title: Cav2.3 channels are critical for oscillatory burst discharges in the reticular thalamus and absence epilepsy.
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 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.
authors.affiliation: Center for Neural Science, Korea Institute of Science and Technology (KIST), Seoul 136-791, Korea.
authors.forename: Tariq
authors.initials: T
authors.lastname: Zaman
authors.forename: Kyoobin
authors.initials: K
authors.lastname: Lee
authors.forename: Cheongdahm
authors.initials: C
authors.lastname: Park
authors.forename: Afshin
authors.initials: A
authors.lastname: Paydar
authors.forename: Jee Hyun
authors.initials: JH
authors.lastname: Choi
authors.forename: Eunji
authors.initials: E
authors.lastname: Cheong
authors.forename: C Justin
authors.initials: CJ
authors.lastname: Lee
authors.forename: Hee-Sup
authors.initials: HS
authors.lastname: Shin
mesh_terms: D015107:4-Butyrolactone / Q000633:toxicity; D000200:Action Potentials / Q000235:genetics / Q000502:physiology*; D000818:Animals; D020908:Calcium Channels, R-Type / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D027682:Cation Transport Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D004569:Electroencephalography / Q000379:methods; D004832:Epilepsy, Absence / Q000139:chemically induced / Q000235:genetics / Q000503:physiopathology*; D051379:Mice; D057507:Mice, 129 Strain; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D012154:Reticular Formation / Q000502:physiology*; D013787:Thalamic Nuclei / Q000502:physiology*
chemical_list: C498916:Cacna1e protein, mouse; D020908:Calcium Channels, R-Type; D027682:Cation Transport Proteins; D015107:4-Butyrolactone