Jay R. Gibson

This study identifies GAA accumulation in gliomas as a driver of neuronal activity and tumor growth, linking cancer metabolism to neuroscience through GABAA receptor activation.

This study identifies gene regulatory programs and cell type-specific molecular mechanisms underlying inferior colliculus development and auditory function.

The paper identifies CEND1 as a regulator of activity-dependent glucose metabolism by facilitating mitochondrial ATP channeling to hexokinase I.

This study shows that reduced CB1 receptor function in GABAergic neurons of FXS model mice rescues cortical hyperexcitability and sensory-driven synchrony deficits.

This study shows that malin-deficient mice accumulate Lafora bodies without observable neurobehavioral decline, suggesting a delay between LB accumulation and clinical symptoms.

This study shows FOXP1 regulates glutamatergic input development in striatal neurons, with potential therapeutic implications for FOXP1 syndrome.

The paper shows that Foxp1 and Foxp2 compensate for each other in D1-SPNs, and their loss causes motor and social deficits, which can be reversed by re-expressing Foxp1.

This study identifies female-specific neocortical circuit dysfunction in a mouse model of autism linked to mGluR5 and estrogen receptor α, leading to hyperexcitability and behavioral deficits.

This study shows that human CLOCK has extra-circadian functions in the neocortex, enhancing cognitive flexibility and neural connectivity through altered gene expression in excitatory neurons.

This study shows that postsynaptic FMRP is required for maturation of callosal synapses in mice, with sensory experience modulating synaptic strength.

The paper shows that FOXP1 reduces intrinsic excitability in D2 striatal projection neurons by increasing potassium currents through transcriptional activation of KIR and KLeak channels.