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High-probability grants
According to our matching algorithm, Brendan M. Walker is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2001 — 2002 |
Walker, Brendan M |
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.). |
Benzodiazepine Modulation of Opiate Reward @ University of California Santa Barbara
DESCRIPTION: (provided by the applicant) The present project proposes to examine the putative enhancing effects of benzodiazepine (BDZ) pretreatment on intravenous opiate drug reward. Clinical case studies have reported numerous examples of apparent opiate drug enhancement in opiate abusers who self-medicate with an oral BDZ tranquilizer prior to their opiate injection. In our laboratory, we have been able to confirm this BDZ-opiate reward interaction in rats. Our preliminary results have demonstrated a reliable potentiation in the size of the heroin-induced place preferences in animals pretreated with low doses of the BDZ, alprazolam; an effect which is blocked by treatment with the BDZ receptor antagonist, flumazenil. The maximal effect is produced at low doses of both heroin and alprazolam that do not produce evidence of drug reward when administered alone. The current proposal builds upon these results in the form of two specific aims: 1) to replicate and extend the preliminary findings by testing the ability of buspirone (a non-BDZ anxiolytic agent) to facilitate opiate reward and to investigate the BDZ-opiate interaction with other measures of drug reward (i.e., operant self-administration); and 2) to identify (using receptor antagonist microinfusions into discrete brain regions) the critical sites in the CNS that might underlie this BDZ-opiate interaction. This work would represent the first systematic animal research on this phenomena and help to elucidate the precise nature and mechanisms underlying BDZ-opiate interactions.
|
0.933 |
2003 — 2006 |
Walker, Brendan M |
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. |
Chronic Ethanol Consumption, Opioids and Dopamine @ Scripps Research Institute
DESCRIPTION (provided by applicant): Due to evidence suggesting that brain reinforcement systems are engaging in allostatic processes to combat the chronic effects of ethanol administration, the present series of experiments are designed to identify changes in basal and ethanol administration-contingent endogenous opioid and dopamine levels in the rat brain during acute and protracted withdrawal in ethanol dependent and non-dependent animals. Furthermore, non-selective and selective opioid receptor antagonists/agonists will be used to pharmacologically study the role of opioids within specific regions of the extended amygdala during acute withdrawal in ethanol dependent and non-dependent rats. These series of experiments will help to classify allostatic changes in brain reinforement systems that could contribute to addiction and dependence and possibly help to identify appropriate pharmacotherapeutics for use in the treatment of alcoholism.
|
0.907 |
2011 — 2017 |
Walker, Brendan M |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
The Role of Dynorphin / Kappa-Opioid Systems in Alcohol Dependence @ Washington State University
DESCRIPTION (provided by applicant): A fundamental characteristic of excessive alcohol use is the comorbidity of alcohol dependence and disorders of affect. Self-medication of these negative affective states likely contributes to excessive alcohol use and relapse. Negative affective states produced by chronic alcohol exposure result from neuroadaptations in motivational and affective neurocircuitry that are not yet understood. The principal investigator's long-term goal is to identify effective pharmacotherapeutic targets for the treatment of alcoholism. The objective of this application, which is the next step in pursuit of that goal, is to understand the neuroadaptations in dynorphin / kappa-opioid systems that occur in response to chronic alcohol exposure and contribute to attenuated motivational and affective states. The central hypothesis is that compensatory neuroadaptations in dynorphin / kappa-opioid systems oppose the acute effects of alcohol, and promote excessive alcohol intake by altering negative affective behaviors. The rationale for the proposed studies is that identification of dynorphin targets will enable the development of pharmacotherapies designed to alleviate motivational and affective symptoms produced by alcohol dependence. The hypothesis will be tested by pursuing the following specific aims: Aim #1 will evaluate kappa opioid receptor antagonism within specific sites of the extended amygdala during acute withdrawal. Aim #2 will site-specifically evaluate the role of extended amygdala dynorphin systems in depressive- and anxiety-like behavior. Specific Aim #3 will maximize dependence-induced alterations in negative affective behaviors during