Sj. Caddick et Da. Hosford, GABA(B)-ACTIVATED GK(+) IN THALAMIC NEURONS IN THE LETHARGIC (LH LH) MOUSE MODEL OF GENERALIZED ABSENCE SEIZURES/, Neuroscience letters, 205(1), 1996, pp. 29-32
Whole-cell voltage-clamp recordings were made from thalamic ventrobasa
l (VB) neurons of age-matched lethargic (VB) 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(+) acti
vated by baclofen. In addition to this, isolated, evoked GABAB-mediate
d currents were recorded in VB cells. There was no significant differe
nce 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 seizu
res.