Open Access. Powered by Scholars. Published by Universities.®

Digital Commons Network

Open Access. Powered by Scholars. Published by Universities.®

Articles 1 - 10 of 10

Full-Text Articles in Entire DC Network

Pharmaceutical And Natural (Exercise) Mechanisms To Mitigate The Negative Impact Of Ptsd And Chronic Stress On Synaptic Plasticity And Memory, Roxanne M. Miller Nov 2017

Pharmaceutical And Natural (Exercise) Mechanisms To Mitigate The Negative Impact Of Ptsd And Chronic Stress On Synaptic Plasticity And Memory, Roxanne M. Miller

Theses and Dissertations

Synapses can be altered due to experiences in a process called synaptic plasticity, which causes memory formations. Synapses can be strengthened through methods known as long-term potentiation (LTP) or weakened through long-term depression (LTD). Stresses can cause changes by altering synapses through either LTP or LTD. Rats were used to study the effects of post-traumatic stress disorder (PTSD)-like symptoms and a prophylactic treatment using pharmaceuticals. The first model used was the single prolonged stress (SPS) with two weeks of chronic light, which was not as effective for causing changes in synaptic plasticity. The second model, seven days of social defeat …


Pharmaceutical And Natural (Exercise) Mechanisms To Mitigate The Negative Impact Of Ptsd And Chronic Stress On Synaptic Plasticity And Memory, Roxanne M. Miller Nov 2017

Pharmaceutical And Natural (Exercise) Mechanisms To Mitigate The Negative Impact Of Ptsd And Chronic Stress On Synaptic Plasticity And Memory, Roxanne M. Miller

Theses and Dissertations

Synapses can be altered due to experiences in a process called synaptic plasticity, which causes memory formations. Synapses can be strengthened through methods known as long-term potentiation (LTP) or weakened through long-term depression (LTD). Stresses can cause changes by altering synapses through either LTP or LTD. Rats were used to study the effects of post-traumatic stress disorder (PTSD)-like symptoms and a prophylactic treatment using pharmaceuticals. The first model used was the single prolonged stress (SPS) with two weeks of chronic light, which was not as effective for causing changes in synaptic plasticity. The second model, seven days of social defeat …


Mri T2 Signal Changes Indicate Tau Pathophysiology In A Murine Alzheimer's Disease Model, Rajan Deep Adhikari Aug 2017

Mri T2 Signal Changes Indicate Tau Pathophysiology In A Murine Alzheimer's Disease Model, Rajan Deep Adhikari

Theses and Dissertations

Pathogenesis, diagnosis and treatment, the essential domains in medical practice, seem helpless to address Alzheimer's disease (AD). With a huge mortality rate, it is looming and threatening the socioeconomic barrier. Despite many different studies, the pathogenesis of AD remains inconclusive. However, growing numbers of studies suggest oxidative stress to contribute to the initiation and progression of AD. We propose an iron hypothesis: iron mediated oxidative damage by reactive oxygen species (ROS), which induces protective roles of amyloid beta and hyper-phosphorylated tau (HP-tau) to sequester iron and limit the disease. We propose to study such mechanism using transgenic mice models for …


Modulation Of Synaptic Plasticity: Endocannabinoids And Novel G-Protein Coupled Receptors Expression And Translational Effects In Interneurons, Katrina M. Hurst Jul 2017

Modulation Of Synaptic Plasticity: Endocannabinoids And Novel G-Protein Coupled Receptors Expression And Translational Effects In Interneurons, Katrina M. Hurst

Theses and Dissertations

Learning and memory are important processes that occur in the brain. The brain is comprised of neurons that make connections with each other known as synapses. Synaptic plasticity is widely believed to be the physiologic mechanism by which learning and memory occur. Synapses can either be strengthened through a process known as long-term potentiation (LTP) or weakened through long-term depression (LTD). The area of the brain that is most studied for its role in learning and memory is the hippocampus, which has been shown to be involved in memory consolidation. The detection of endocannabinoids and their receptors has opened a …


Chemogenetic Stimulation Of Electrically Coupled Midbrain Gaba Neurons In Alcohol Reward And Dependence, Stephanie Suzette Pistorius May 2017

Chemogenetic Stimulation Of Electrically Coupled Midbrain Gaba Neurons In Alcohol Reward And Dependence, Stephanie Suzette Pistorius

Theses and Dissertations

The prevailing view is that enhancement of dopamine (DA) transmission in the mesolimbic system leads to the rewarding properties of alcohol. The mesolimbic DA system, which plays an important role in regulating reward and addiction, consists of DA neurons in the midbrain ventral tegmental area (VTA) that innervate the nucleus accumbens (NAc). It is believed that VTA DA neurons are inhibited by local gamma-aminobutyric acid (GABA) interneurons that express connexin-36 (Cx36) gap junctions (GJs). We have previously demonstrated that blocking Cx36 GJs suppresses electrical coupling between VTA GABA neurons and reduces ethanol intoxication and consumption suggesting that electrical coupling between …


