| First Author | Kim D | Year | 2001 |
| Journal | Neuron | Volume | 31 |
| Issue | 1 | Pages | 35-45 |
| PubMed ID | 11498049 | Mgi Jnum | J:70557 |
| Mgi Id | MGI:2137777 | Doi | 10.1016/s0896-6273(01)00343-9 |
| Citation | Kim D, et al. (2001) Lack of the burst firing of thalamocortical relay neurons and resistance to absence seizures in mice lacking alpha(1G) T-type Ca(2+) channels. Neuron 31(1):35-45 |
| abstractText | T-type Ca(2+) currents have been proposed to be involved in the genesis of spike-and-wave discharges, a sign of absence seizures, but direct evidence in vivo to support this hypothesis has been lacking. To address this question, we generated a null mutation of the alpha(1G) subunit of T-type Ca(2+) channels. The thalamocortical relay neurons of the alpha(1G)-deficient mice lacked the burst mode firing of action potentials, whereas they showed the normal pattern of tonic mode firing. The alpha(1G)-deficient thalamus was specifically resistant to the generation of spike-and-wave discharges in response to GABA(B) receptor activation. Thus, the modulation of the intrinsic firing pattern mediated by alpha(1G) T-type Ca(2+) channels plays a critical role in the genesis of absence seizures in the thalamocortical pathway. |
