Mary Sommer

This study shows that a single closed-head mild traumatic brain injury (mTBI) in mice temporarily increases atypical astrocytes (AtAs) but they do not persist long-term, unlike in repeated mTBI.

This study shows that glutamate uptake is temporarily reduced in the perilesional cortex after TBI, contributing to excitotoxicity, but returns to normal levels by 14 days post-injury.

This study shows that traumatic brain injury disrupts functional connectivity in mice, with recovery and state-dependent changes in connectivity and theta power during stillness.

This study shows that APC conditional knockout mice exhibit altered parvalbumin-positive interneuron development and inhibitory synaptic dysfunction, contributing to ISS-like phenotypes.

Genetically encoded voltage imaging reveals presynaptic neuronal activity drives focal astrocyte depolarization, inhibiting glutamate uptake during neuronal activity.

In vivo treatment with 2-deoxyglucose after traumatic brain injury in mice prevented cortical hyperexcitability, synaptic changes, and loss of GABAergic interneurons.