Investigating the mechanism by which Tacr1 Neurons Regulate Neurovascular Coupling
研究 Tacr1 神经元调节神经血管耦合的机制
基本信息
- 批准号:10678077
- 负责人:
- 金额:$ 4.77万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2023
- 资助国家:美国
- 起止时间:2023-05-01 至 2026-04-30
- 项目状态:未结题
- 来源:
- 关键词:BrainBrain imagingCalciumCerebrovascular CirculationCerebrovascular DisordersComplexDevelopmentDiseaseElectroencephalographyEnsureEnzymesFellowshipFrequenciesFunctional Magnetic Resonance ImagingFutureG-Protein-Coupled ReceptorsGoalsHealthHumanImageKnowledgeLaser-Doppler FlowmetryLigandsLinkMeasuresMediatingMediatorMentorsMicroscopyMolecularMusNeuronsNeuropeptidesNitric OxideNitric Oxide Synthase Type INitric Oxide Synthetase InhibitorNutrientOxygenParvalbuminsPathway interactionsPerfusionProcessProductionResearch PersonnelResearch TrainingRiskScientistSignal TransductionSleepSomatosensory CortexSourceStrokeSubstance PTAC1 geneTACR1 geneTestingTherapeuticTissuesTrainingTranslatingVasodilationVasodilator AgentsViralWakefulnessantagonistawakeblood oxygen level dependentbrain healthbrain tissuecerebrovascularexperimental studyhemodynamicsimaging studyin vivoinhibitory neuronleadership developmentnervous system disorderneuralneurovascularneurovascular couplingneurovascular unitoptogeneticsresponsetraining opportunitytwo-photon
项目摘要
PROJECT SUMMARY/ABSTRACT
Neurovascular coupling (NVC) is a mechanism that translates neural activity into either slow or fast
hemodynamic responses. This mechanism is critical for blood oxygen level dependent (BOLD) functional
magnetic resonance imaging (fMRI) studies, and for maintaining healthy brain tissue. Also, disruptions to NVC
have been linked to an increased risk of cerebrovascular disorders, such as stroke. Despite the importance NVC
has in ensuring a functional brain, the exact process of this complex mechanism is poorly understood. Different
mediators responsible for the hemodynamic responses have been proposed. One of these proposed mediators
is nitric oxide (NO), a strong vasodilator. NO is catalyzed by the enzyme neuronal nitric oxide synthase (nNOS)
in specific neurons. Our lab has identified a subset of cortical inhibitory neurons that co-express nNOS and
Tachykinin Receptor 1 (TACR1), also known as substance P receptor. These Tacr1 neurons have been
observed to be in proximity with the neurovascular unit. Moreover, optogenetic stimulation of Tacr1 neurons
results in increased cerebral blood flow (CBF). Based on our findings, Tacr1 neurons mediate NVC. Even though
Tacr1 neurons express nNOS, whether NO is responsible for the observed changes in CBF during optogenetic
stimulation is unknown. Furthermore, no studies have investigated the cellular inputs that activate Tacr1 neurons.
Previous studies suggest that Tacr1 neurons are depolarized by substance P (SP), but where the source of SP
is coming from is unknown. One possibility is parvalbumin (PV) neurons, which are known to release SP.
Additionally, PV neurons are known to produce gamma-band oscillations, which are strongly correlated to the
BOLD signal . PV neurons may be providing a source of SP for Tacr1 neurons
during high gamma-band activity. As such, Tacr1 neuron activity may increase during high gamma-band activity
causing the release of NO. I propose to determine whether
My proposal comprises of the following aims: Aim 1: Determine the
molecular mechanism through which Tacr1 neuron activity increases cerebral blood flow (CBF). Aim 2: Examine
the cellular inputs that activate Tacr1 neurons. Aim 3: Characterize the endogenous activity of Tacr1 neurons
across brain states. Together, these experiments may reveal the circuitry underlying NVC and the association
with state-dependent changes. This knowledge is fundamental to our understanding of BOLD signal and
cerebrovascular disorders. Finally, in this proposal, I outlined a combination of rigorous mentored research
training, coursework, and professional and leadership development activities that along with this fellowship
training period will be instrumental in my development as an aspiring independent investigator.
(an indirect measure of NVC)
SP causes a state-dependent increase in Tacr1
neuron activity, resulting in vasodilation.
项目总结/文摘
项目成果
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Maria Fernanda Juarez Anaya其他文献
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