Long-lasting remodeling of astrocytes in an Scna1+/- mouse model of Dravet syndrome - PubMed

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Dravet syndrome (DS) is caused by mutations in the SCN1A gene, leading to loss of function of the Na��1.1 sodium channel.
The study uses a heterozygous Scn1a knockout (Scn1a+/-) mouse model to explore astrocyte remodeling in DS.
Increased hippocampal and cortical GFAP transcript and protein levels were observed in Scn1a+/- mice from disease aggravation to long-term stabilization.
Astrocyte branching increased during the aggravation phase but was not sustained long-term.
No association was found between astrocyte modifications and macroscopic hippocampal sclerosis or cortical atrophy.
Long-term astrocyte-astrocyte network expansion and increased connexin protein levels were observed in Scn1a+/- mice.
Impaired astrocytic hemichannel function was indicated by an ethidium bromide uptake assay.
Astrocyte remodeling in DS is independent of tissue damage and may be linked to seizures, synaptic, and cognitive deficits.

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