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High-probability grants
According to our matching algorithm, Astrid A. Prinz is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2007 — 2011 |
Prinz, Astrid Antonia |
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. |
Activity-Dependent Homeostatic Regulation in Neural Networks
[unreadable] DESCRIPTION (provided by applicant): Neuronal networks must function reliably throughout life in spite of molecular turnover and developmental and environmental changes. This is most evident for pattern-generating neural circuits underlying vital behaviors such as breathing. Activity-dependent homeostatic regulation (ADHR) of network properties supports stable network function through a feedback loop between a circuit's electrical activity and the underlying cellular and synaptic properties. Intracellular calcium levels play an important role in this feedback loop because they act as sensors of electrical activity and are involved in intracellular signaling, but the pathways underlying ADHR are not understood. This grant will use computational brute force to examine millions of different models of ADHR, with the aim of identifying regulatory pathway structures that support stable network function and can restore it after perturbations. Analyzing the common properties of successful regulation models will identify key features of ADHR pathways and reveal how neuronal networks can maintain stable function. The proposed research will use the lobster pyloric pattern-generating circuit as an established model system in which ADHR has been demonstrated at the cellular and network levels. Simulations will proceed in three steps: 1) identifying calcium-based activity sensors that distinguish functional from non-functional network activity, 2) determining how these sensors feed back onto neuronal properties to achieve homeostasis at the cellular level, and 3) testing regulation mechanisms that are successful at the cellular level for their ability to support homeostasis at the network level. Because little is know about ADHR of synaptic properties in pattern-generating circuits, experiments will determine whether and how synapses in the pyloric circuit are homeostatically regulated, and results from these experiments will inform the final network level simulations. RELEVANCE: Maintaining stable neural network function, especially in pattern-generating circuits, is of vital importance for any animal, including humans. Homeostatic regulation failure can lead to dysfunctional network outputs including silence or seizure-like activity, and has been implicated in epilepsy and other seizure disorders and in the response of brain tissue to trauma or hypoxia. This grant will contribute to a better understanding of homeostatic regulation processes in neural circuits and will thus lay the groundwork for potential treatments of these disorders. [unreadable] [unreadable] [unreadable]
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2017 — 2021 |
Hochman, Shawn [⬀] Prinz, Astrid Antonia |
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. |
Recruitment Principles and Injury-Induced Plasticity in Thoracic Paravertebral Sympathetic Postganglionic Neurons
Project Summary The present project explores a barely studied and poorly-understood area of vertebrate autonomic neuroscience: the recruitment properties of thoracic paravertebral sympathetic postganglionic neurons (tSPNs). The prominent role of thoracic paravertebral sympathetic chain ganglia is as the final neural control element regulating vasomotor tone. Given their strategic nodal site in autonomic signaling to body, any plasticity in tSPNs is likely to be of high significance. Unfortunately, tSPNs are largely inaccessible for in vivo study, so operational principles are inferred from studies in cervical and lumbar chain ganglia. Only 3 in vitro studies have revealed tSPN electrophysiological properties: none accurately measure cellular integrative properties or underlying recruitment principles due to electrode impalement injury. We undertook the first physiological studies on caudal thoracic chain ganglia in the adult mouse by developing an ex vivo preparation with intact segmental preganglionic and rostrocaudal interganglionic connections. We obtained the first whole- cell patch clamp recordings of tSPNs and observed fundamentally different integrative and firing properties are than previously observed. This reliable data set is a critical prerequisite to realistic computational simulation. We propose to interleave experimental testing with modeling to understand tSPN recruitment principles and their integrative properties. [SA1] We will test the hypothesis that tSPNs have heterogeneous synaptic, cellular, and network properties, and are active participants in input-output recruitment strategies. Higher thoracic spinal cord injuries (SCI) disrupt the brainstem pathways that regulate tSPN excitability via spinal preganglionic loops. Such disruption can lead to sudden life-threatening tSPN mediated hypertensive crises (autonomic dysreflexia). Whether paravertebral sympathetic chain ganglia dysfunction contributes to amplification in a vasomotor response is unknown. To fill this significant gap in knowledge, experimental studies will disclose plasticity in the cellular and synaptic organizational rules serving tSPN recruitment. [SA2] We will test the hypothesis that tSPNs increased their intrinsic excitability and convert from linear to non-linear gain amplifiers after SCI. Computational simulation will construct a database amenable to realistic modeling of recruitment principles of potential clinical relevance that could be transformative to the field. The relative simplicity of the organization makes discovery of principles through modeling more assured than in more complex systems. Realistic simulation of the neural bases of tSPN function and emergent dysfunction could catalyze predictive drug discovery-based high throughput simulations that normalize function for rapid preclinical testing. Significance: we aim to uncover the operational principles governing the final neural command pathways regulating vascular tone. As sympathetic hyperactivity is implicated in various autonomic disorders, a database amenable to realistic modeling studies will be of broad predictive use in preclinical and translational studies.
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