{"id":5909,"date":"2021-07-12T13:47:47","date_gmt":"2021-07-12T17:47:47","guid":{"rendered":"https:\/\/neuroid.uprrp.edu\/?page_id=5909"},"modified":"2022-11-11T13:40:22","modified_gmt":"2022-11-11T17:40:22","slug":"wilma-richiez-mateo","status":"publish","type":"page","link":"https:\/\/neuroid.uprrp.edu\/index.php\/wilma-richiez-mateo\/","title":{"rendered":"Wilma Richiez Mateo"},"content":{"rendered":"\n
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Wilma V. Richiez Mateo<\/strong>
Undergraduate Student
Faculty of Biology
Dept. of Biology with a Human Approach
University of Puerto Rico
Bayam\u00f3n Campus<\/p>\n<\/div>\n\n\n\n

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Home Research<\/strong><\/span><\/p>\n\n\n\n

Mentor:<\/strong> Jennifer Barreto, PhD<\/p>\n\n\n\n

Project:\u00a0<\/strong>Extinction of morphine place preference and BDNF expression in the mesolimbic reward system of male and female rats.<\/p>\n\n\n\n

Project Description<\/strong>:<\/strong> The current opioid crisis in the United States is one of the leading causes of death, resulting in over 100,000 opioid-related overdoses in 2021. Therefore, it is imperative to understand the underlying biological mechanisms of addiction, to mitigate this crisis and improve overall public health. Substance use disorder (SUD) is a cognitive disorder of chronic relapse in which an organism develops a dependency to a substance. Although SUDs are not fully understood, it is believed to be caused by neuroplasticity changes in the neural circuits of the reward mesolimbic system and it often leads to a lack of extinction of persistent drug-seeking behavior. Brain-derived neurotrophic factor (BNDF), on the other hand, is a protein that aids in neuromaturation and neuroplasticity within the Mesolimbic Reward System. For this reason, we believe that BDNF is a pro-extinction protein that reinforces healthy neuronal connections. Consequently, this research evaluates the BDNF expression within the different sections of the reward mesolimbic system, as well as comparing these results to animals that extinguish or persist their morphine preferences within a conditioned placed preference paradigm (CPP). Behavioral changes will also be evaluated in order to assess withdrawal symptoms and anxiety-like behavior to compare it to morphine extinction. Finally, these results will be compared between male and female rats to evaluate any sexual differences. We hypothesize that those animals that extinguish their morphine-induced CPP will have a higher expression of BDNF, as well as they will present fewer withdrawal symptoms.\u00a0<\/p>\n<\/div>\n\n\n\n

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Summer Research<\/strong><\/span><\/p>\n\n\n\n

Mentor:<\/strong> Dorothy P. Schafer<\/p>\n\n\n\n

Project:\u00a0<\/strong>Lipofuscin-like autofluorescent accumulation within microglia across development<\/p>\n\n\n\n

Project Description<\/strong>:<\/strong>\u00a0Microglia<\/strong>\u00a0are tissue-resident self-sustaining macrophages of the central nervous system (CNS) that play a pivotal role in maintaining homeostatic conditions in tissue by engulfing apoptotic cells and coordinating inflammatory responses. Over time, different components start accumulating within microglia lysosomes.\u00a0\u00a0Consequently, the lysosomes of microglia are obstructed, and their degradative capacity diminishes, resulting in the accumulation of unwanted debris in the extracellular space. This accumulation of debris often leads to the development of neurodegenerative diseases such as Alzheimer\u2019s Disease and Amyotrophic Lateral Sclerosis. Therefore, it is important to understand when and where these particles start accumulating. These accumulations within microglia\u00a0\u00a0have been previously associated with\u00a0lipofuscin (LF)<\/strong>. LF is an autofluorescent (AF) material composed of lipids, metals, and misfolded proteins that accumulate in the lysosomes with time. In previous research, we and others have observed lipofuscin-like AF accumulation in microglia in 90-day-old mice.\u00a0\u00a0Therefore, this research evaluated the time and origin of AF accumulation within microglia at earlier stages of development. This way, we may further understand when this accumulation starts, and how we may combat it. We hypothesized that the accumulation of AF starts within the white matter during development, given that it is largely composed of myelinated axons, which has previously been implicated in driving AF accumulation within microglia. To interrogate AF accumulation, immunostained coronal sections of the cortex and the corpus callosum of P5-P8, P30, and P90 mice were evaluated. These slides were imaged on a spinning disk confocal microscope followed by quantification of AF volume within microglia.\u00a0<\/p>\n<\/div>\n\n\n\n

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