Measuring synaptic activity in critical illness survivors through excitatory post-synaptic currents – UROP Spring Symposium 2022

Measuring synaptic activity in critical illness survivors through excitatory post-synaptic currents

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Niyati Puranik

Pronouns: she/her

Research Mentor(s): Benjamin Singer
Co-Presenter:
Research Mentor School/College/Department: Internal Medicine / Pulmonary and Critical Care Medicine / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 1 – 10am – 10:50am
Room: League Ballroom
Authors: Niyati Puranik, Shannon Moore, Benjamin Singer
Presenter: 114

Abstract

It’s well known that sepsis survivors carry an increased risk of long-term cognitive impairment. This is thought to be the result of systemic neuroinflammation through the activation of microglia, which causes synaptic phagocytosis. The amyloid-beta (Aß) pathology that underlies many Alzheimer’s diagnoses is also found in 20-50% of the population over 60 years old in the U.S., raising the question of whether populations with this pathology are more susceptible to the long term cognitive impairment that can follow sepsis. Using animal models, we compare control groups to those who have survived bacterial pneumonia with and without Alzheimer’s disease pathology (5XFAD model). In order to quantify changes in synaptic activity, electrophysiologic measurements will be used as direct evidence of brain dysfunction. By looking at the frequency, amplitudes and cluster patterns of excitatory post-synaptic currents (EPSCs) in single cell recordings of pyramidal cells in the hippocampus, we aim to compare general synaptic activity between our experimental groups. The electrophysiology recordings will be analyzed using MOD (Machine-learning Optimal-filtering Detection-procedure), a supervised machine learning method for detecting synaptic events. By automating the process beyond training the artificial intelligence, we minimize subjectivity in event characterization and significantly decrease the time needed for processing the recordings. We hypothesize that mice with a combination of Aß pathology (5XFAD Alzheimer’s disease) and history of sepsis (recovery from bacterial pneumonia) will have decreased synaptic activity as compared to the control groups.

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Natural/Life Sciences

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