Insulin And Ketones: Their Roles In Brain Mitochondrial Function, Sheryl Teresa Carr May 2017

Insulin And Ketones: Their Roles In Brain Mitochondrial Function, Sheryl Teresa Carr

Theses and Dissertations

The prevalence of both Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) is increasing worldwide, and the trends are unfortunately expected to continue. AD has recently been tied with mitochondrial dysfunction and insulin resistance, creating a mechanistic tie between AD and T2DM. Unfortunately, insulin resistance is often increased with aging and therefore, all individuals are at risk of brain mitochondrial dysfunction. Without proper mitochondrial function, the brain will degenerate, causing impaired cognitive function and reduced quality of life. The purpose of this study is two-fold: first, to understand the role of ceramides in insulin-induced brain mitochondrial dysfunction, and; second, …


Insulin And Ketones: Their Roles In Brain Mitochondrial Function, Sheryl Teresa Carr May 2017

Insulin And Ketones: Their Roles In Brain Mitochondrial Function, Sheryl Teresa Carr

Theses and Dissertations

The prevalence of both Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) is increasing worldwide, and the trends are unfortunately expected to continue. AD has recently been tied with mitochondrial dysfunction and insulin resistance, creating a mechanistic tie between AD and T2DM. Unfortunately, insulin resistance is often increased with aging and therefore, all individuals are at risk of brain mitochondrial dysfunction. Without proper mitochondrial function, the brain will degenerate, causing impaired cognitive function and reduced quality of life. The purpose of this study is two-fold: first, to understand the role of ceramides in insulin-induced brain mitochondrial dysfunction, and; second, …


Chemogenetic Stimulation Of Electrically Coupled Midbrain Gaba Neurons In Alcohol Reward And Dependence, Stephanie Suzette Pistorius May 2017

Chemogenetic Stimulation Of Electrically Coupled Midbrain Gaba Neurons In Alcohol Reward And Dependence, Stephanie Suzette Pistorius

Theses and Dissertations

The prevailing view is that enhancement of dopamine (DA) transmission in the mesolimbic system leads to the rewarding properties of alcohol. The mesolimbic DA system, which plays an important role in regulating reward and addiction, consists of DA neurons in the midbrain ventral tegmental area (VTA) that innervate the nucleus accumbens (NAc). It is believed that VTA DA neurons are inhibited by local gamma-aminobutyric acid (GABA) interneurons that express connexin-36 (Cx36) gap junctions (GJs). We have previously demonstrated that blocking Cx36 GJs suppresses electrical coupling between VTA GABA neurons and reduces ethanol intoxication and consumption suggesting that electrical coupling between …


Lkb1 Regulation Of High-Fat Diet-Induced Adaptation In Mouse Skeletal Muscle, Ting Chen Mar 2017

Lkb1 Regulation Of High-Fat Diet-Induced Adaptation In Mouse Skeletal Muscle, Ting Chen

Theses and Dissertations

Ad libitum high-fat diet (HFD)-induced obesity leads to insulin resistance in skeletal muscle, altered gene expression, and altered growth signaling, all of which contributes to pathological changes in metabolism. Liver kinase B1 (LKB1) is an important metabolism regulator. The purpose of this dissertation was to understand how knocking out LKB1 influences HFD induced adaptations in mouse skeletal muscle. To do so, control and skeletal muscle LKB1 knock-out (LKB1-KO) mice were put on either standard diet (STD) or HFD for 1 week or 14 weeks, or put on the HFD for 14 weeks and then switched to STD for 1 week …


Alterations In Tight Junctional Proteins And Their Effects On Pulmonary Inflammation, Joshua B. Lewis Mar 2017

Alterations In Tight Junctional Proteins And Their Effects On Pulmonary Inflammation, Joshua B. Lewis

Theses and Dissertations

The lungs represent one of the earliest interfaces for pathogens and noxious stimuli to interact with the body. As such, careful maintenance of the permeability barrier is vital in providing homeostasis within the lung. Essential to maintaining this barrier is the tight junction, which primarily acts as a paracellular seal and regulator of ionic transport, but also contributes to establishing cell polarity, cell-to-cell integrity, and regulating cell proliferation and differentiation. The loss of these tight junctions has been documented to result in alterations in inflammation, and ultimately the development of many respiratory disorders such as COPD, Asthma, ARDS, and pulmonary …