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High-probability grants
According to our matching algorithm, Caroline E. Bass is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2008 — 2011 |
Bass, Caroline Evelyn |
K01Activity Code Description: For support of a scientist, committed to research, in need of both advanced research training and additional experience. |
Cb1 and Da Receptor Deletion by Rnai in Cocaine Self-Administration @ Wake Forest University Health Sciences
[unreadable] DESCRIPTION (provided by applicant): This K01 Mentored Research Career Development Award is to train Caroline E. Bass, junior faculty in the Dept. Physiology & Pharmacology at Wake Forest Univ., to develop an independent hypothesis-driven research project to investigate addiction processes that are modulated by dopamine and cannabinoid receptors in the mesocorticolimbic system. Dr. Bass will apply her skills in the development of adenoassociated virus (AAV) vectors for the delivery of RNA interference (RNAi) transgenes to develop her own project focused on the knock down of D1, D2 and CB1 receptors in strategically defined brain loci, the impact this has on the reinforcing efficacy of cocaine, and how the cananbiniod and dopamine systems interact in a cocaine self-administration model of drug abuse. Dr. Bass's mentoring in cannabinoid pharmacology and gene expression changes will come from Dr. Allyn C. Howlett, and her mentoring in the behavioral models, particularly rat self-administration, will come from Dr. David C.S. Roberts, who are distinguished scientists in these respective areas. Other mentoring will cover all aspects of professional skills commensurate with academic promotion and national recognition. The following specific aims are proposed to meet the goals of this proposal: 1) Generate and characterize AAV vectors containing RNAi expression cassettes that cause the degradation of D1, D2 and CB1 receptor mRNA in rats and determine the compensatory changes in molecular components of dopamine and endocannabinoid neurotransmission resulting from this manipulation; 2) Investigate the site(s) of action of non-conditioned behavioral effects of THC by injecting the CB1 RNAi-AAV into the striatum and medulla and assessing the efficacy of THC in inducing antinociception, hypoactivity, hypothermia, and catalepsy; 3) delineate and define the contribution of D1 and D2 receptors in the ventral striatum, dorsal striatum and VTA in the reinforcing effects of cocaine by site specific injection of D1 or D2 RNAi-AAV in rats self-administering cocaine; 4) Characterize the impact of CB1 receptor ablation from the ventral striatum, dorsal striatum and VTA on cocaine self-administration. Specifically, the CB1 RNAi-AAV will be injected into these regions and the reinforcing efficacy of cocaine will be assessed. During all stages of these aims the compensatory mechanisms in cannabinoid and dopamine neurotransmission will be assessed to determine how these receptor systems are interacting in modulating cocaine intake. These studies will address fundamental gaps in our knowledge of dopamine receptor function in reinforcement and serve as a basis for understanding how cannabinoid and dopamine receptor systems interact to regulate addictive behaviors. These findings may lead to the development of novel and more effective therapeutic interventions for drug addiction. [unreadable] [unreadable] [unreadable]
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1 |
2017 — 2018 |
Bass, Caroline Evelyn |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Targeted Chemogenetic Stimulation of Rat Vta Gaba Neurons in Cocaine Extinction and Reinstatement @ State University of New York At Buffalo
Dopaminergic neurons originating from the ventral tegmental area (VTA) regulate a variety of reward and drug- related behaviors. However, up to 20% of VTA neurons are GABAergic interneurons, and ~5% are GABA projection neurons (GPNs) that send projections to several brain regions involved in drug reward, including the nucleus accumbens (NAc). Recently the role of VTA GABA neurons and GPNs in reinforcement has been explored using transgenic mice that allow for selective manipulation of VTA GABA neurons. However, the role of these GABAergic neurons in drug-related behaviors is much less understood. We propose to use a novel combinatorial adeno-associated viral (AAV) vector system to target gene expression to either VTA GABA neurons or VTAà?NAc core GPNs in wildtype rats that have been trained to self-administer cocaine. The targeted GABA neurons will express DREADDs (designer receptors exclusively activated by designer drugs) which will allow us to selectively stimulate these neuronal subtypes during extinction of cocaine self- administration, and reinstatement of cocaine-seeking behavior, a rat model of relapse. We hypothesize that VTA GABA neurons will enhance responding during extinction learning and cocaine- and cue-induced reinstatement by disrupting learned cue-reward associations. Furthermore, we believe that VTAà?NAc core GPN activation will selectively enhance cue-induced reinstatement, but have little influence on cocaine-induced reinstatement or extinction. In aim 1 of this proposal, we will determine the role of VTA GABA neurons in extinction learning and reinstatement of cocaine-seeking. We will also undertake a pilot study in female rats to determine if sex differences exist. In aim 2 we will selectively target the VTA GPNs projecting to the NAc core. By contrasting these results of aim 1 and 2, we will determine if the VTAà?NAc core GPN effects differ substantially from stimulating all VTA GABA neurons, and whether these specific projections alone may serve as a potential target for therapeutic intervention. These experiments will establish the role of VTA GABA neurons in drug-seeking behaviors, and will provide the necessary groundwork for future exploration into the mechanisms underlying VTA GABA neuron effects on responding to drug cues and the processes underlying relapse.
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