GABAB-activated gK+ in thalamic neurons in the lethargic (lh/lh) mouse model of generalized absence seizures.
Whole-cell voltage-clamp recordings were made from thalamic ventrobasal (VB) 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 (gK+) activated by the GABAB receptor agonist baclofen was measured and compared between the two groups. VB cells from +/+ and lh/lh displayed no significant differences in resting conductance (gIN) or gK+ activated by baclofen. In addition to this, isolated, evoked GABAB-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 GABAB receptor-mediated function is not altered in VB thalamic neurones in this model of absence seizures.
Caddick
S J
SJ
Division of Neurology, Duke University and Durham VA Medical Centers, NC 27705, USA. sajaca@acpub.duke.edu
Hosford
D A
DA
D000818:Animals; D001418:Baclofen / Q000494:pharmacology*; D004195:Disease Models, Animal; D004832:Epilepsy, Absence / Q000503:physiopathology; D051379:Mice; D008815:Mice, Inbred Strains; D015221:Potassium Channels / Q000187:drug effects*; D018080:Receptors, GABA-B / Q000187:drug effects*; D013788:Thalamus / Q000187:drug effects*
D015221:Potassium Channels; D018080:Receptors, GABA-B; D001418:Baclofen