Repeated swim exposure and PKN1a knockout enhance group I mGluR-dependent excitability associated with reduced EAAT3 expression in mouse dentate granule cells
Stress-related experiences alter glutamatergic signaling and neuronal excitability, but the mechanisms that couple experience to dentate granule cell function remain incompletely understood. Here, we examined how protein kinase N1a (PKN1a), a protein kinase C-like serine/threonine kinase, and repeated swim exposure regulate mouse hippocampal dentate granule cell excitability, with a focus on the…
Repeated swim exposure and the absence of a gene called PKN1a in mice can lead to heightened excitability in a specific type of brain cell called dentate granule cells. This increased activity is linked to a decrease in the expression of a protein called EAAT3, which is involved in transporting the neurotransmitter glutamate in and out of cells.
When researchers blocked the activity of certain receptors in the brain using specific drugs, they found that the enhanced excitability caused by swim exposure and the absence of PKN1a was reduced. This suggests that the transport of glutamate plays a role in regulating the excitability of these cells. Additionally, the reduced expression of EAAT3 and increased excitability were also associated with lower anxiety-like behavior in the mice, as measured by their movements in a special maze designed to test anxiety-related behavior.
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