Peter A. Groblewski - US grants
Affiliations: | Oregon Health and Science University, Portland, OR |
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High-probability grants
According to our matching algorithm, Peter A. Groblewski is the likely recipient of the following grants.| Years | Recipients | Code | Title / Keywords | Matching score |
|---|---|---|---|---|
| 2008 — 2010 | Groblewski, Peter A | 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.). |
The Neurobiology of Cue-Induced Relapse to Ethanol-Seeking Behavior in Mice @ Oregon Health and Science University [unreadable] DESCRIPTION (provided by applicant): The transition from alcohol abuse to addiction is greatly influenced by the control with which both external (environmental) and internal (biological) cues exert over alcohol-seeking behavior. The new learning that occurs during the extinction of this behavior is thought to be more vulnerable to disturbance than the initial association and can therefore be easily disrupted by simple presentation of alcohol and/or the previously alcohol-associated cues. Because of the ease with which it can be triggered, relapse to alcohol and drug-seeking behavior has proven to be one of the most difficult aspects of rehabilitation therapy in human addicts. In fact, it has been reported that 50-90% of dependent patients will relapse following treatment. As such, it is imperative to better understand the factors that dictate the drive to relapse in order to reduce the likelihood that rehabilitated individuals return to harmful alcohol and drug-related behaviors. As alcohol continues to be the most commonly used psychoactive drug, understanding how alcohol-paired cues trigger alcohol-seeking behavior following rehabilitation is of great importance to the prevention of relapse. This project is specifically aimed at understanding the neurobiological mechanisms underlying the extinction of, and relapse to, alcohol-seeking behavior in mice. Using a novel behavioral procedure that combines alcohol-conditioned place preference (CPP) and Pavlovian-lnstrumental Transfer (PIT) procedures, we will first use the expression of activated transcription factors to identify the brain regions stimulated by a relapse-inducing cue and then examine the effects of neuronal inactivation of these regions on the expression of cue-induced relapse behavior. Aim 1 proposes to use immunohistochemical mapping [unreadable] techniques to assess the regional protein expression of the phosphorylated transcription factors, pCREB and pElk-1 immediately following exposure to a cue that induces relapse to alcohol-seeking behavior in mice. Aim 2 will compliment these experiments by examining the contributions of different brain regions to the expression of cue-induced relapse by manipulating the neuronal activity of these regions using site-specific microinjections of lidocaine. By combining molecular, neuropharmacological, and behavioral techniques, these proposed experiments are specifically aimed at furthering our understanding the neurobiological mechanisms underlying cue-induced relapse to alcohol abuse following treatment. [unreadable] [unreadable] [unreadable] |
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| 2013 | Groblewski, Peter A | 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. |
Prefrontal Control of Kappa-Opioid Receptor Mediated Stress-Induced Relapse. @ University of Washington DESCRIPTION (provided by applicant): One of the major triggers of relapse among patients recovering from substance use disorders is exposure to stressful or traumatic events. In animal models of drug-seeking behaviors including conditioned place preference (CPP), exposure to a stressor, including forced swim or social defeat stress (SDS), results in significant reinstatement of an extinguished cocaine-induced CPP. SDS- but not cocaine-primed reinstatement depends on activation of kappa opioid receptors (KORs) located on the serotonergic neurons of the dorsal raphe nucleus (DRN). However, it remains unknown what upstream, cortical areas are responsible for controlling the DRN during expression of stress-induced reinstatement of drug-seeking behavior. Interestingly, the DRN possesses a number of direct inputs from KOR-expressing regions of the prefrontal cortex (PFC)-an area previously found to play an important role in stress and drug-seeking behavior. This proposal therefore aims to identify and characterize the involvement of cortical-KORs in mediating reinstatement of cocaine- seeking behavior in hopes of better understanding the therapeutic potential of the KOR system. Using a combination of retrograde tract tracing, Fos, and KOR immunohistochemistry, Specific Aim 1 will first identify the cortical regions, and KOR activity within these regions, that are responsibe for controlling DRN activity during reinstatement of cocaine-CPP induced by social-defeat stress (SDS). Additionally, Aim 1 will identify the involvement of KORs on the known subset of PFC neurons that simultaneously project to the DRN and ventral tegmental area in reinstatement of CPP. Specific Aim 2 will then directly manipulate KOR activity within these connections to determine a causal role of cortical-KORs in reinstatement of cocaine-CPP. Using site- and connection-specific viral-mediated re-expression of KORs, the experiments of Aim 2 will assess the ability of KOR re-expression in the DRN and on DRN-projecting PFC neurons to rescue a deficit in SDS- reinstatement exhibited by KOR-KO mice. This proposal requires extensive training in molecular, genetic, biochemical and behavioral techniques, and the results of these experiments will provide unique insight into the involvement of the cortical and subcortical KOR systems in regulating stress-induced reinstatement of cocaine-CPP. Overall, these experiments are intended to further our understanding of how the KOR system is involved in the convergence of the stress and reward pathways that is required for expression of stress- induced relapse. |
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