acute and protracted withdrawal. All three aims will utilize animal models of ethanol reinforcement and affective behavior to allow for the systematic investigation of neurotransmitter systems and neurocircuitry that contribute to altered motivational and affective states produced by chronic ethanol exposure. These three specific aims will collectively help to identify important neuroadaptations that result from chronic alcohol exposure and provide much needed information regarding the neurocircuitry involved in altered motivational and affective systems. Such a contribution is significant because it will help to develop pharmacotherapeutic targets for the treatment of alcoholism that focus on the removal of attenuated motivational and negative affective states;a strategy that should greatly increase medication compliance and decrease rates of relapse. PUBLIC HEALTH RELEVANCE: This proposal is relevant to public health and will have an important positive impact because there are currently no pharmacotherapies designed to alleviate the negative affective and attenuated motivational aspects of alcohol withdrawal and dependence. In addition to the site-specific investigation of dynorphin / kappa-opioid systems in reinforcement paradigms, the benefits of this proposal are the assessment of dynorphin / kappa-opioid systems in depressive- and anxiety-like behaviors associated with alcohol dependence. The proposed experiments will assist with the development of pharmacological targets for alcoholism based on the alleviation of negative affect and result in increased compliance and treatment success for the individual and less alcoholism-associated societal costs.
|
1 |
2019 — 2021 |
Walker, Brendan M |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
The Role of Kappa-Opioid Receptors in Alcohol Use Disorders @ University of South Florida
Project Summary. A fundamental characteristic of alcohol use disorders is the loss of control over alcohol consumption that results in progressively escalating levels of alcohol use and facilitates the progression to alcohol-dependence. Given the comorbidity of alcohol dependence and disorders of affect such as de-pression is extremely high, it has been posited that self-medication of negative affective states contributes to continued excessive alcohol use and relapse. Furthermore, negative affective states produced by chronic alcohol exposure can influence the neurocircuitry of cognitive control systems to perpetuate further excessive alcohol use. Once that degree of dysregulation is reached, components of the dependence cycle serve to facilitate each other in a manner that is extremely deleterious to personal, familial and societal welfare. The principal investigator?s long-term goal is to identify effective therapeutic targets and strategies for the treatment of AUDs. The objective of this renewal application, which is the next step in pursuit of that goal, is to understand the neuroadaptations in dynorphin (DYN) / kappa-opioid receptor (KOR) systems that occur in response to chronic alcohol exposure and contribute to maladaptive behavioral regulation in the form of maladaptive behavioral regulation. The central hypothesis is that the DYN / KOR system becomes progressively dysregulated in a manner that promotes the continued excessive consumption of alcohol and perpetuates the cycle of alcohol dependence. The rationale for the proposed studies is that identification of novel DYN / KOR- related treatment targets will enable the development of effective therapies designed to alleviate maladaptive behavioral regulation produced by dysphoria and alcohol dependence. This hypothesis will be tested by pursuing the following specific aims: Aim #1 evaluates kappa-opioid receptor dysregulation within cortical nuclei during acute withdrawal within working memory and impulse control domains. Aim #2 assesses the role of KORs in amygdalar nuclei in response to non-dependent dysphoria cues and alcohol-dependent withdrawal cue-induced maladaptive behavioral regulation using a combination of pharmacological and inducible genetic approaches. Animal models of self-administration, negative affective-like behavior, working memory and impulse control will serve as functional end-points to systematically investigate the mechanisms that contribute to maladaptive behavioral regulation in AUDs. These specific aims will collectively help to identify important neuroadaptations in DYN / KOR systems that can promote the transition to, and perpetuation of, AUDs and will provide much needed information regarding the influence of DYN / KORs on the neurocircuitry maladaptive behavioral regulation. Such a contribution is significant because it will help develop personalized therapeutic targets to treat AUDs that focus on the removal of maladaptive phenotypes; a strategy that should greatly increase medication compliance and decrease rates of relapse.
|
0.934 |