| First Author | Zaman T | Year | 2011 |
| Journal | Neuron | Volume | 70 |
| Issue | 1 | Pages | 95-108 |
| PubMed ID | 21482359 | Mgi Jnum | J:174708 |
| Mgi Id | MGI:5140651 | Doi | 10.1016/j.neuron.2011.02.042 |
| Citation | Zaman T, et al. (2011) Cav2.3 channels are critical for oscillatory burst discharges in the reticular thalamus and absence epilepsy. Neuron 70(1):95-108 |
| abstractText | Neurons of the reticular thalamus (RT) display oscillatory burst discharges that are believed to be critical for thalamocortical network oscillations related to absence epilepsy. Ca(2)+-dependent mechanisms underlie such oscillatory discharges. However, involvement of high-voltage activated (HVA) Ca(2)+ channels in this process has been discounted. We examined this issue closely using mice deficient for the HVA Ca(v)2.3 channels. In brain slices of Ca(v)2.3/, a hyperpolarizing current injection initiated a low-threshold burst of spikes in RT neurons; however, subsequent oscillatory burst discharges were severely suppressed, with a significantly reduced slow afterhyperpolarization (AHP). Consequently, the lack of Ca(v)2.3 resulted in a marked decrease in the sensitivity of the animal to gamma-butyrolactone-induced absence epilepsy. Local blockade of Ca(v)2.3 channels in the RT mimicked the results of Ca(v)2.3/ mice. These results provide strong evidence that Ca(v)2.3 channels are critical for oscillatory burst discharges in RT neurons and for the expression of absence epilepsy. |
