Grace Vollmar
Research Mentor(s): Wei-Chih Chang
Mentor Department: Molecular and Integrative Physiology
Authors: Grace Vollmar, Geoffrey Murphy, Wei-Chih Chang
Session: Session 3 (11:00am – 11:50am)
Presentation Type: Oral
Abstract
The Plexin A2 receptor modulates axonal growth by preventing axons from targeting inappropriate areas during development. Genome-wide association studies suggest Plexin A2 is associated with brain disorders affecting learning and memory, and psychiatric disorders such as schizophrenia. In Plxna2 knockout mice, migration of progenitor cells is interrupted, and the hippocampal dentate gyrus is deformed. These mice presented behaviors linked to schizophrenia and impaired learning, but the mechanisms behind these dysfunctions are unknown. We investigated induced neuronal network activities as functional markers to understand how the hippocampus is disturbed in Plxna2 knockout mice. No Mg2+, 6 mM K+ artificial cerebrospinal fluid was used to excite neurons in the horizontal hippocampal brain slices (400 µm) from mice with genetic modifications of Plxna2 (+/+, +/-, and -/-). Electrodes were placed in the dentate gyrus, CA1 and CA3 regions of the hippocampus, and the entorhinal cortex to record the neuronal network activities. These recordings were analyzed to identify any differences in network propagation through the different areas of the brain, as well as if the neurons in the network remain functional in Plxna2 knockout mice. Two types of synchronous network activities were observed between the recorded regions, with a CA3-driven propagation and an entorhinal cortex-driven propagation from the Plxna2 +/+ mice. However, in the slices from Plxna2 -/- mice, the entorhinal cortex-driven events were significantly suppressed. These experiments suggest that the disrupted migration of progenitor cells impaired signal transmission and network synchrony between the hippocampus and the entorhinal cortex.
