmental and genetic factors contribute to schizophrenia etiology, yet few studies have demonstrated how environmental stimuli impact genes associated with the disorder. Immediate early genes (IEGs) are of great interest

Environmental and genetic factors contribute to schizophrenia etiology, yet few studies have demonstrated how environmental stimuli impact genes associated with the disorder. Immediate early genes (IEGs) are of great interest to schizophrenia research because they are activated in response to physiological stress from the environment, and subsequently regulate the expression of downstream genes that are essential to neuropsychiatric function. An IEG, early growth response 3 (EGR3) has been identified as a main gene involved in a network of transcription factors implicated in schizophrenia susceptibility. The serotonin 2A receptor (5-HT2AR) seems to play an important role in schizophrenia and the dysfunction of the 5-HT2AR encoding gene, HTR2A, within the prefrontal cortex (PFC) contributes to multiple psychiatric illnesses including schizophrenia. EGR3's role as a transcription factor that is activated by environmental stimuli suggests it may regulate Htr2a transcription in response to physiological stress, thus affecting 5-HT2AR function in the prefrontal cortex (PFC). The aim of this study was to examine the relationship between Egr3 activation and Htr2a expression after an environmental stimulus. Sleep deprivation is an acute physiological stressor that activates Egr3. Therefore to examine the relationship between Egr3 and Htr2a expression after an acute stress, wild type and Egr3 knockout mice that express EGFP under the control of the Htr2a promoter were sleep deprived for 8 hours. We used immunohistochemistry to determine the location and density of Htr2a-EGFP expression after sleep deprivation and found that Htr2a-EGFP expression was not affected by sex or subregions of the PFC. Additionally, Htr2a-EGFP expression was not affected by the loss of Egr3 or sleep deprivation within the PFC. The LPFC subregions, layers V and VI showed significantly more Htr2a-EGFP expression than layers I-III in all animals for both sleep deprivation and control conditions. Possible explanations for the lack of significant effects in this study may be the limited sample size or possible biological abnormalities in the Htr2a-EGFP mice. Nonetheless, we did successfully visualize the anatomical distribution of Htr2a in the prefrontal cortex via immunohistochemical staining. This study and future studies will provide insight into how Egr3 activation affects Htr2a expression in the PFC and how physiological stress from the environment can alter candidate schizophrenia gene function.

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Date Created
  • 2014-05

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The Combined Effects of Methamphetamine and Alcohol on Brain Reward Function as Assessed Using Intracranial Self-Stimulation

Description

Polysubstance abuse is far more common than single substance abuse. One of the most widely abused, yet greatly understudied combination of drugs is the simultaneous use of methamphetamine (meth) and

Polysubstance abuse is far more common than single substance abuse. One of the most widely abused, yet greatly understudied combination of drugs is the simultaneous use of methamphetamine (meth) and alcohol. Because little research has been conducted on the co-abuse of meth and alcohol, it is important to study the behavioral and neural mechanisms underlying the use of both to combat addiction and come closer to finding an effective treatment of this form of drug abuse. This study uses a rodent model to attempt to identify the mechanisms underlying this co-abuse through the stimulation of the medial forebrain bundle (MFB) and thus the activation of the mesocorticolimbic pathway, the brain's pleasure circuit. First, self-stimulation thresholds (the lowest electrical current the rats are willing to respond for) were determined using a process called Discrete Trials Training. This threshold was later used as a baseline measure to reference when the rats were administered the drugs of abuse: meth and alcohol, both alone and in combination. Our overall results did not show any significant effects of combining alcohol and meth relative to the effects of either drug alone, although subject attrition may have resulted in sample sizes that were statistically underpowered. The results of this and future studies will help provide a clearer understanding of the neural mechanisms underlying the polyabuse of meth and alcohol and can potentially lead to more successfully combating and treating this addiction.

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  • 2016-12

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Assessing the Role of the Transcription Factor EGR3 in Activity-Induced DNA Damage Response

Description

Immediate early genes (IEGs) are rapidly activated in response to an environmental stimulus, and most code for transcription factors that mediate processes of synaptic plasticity, learning, and memory. EGR3, an

Immediate early genes (IEGs) are rapidly activated in response to an environmental stimulus, and most code for transcription factors that mediate processes of synaptic plasticity, learning, and memory. EGR3, an immediate early gene transcription factor, is a mediator of biological processes that are disrupted in patients with schizophrenia (SCZ). A microarray experiment conducted by our lab revealed that Egr3 also regulates genes involved in DNA damage response. A recent study revealed that physiological neuronal activity results in the formation of DNA double-stranded breaks (DSBs) in the promoters of IEGs. Additionally, they showed that these DSBs are essential for inducing the expression of IEGs, and failure to repair these DSBs results in the persistent expression of IEGs. We hypothesize that Egr3 plays a role in repairing activity- induced DNA DSBs, and mice lacking Egr3 should have an abnormal accumulation of these DSBs. Before proceeding with that experiment, we conducted a preliminary investigation to determine if electroconvulsive stimulation (ECS) is a reliable method of inducing activity- dependent DNA damage, and to measure this DNA damage in three subregions of the hippocampus: CA1, CA3, and dentate gyrus (DG). We asked the question, are levels of DNA DSBs different between these hippocampal subregions in animals at baseline and following electroconvulsive stimulation (ECS)? To answer this question, we quantified γ-H2AX, a biomarker of DNA DSBs, in the hippocampal subregions of wildtype mice. Due to technical errors and small sample size, we were unable to substantiate our preliminary findings. Despite these shortcomings, our experimental design can be modified in future studies that investigate the role of Egr3 in activity-induced DNA damage repair.

