The role of BRSK1, a PKC epsilon substrate, in behavioral and physiological responses to ethanol
PKC epsilon 底物 BRSK1 在乙醇行为和生理反应中的作用
基本信息
- 批准号:10748283
- 负责人:
- 金额:$ 2.41万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2022
- 资助国家:美国
- 起止时间:2022-09-01 至 2023-12-31
- 项目状态:已结题
- 来源:
- 关键词:AcuteAlcohol consumptionAlcoholic IntoxicationAlcoholsAmygdaloid structureAtaxiaBehavioralBehavioral AssayBindingBrainBrain regionConsumptionCyclic AMP-Dependent Protein KinasesDevelopmentDrug TargetingEthanolExocytosisFutureGenetic ScreeningImageInterruptionKnock-outKnockout MiceKnowledgeMeasuresMediatingMethodsMolecularMusNeuronsPersonsPharmacological TreatmentPhenotypePhosphorylationPhysiologicalPlayProbabilityProceduresProcessProtein InhibitionProtein-Serine-Threonine KinasesRNA InterferenceRegulationRewardsRoleSerineSignal TransductionSocietiesSynapsesSynaptic TransmissionSynaptic VesiclesTestingTotal Internal Reflection FluorescentWild Type MouseWorkalcohol abuse therapyalcohol behavioralcohol consequencesalcohol responsealcohol rewardalcohol sensitivityalcohol testingalcohol use disorderbehavioral responsechemical geneticsconditioned place preferencecostdrinkingdruggable targetexperimental studygamma-Aminobutyric Acidinhibitorknock-downneurotransmissionneurotransmitter releasenew therapeutic targetnovelpharmacologicpreferencepresynapticprotein kinase C epsilontransmission processvesicular release
项目摘要
Project Summary/Abstract:
Alcohol use disorder effects numerous people around the world and creates an enormous cost on society. The
pharmacological treatments available are limited and modestly effective. One mechanism by which alcohol
perturbs brain function is by altering synaptic transmission by altering the release probability of synaptic
vesicles. The molecular mechanisms underlying this action are not known. Protein kinase C epsilon (PKCε)
regulates both synaptic vesicle release and alcohol consumption in mice. Alcohol enhancement of inhibitory
neurotransmission in the central amygdala (CeA), which is implicated in regulating alcohol consumption, is a
process dependent on PKCε, and inhibition of PKCε in the CeA decreases alcohol consumption in mice. It is
not known how PKCε regulates synaptic vesicle release. Brain serine/threonine kinase 1 (BRSK1) is
phosphorylated by PKCε, colocalizes with pre-synaptic markers, and increases the release probability of
synaptic vesicles. The objective of this project is to determine the role of BRSK1 in behavioral and
physiological responses to alcohol and its relation to PKCε signaling. Based on preliminary evidence, the
hypothesis is that BRSK1 via PKCε signaling mediates alcohol-induced GABA release in the CeA, limits
sensitivity to ethanol intoxication, and promotes ethanol consumption and reward. This project will utilize
several behavioral and pharmacological methods to determine the role of BRSK1 in behavioral responses to
alcohol (Aim 1). The role of BRSK1 in alcohol-enhancement of inhibitory neurotransmission in primary neurons
from the central amygdala will also be examined (Aim 2). The results of this project will increase understanding
of the downstream signals that mediate PKCε regulation of alcohol related behaviors and alcohol’s
enhancement of inhibitory transmission in neurons of the CeA. This project may also provide evidence for
BRSK1 as a drug target for the development of novel treatments for alcohol use disorder.
项目总结/文摘:
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Michael P Dugan其他文献
Michael P Dugan的其他文献
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{{ truncateString('Michael P Dugan', 18)}}的其他基金
The role of BRSK1, a PKC epsilon substrate, in behavioral and physiological responses to ethanol
PKC epsilon 底物 BRSK1 在乙醇行为和生理反应中的作用
- 批准号:
10538025 - 财政年份:2022
- 资助金额:
$ 2.41万 - 项目类别:
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