Theresa Fadool
Research Mentor(s): Wei-Chih Chang
Mentor Department: Molecular and Integrative Physiology
Authors: Theresa Fadool, Geoffrey Murphy, Wei-Chih Chang
Session: Session 2 (10:00am – 10:50am)
Presentation Type: Poster 22
Abstract
A high-fat but low-protein and low-carbohydrate diet, commonly known as a keto diet, promotes fatty acid oxidation and ketone production. This ketogenic diet has been known to have an anticonvulsant effect for decades, but the mechanisms of how it aids in treating epilepsies are still uncertain. Potassium flux through the voltage-gated potassium channels (Kv) decreases membrane potentials and makes neurons difficult to fire. Kv is modulated by auxiliary proteins, like Kvß2. Activated by reducing ketones, Kvß2 keeps the potassium channel open, increases potassium flux, and stabilizes neurons. We hypothesize that the anti-epileptic effect of the ketogenic diet is mediated by Kvß2 and reduces the excitability of neuronal networks; this UROP project addresses how Kvß2 stabilizes network activity. I prepared slices from the hippocampus (sagittal, 400 µm) of mice with and without Kvß2 (Kvß2 +/+, +/-, and -/-). The hippocampal slices were held in a modified artificial cerebrospinal fluid (0 mM Mg2+ and 6 mM K+) to measure spontaneous neuronal network activity. I used wire electrodes to record the neuronal network events from the hippocampus and cortex. I expect to observe more frequent and complicated neuronal network events from the slices without Kvß2 (-/-) in accordance with our hypothesis.
