Structural and functional abnormalities in thalamic neurons following neocortical focal status epilepticus.

Status epilepticus (SE) is a life-threatening emergency that can result in de novo development or worsening of epilepsy. We tested the hypothesis that the aberrant cortical output during neocortical focal status epilepticus (FSE) would induce structural and functional changes in the thalamus that might contribute to hyperexcitability in the thalamocortical circuit. We induced neocortical FSE by unilateral epidural application of convulsant drugs to the somatosensory cortex of anesthetized mice of both sexes.

Dopamine D and Adenosine A Receptors Interaction on Ca Current Modulation in a Rodent Model of Parkinsonism.

A receptor required previous D receptor activation to modulate Ca currents. Istradefylline decreases pramipexole modulation on Ca currents. Istradefylline reduces A + neurons activity in striatial microcircuit, but pramipexole failed to further reduce neuronal activity.

Prolonged prophylactic effects of gabapentin on status epilepticus-induced neocortical injury.

Long-term consequences of status epilepticus (SE) occur in a significant proportion of those who survive the acute episode. We developed an in vivo model of acute focal neocortical SE (FSE) to study long-term effects on local cortical structure and function and potential strategies to mitigate adverse consequences of SE. An acute 2 h episode of FSE was induced in anesthetized mice by epidural application of gabazine +4-aminopyridine over sensorimotor neocortex.