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Date Created
  • 2020-05

A Methodology for Determining the Dendritic Complexity of Hippocampal Neurons in Chronically Stressed Rats

Description

Chronic stress is a risk factor for many diseases that impact the brain, including Alzheimer’s Disease. Unlike acute stress, chronic stress reduces neuronal plasticity, which can lead to neuronal remodeling

Chronic stress is a risk factor for many diseases that impact the brain, including Alzheimer’s Disease. Unlike acute stress, chronic stress reduces neuronal plasticity, which can lead to neuronal remodeling and suppression. This project investigates the effect of stress on the dendritic complexity of hippocampal neurons in rats, demonstrating a methodology for procuring and analyzing these neurons. The brains of the 160 rats from the Sustained Threat and Timing (STAT) experiment were frozen. The STAT experiment investigated the effect chronic variable stress had on prospective and retrospective timing in rodents. Using a cryostat, thin coronal slices of brain tissue were placed on microscopic slides. The tissue samples were then stained using the Golgi method of silver staining. Hippocampal neurons were assessed using Sholl Analysis; the dendritic complexity of these neurons was quantified. The method of using Sholl Analysis was found to be an effective process in measuring dendritic length of hippocampal neurons.

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Date Created
  • 2020-05

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Assessing the Use of Electroconvulsive Stimulation to Induce DNA Damage in the Hippocampus

Description

Damage to DNA can affect the genes it encodes; if this damage is not repaired, abnormal proteins may be produced and cellular functions may be disturbed. DNA damage has been

Damage to DNA can affect the genes it encodes; if this damage is not repaired, abnormal proteins may be produced and cellular functions may be disturbed. DNA damage has been implicated in the initiation and progression of a variety of diseases. Conversely, DNA damage has also been discovered to contribute to beneficial biological processes. Madabhushi and colleagues (2015) determined that activity-dependent DNA double strand breaks (DSBs) in the promoter region of immediate early genes (IEGs) induced their expression. EGR3 is an IEG transcription factor which regulates the expression of growth factors and synaptic plasticity-associated genes. In a previously conducted microarray experiment, it was revealed that EGR3 regulates the expression of genes associated with DNA repair such as Cenpa and Nr4a2. These findings inspired us to investigate if EGR3 affects DNA repair in vivo. Before conducting this experiment, we sought to standardize and optimize a method of inducing DNA damage in the hippocampus. Electroconvulsive stimulation (ECS) is utilized to induce neuronal activity. Since neuronal activity leads to the formation of DNA DSBs, we theorized that ECS could be used to induce DNA DSBs in the hippocampus. We predicted that mice that receive ECS would have more DNA DSBs than those that receive the sham treatment. Gamma H2AX, a biomarker for DNA damage, was utilized to quantify DNA DSBs. Gamma H2AX expression in the dentate gyrus, CA1 and CA3 regions of the hippocampus was compared between mice that received the sham treatment and mice that received ECS. Mice that received ECS were sacrificed either 1 or 2 hours post-administration, constituting treatment conditions of 1 hr post-ECS and 2 hrs post-ECS. Our results suggest that ECS has a statistically significant effect exclusively in the CA1 region of the hippocampus. However, our analyses may have been limited due to sample size. A power analysis was conducted, and the results suggest that a sample size of n=4 mice will be sufficient to detect significant differences across treatments in all three regions of the hippocampus. Ultimately, future studies with an increased sample size will need to be conducted to conclusively assess the use of ECS to induce DNA damage within the hippocampus.

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  • 2020-05

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Investigation of Sniffing as a Viable Measure of Odor Habituation in Mice

Description

Mammalian olfaction relies on active sniffing, which both shapes and is shaped by olfactory stimuli. Habituation to repeated exposure of an olfactory stimuli is believed to be mediated by decreased

Mammalian olfaction relies on active sniffing, which both shapes and is shaped by olfactory stimuli. Habituation to repeated exposure of an olfactory stimuli is believed to be mediated by decreased sniffing; however, this decrease may be reserved by exposure to novel odorants. Because of this, it may be possible to use sniffing itself as a measure of novelty, and thus as a measure of odorant similarity. Thus, I investigated the use of sniffing to measure habituation, cross-habituation, and odorant similarity. During habituation experiments, increases in sniff rate seen in response to odorant presentation decreased in magnitude between the first and second presentations, suggesting of habituation. Some of this reduction in sniff rate increases was revered by the presentation of a novel odorant in cross-habituations. However the effect sizes in cross-habituation experiments were low, and the variability high, forestalling the conclusion that sniffing accurately measured cross-habituation. I discuss improvements to the experimental protocol that may allow for cross-habituation to be more accurately measured using sniffing alone in future experiments.

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Date Created
  • 2015-12

Joint Action Produces Super Mirror Neurons

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Abstract: Behavioral evidence suggests that joint coordinated movement attunes one's own motor system to the actions of another. This attunement is called a joint body schema (JBS). According to the

Abstract: Behavioral evidence suggests that joint coordinated movement attunes one's own motor system to the actions of another. This attunement is called a joint body schema (JBS). According to the JBS hypothesis, the attunement arises from heightened mirror neuron sensitivity to the actions of the other person. This study uses EEG mu suppression, an index of mirror neuron system activity, to provide neurophysiological evidence for the JBS hypothesis. After a joint action task in which the experimenter used her left hand, the participant's EEG revealed greater mu suppression (compared to before the task) in her right cerebral hemisphere when watching a left hand movement. This enhanced mu suppression was found regardless of whether the participant was moving or watching the experimenter move. These results are suggestive of super mirror neurons, that is, mirror neurons which are strengthened in sensitivity to another after a joint action task and do not distinguish between whether the individual or the individual's partner is moving.

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Date Created
  • 2015-12