• Tariq Zaman, Kyoobin Lee, Cheongdahm Park, Afshin Paydar, Jee Hyun Choi, Eunji Cheong, C Justin Lee, and Hee-Sup Shin.
• Center for Neural Science, Korea Institute of Science and Technology (KIST), Seoul 136-791, Korea.
• Neuron. 2011 Apr 14; 70 (1): 95-108.

AbstractNeurons of the reticular thalamus (RT) display oscillatory burst discharges that are believed to be critical for thalamocortical network oscillations related to absence epilepsy. Ca²+-dependent mechanisms underlie such oscillatory discharges. However, involvement of high-voltage activated (HVA) Ca²+ 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 γ-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.Copyright © 2011 Elsevier Inc. All rights reserved.

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