Chris G. Dulla

TL;DR: It is proposed that CO(2)-induced changes in neuronal function arise from a pH-dependent modulation of adenosine and ATP levels, and this findings demonstrate a mechanism for the bidirectional effects ofCO(2) on neuronal excitability in the forebrain.

TL;DR: Investigating isolated nerve terminals in brain slices by transecting hippocampal Schaffer collaterals and cortical layer I axons identifies an activity-dependent reduction in synaptic efficacy that correlated with reduced glutamate release, providing direct electrophysiological evidence that an astrocyte-dependent glutamate-glutamine cycle is required to maintain active neurotransmission at excitatory terminals.

TL;DR: The results suggest that specific cortical neuronal microcircuits may initiate and facilitate the spread of epileptiform activity following TBI, and increased glutamatergic signaling due to loss of GABAergic control may provide a mechanism by which TBI can give rise to post-traumatic epilepsy.

TL;DR: These results show that astrocytic clearance of extracellular glutamate is slowed in a temporally and spatially specific manner following bursts of neuronal activity ≥30 Hz and that these changes affect the neuronal response to released glutamate.

TL;DR: It is found that astroglial glutamate transporter subtype glutamate transporter 1 (GLT1) and glutamate uptake is significantly reduced in the cortex of fmr1(-/-) mice, and the dysregulation of GLT1 and reduced glutamate uptake may potentially contribute to enhanced neuronal excitability observed in the mouse model of FXS.