| First Author | Di Pasquale E | Year | 1997 |
| Journal | J Neurophysiol | Volume | 77 |
| Issue | 2 | Pages | 621-31 |
| PubMed ID | 9065835 | Mgi Jnum | J:40687 |
| Mgi Id | MGI:708065 | Doi | 10.1152/jn.1997.77.2.621 |
| Citation | Di Pasquale E, et al. (1997) Increased excitability and inward rectification in layer V cortical pyramidal neurons in the epileptic mutant mouse Stargazer. J Neurophysiol 77(2):621-31 |
| abstractText | The excitability of layer V cortical pyramidal neurons was studied in vitro in the single-locus mutant mouse stargazer (stg), a genetic model of spike wave epilepsy. Field recordings in neocortical slices from mutant mice bathed in artificial cerebrospinal fluid revealed spontaneous synchronous network discharges that were never present in wild-type slices. Intracellular and whole cell recordings from stg/stg neurons in deep layers showed spontaneous giant depolarizing excitatory post-synaptic potentials generating bursts of action potentials, and a 78% reduction in the afterburst hyperpolarization. Whole cell recordings revealed gene-linked differences in active membrane properties in two types of regular spiking neurons. Single action potential rise and decay times were reduced, and the rheobase current was decreased by 68% in mutant cells. Plots of spike frequency-current relationships revealed that the gain of this relation was augmented by 29% in the mutant. Comparisons of visually identified pyramidal neurons firing properties in both genotypes revealed no difference in single action potential afterhyperpolarization. Voltage-clamp recordings showed an approximately threefold amplitude increase in a cesium-sensitive inward rectifier. No cell density or soma size differences were observed in the layer V pyramidal neuron population between the two genotypes. These results demonstrate an autonomous increase in cortical network excitability in a genetic epilepsy model. This defect could lower the threshold for aberrant thalamocortical spike wave oscillations in vivo, and may contribute to the mechanism of one form of inherited absence epilepsy. |
