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Memory acquisition and encoding are modulated by neural network activity between the hippocampus (HPC) and prefrontal cortex (PFC). Research has shown that neuroimmune defense cells, glia, interact with neurons in both brain regions. However, little is known about glial-neuronal interactions, and how these interactions affect memory network activity and in turn, memory recall. Memory network activity involves a host of cellular excitation and inhibition. The primary neurotransmitter involved in inhibition is γ-aminobutyric acid (GABA), and receptors for this neurotransmitter can also be found on microglia. To better understand glial-neuronal interactions between the HPC and PFC, we utilized a mouse model (GABABFlox) with a knockdown of GABAB receptors on microglia, to alter microglial activity. Our lab utilizes electrophysiological recordings of neuronal activity related to learning and memory in the HPC and PFC. Mice were implanted with 64-channel implants to record from single cells and local field potentials (LFPs) while completing a conditioned place preference task to measure remote recall. Results showed that GABABFlox mice had remote recall (18days) deficits but intact recent recall (1day). We also found that GABABFlox mice had changes in multiple electrophysiological signals associated with memory processing, including: decreased gamma power in the HPC, impairments in theta-gamma comodulation in the cortex, theta and delta hypersynchrony between the HPC and cortex, and fewer sharp-wave ripples in the HPC. These findings suggest that GABAergic signaling on microglia may facilitate neural network systems involved in memory formation and recall, and that alterations in microglia may impair functions necessary for memory formation.

Publication Date

Fall 11-15-2021




Neuroscience; Neural Circuitry; Hippcampus; Anterior Cingulate Cortex; Learning and Memory

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Faculty Mentor: James Hyman, Ph.D.


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The Effects of Altered GABAergic Signaling in Microglia on Hippocampal-cortical Network Activity and Remote Recall