Samantha Poplawski
Research Mentor: Wei-Chih Chang
Mentor Department: Molecular and Integrative Physiology, Medicine
Author(s): Samantha Poplawski, Geoffrey G. Murphy, Wei-Chih Chang
Session: Session 5 (2:00 PM – 2:50 PM)
Presentation Type: Poster 66
Abstract
In genome-wide association studies, PLXNA2 has been linked to a number of psychiatric disorders, such as schizophrenia. Plxna2-/- mice have demonstrated reduced fear memory, suggesting impaired learning and memory consolidation, which aligns with the symptoms of schizophrenia. Deletion of Plxna2 disrupts the migration of granule cells during brain development, contributing to the abnormal structure of the dentate gyrus seen in Plxna2-/- mice. Using ex vivo neuronal network activity as a functional index of the hippocampus and the neighboring entorhinal cortex (EC), the host lab recently revealed that Plxna2-/- brain slices had fewer EC-driven network activity compared to Plxna2+/+, in which network activity was equally driven by the hippocampus and the EC. In this project, I tested if the ectopic network activity is mitigated by modern antipsychotic medicine, such as cariprazine. Brain slices were prepared from Plxna2+/+ and Plxna2-/- mice, and I used high potassium (8 mM), no magnesium artificial cerebrospinal fluid to induce neuronal network activity. The electrodes were placed in the EC and the cellular lines in three regions of the hippocampus—CA1, CA3, and dentate gyrus—to record electrographic activity. I quantified the network activity before and after applying cariprazine, a dopaminergic agonist. I found cariprazine restores the EC-driven network activity, implying that the learning or memory impairment in schizophrenia patients with similar interrupted signal transmissions as in the Plxna2-/- mice may be prevented in the same fashion.
