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High-probability grants
According to our matching algorithm, Melissa Malvaez is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2010 — 2011 |
Malvaez, Melissa F. |
F31Activity Code Description: To provide predoctoral individuals with supervised research training in specified health and health-related areas leading toward the research degree (e.g., Ph.D.). |
Epigenetic Gene Regulation Underlying Cocaine-Induced Memories @ University of California-Irvine
DESCRIPTION (provided by applicant): Drugs of abuse cause persistent changes in brain function, leading to long lasting changes in behavior that are extremely resistant to extinction (an experience-dependent process by which a previously learned behavior is reduced). A common finding from studies of drug abuse is that exposure to the context in which drug use occurs elicits memories and behaviors that result in relapse to drug-seeking behavior and subsequent drug use. Accumulating evidence shows that these persistent changes in brain function are mediated by altered gene transcription. Recently, it has become clear that regulation of gene transcription necessary for drug- associated memories involves the concerted action of multiple transcription factors and cofactors that interact with chromatin, a protein complex that packages DNA. Chromatin modification via histone acetylation (a form of epigenetic gene regulation) is emerging as a major molecular pathway involved in regulation of gene expression required for long-term memory as well as substance abuse. However, the role of the specific histone modifying enzymes involved in the acquisition and extinction of drug-induced memories remains unknown. The primary goal of this proposal incorporates behavioral, pharmacological, and molecular approaches to examine the role of histone acetylating/deacetylating enzymes that may underlie the formation and extinction of drug-induced memories. The first aim of this research proposal is to determine the ability of histone deacetylase inhibition, which relaxes chromatin structure and thereby enhances gene transcription, to enhance the rate and persistence of extinction of drug-associated memories. Epigenetic gene regulation has been shown to underlie persistent long-term changes at the cellular level as well as the behavioral level, which raises the possibility that histone deacetylase inhibition may generate a form of extinction that is refractive to reinstatement of drug-seeking behavior. The second aim will examine the role of CREB-binding protein (CBP), a histone acetyltransferase and transcriptional coactivator, in the acquisition of drug-associated memories. The focus of the third aim is to examine the role of CBP in the extinction of drug-associated memories. In both the second and third aims, I will be using novel genetic techniques to generate site specific deletions of the Cbp gene in the nucleus accumbens. My research plan focuses on epigenetic mechanisms underlying the formation and extinction of drug-associated memories. By understanding the epigenetic mechanisms involved in the formation and extinction of drug-associated memories, we can identify a potential therapeutic approach for the treatment of cocaine addiction. The translational value of these findings has the potential to greatly impact the number of people who complete a treatment program. Further, HDAC inhibitors are FDA approved drugs, which significantly increases the potential translational value of this research. PUBLIC HEALTH RELEVANCE: Cocaine addiction is a major public health problem in the United States. By understanding the epigenetic mechanisms involved in the formation and extinction of drug-associated memories, we can identify a potential therapeutic approach for the treatment of cocaine addiction.
|
0.958 |
2014 — 2015 |
Malvaez, Melissa F. |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
The Role of Rapid Bla Glutamatergic Signaling in Reward-Seeking Decisions @ University of California Los Angeles
DESCRIPTION (provided by applicant): Drugs of abuse cause persistent changes in brain function, leading to long lasting changes in behavior. A common finding from studies of drug abuse is that drug exposure may result in disruption of the cognitive processes normally responsible for adaptive decision making, resulting in relapse to drug-seeking behavior and subsequent drug use. Accumulating evidence shows that these persistent changes in brain function are mediated by altered excitatory glutamatergic neurotransmission. Recently, it has become clear that excitatory glutamatergic neurotransmission is involved in normal reward-seeking actions. Several things, such as cues in the environment that trigger actions, can control reward-seeking actions. Importantly, reward-seeking decisions are also controlled by the anticipated value of an outcome, which enables us to choose a path leading to the most desirable outcome. A major gap in the literature remains in the neurochemical mechanisms and circuits underlying value-based decision-making under normal need-states and drug-induced disorder. The primary goal of this proposal incorporates sophisticated behavioral, pharmacological, and advance neurochemical monitoring approaches to examine how glutamatergic signaling relates to value-guided decisions. The first aim of this research proposal is to determine how rapid glutamate transients relate to discrete behaviors of reward seeking. Glutamate processes have been implicated in learning about reward values to guide decisions and very recently, rapid changes in glutamate concentrations have recently been shown to predict reward seeking generally. This raises the possibility that rapid changes in glutamate concentrations are involved in learning about reward values necessary for adaptive decision-making. The second aim will examine cortical inputs contributing to glutamatergic signals related to value-guided decision-making. The focus of the third aim is to examine how glutamatergic signals are altered by chronic opiate exposure. In all three aims, I will be using an innovative electroenzymatic method that allows for the temporally and spatially precise detection of rapid glutamate concentration changes. The experiments in this proposal will elucidate the role of glutamatergic signaling in value-guided reward seeking. This will not only significantly impact our basic understanding of decision-making processes, but more importantly, could also elucidate why addicts engage in maladaptive decisions and provide new strategies to prevent its occurrence.
|
0.938 |