GABAB-activated gK+ in thalamic neurons in the lethargic (lh/lh) mouse model of generalized absence seizures.

Abstract Whole-cell voltage-clamp recordings were made from thalamic ventrobasal (V13) neurons of age-matched lethargic ( lh lh ) and wildtype (+/+) mice. Hyperpolarizing voltage commands (40 mV) from a holding potential of −60 mV were delivered to the cell and the resulting K + conductance ( g K + ) activated by the GABA B receptor agonist baclofen was measured and compared between the two groups. VB cells from +/+ and lh lh displayed no significant differences in resting conductance ( g IN) or g K + activated by baclofen. In addition to this, isolated, evoked GABA B -mediated currents were recorded in VB cells. There was no significant difference in peak amplitude or latency to peak noted between the two groups. These data suggest that postsynaptic GABA B receptor-mediated function is not altered in VB thalamic neurones in this model of absence seizures.