CaV2.3 Channels Are Critical for Oscillatory Burst Discharges in the Reticular Thalamus and Absence Epilepsy

Tariq Zaman, Kyoobin Lee, Cheongdahm Park, Afshin Paydar, Jee Hyun Choi, Eunji Cheong, C. Justin Lee, Hee Sup Shin

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51 Citations (Scopus)

Abstract

Neurons 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 CaV2.3 channels. In brain slices of CaV2.3-/-, 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 CaV2.3 resulted in a marked decrease in the sensitivity of the animal to γ-butyrolactone-induced absence epilepsy. Local blockade of CaV2.3 channels in the RT mimicked the results of CaV2.3-/- mice. These results provide strong evidence that CaV2.3 channels are critical for oscillatory burst discharges in RT neurons and for the expression of absence epilepsy.

Original languageEnglish
Pages (from-to)95-108
Number of pages14
JournalNeuron
Volume70
Issue number1
DOIs
Publication statusPublished - 2011 Apr 14

ASJC Scopus subject areas

  • Neuroscience(all)

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    Zaman, T., Lee, K., Park, C., Paydar, A., Choi, J. H., Cheong, E., Lee, C. J., & Shin, H. S. (2011). CaV2.3 Channels Are Critical for Oscillatory Burst Discharges in the Reticular Thalamus and Absence Epilepsy. Neuron, 70(1), 95-108. https://doi.org/10.1016/j.neuron.2011.02.042