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J. Biol. Chem., Vol. 283, Issue 18, 12093-12101, May 2, 2008

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Ablation of Ca²⁺ Channel β3 Subunit Leads to Enhanced N-Methyl-D-aspartate Receptor-dependent Long Term Potentiation and Improved Long Term Memory^*

Daejong Jeon, Inseon Song, William Guido^¶, Karam Kim^||, Eunjoon Kim^||, Uhtaek Oh¹, and Hee-Sup Shin²

From the Center for Neural Science, Korea Institute of Science and Technology, Seoul 136-791, Korea, National Creative Research Initiative Center for Sensory Research, Seoul National University, College of Pharmacy, Seoul 151-742, Korea, the ^¶Department of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298, and ^||National Creative Research Initiative Center for Synaptogenesis, Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea

The β subunits of voltage-dependent Ca²⁺ channels (VDCCs) have marked effects on the properties of the pore-forming ₁ subunits of VDCCs, including surface expression of channel complexes and modification of voltage-dependent kinetics. Among the four different β subunits, the β₃ subunit (Ca_vβ3) is abundantly expressed in the hippocampus. However, the role of Ca_vβ3 in hippocampal physiology and function in vivo has never been examined. Here, we investigated Ca_vβ3-deficient mice for hippocampus-dependent learning and memory and synaptic plasticity at hippocampal CA3-CA1 synapses. Interestingly, the mutant mice exhibited enhanced performance in several hippocampus-dependent learning and memory tasks. However, electrophysiological studies revealed no alteration in the Ca²⁺ current density, the frequency and amplitude of miniature excitatory postsynaptic currents, and the basal synaptic transmission in the mutant hippocampus. On the other hand, however, N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic currents and NMDAR-dependent long term potentiation were significantly increased in the mutant. Protein blot analysis showed a slight increase in the level of NMDAR-2B in the mutant hippocampus. Our results suggest a possibility that, unrelated to VDCCs regulation, Ca_vβ3 negatively regulates the NMDAR activity in the hippocampus and thus activity-dependent synaptic plasticity and cognitive behaviors in the mouse.

Received for publication, January 31, 2008 , and in revised form, March 12, 2008.

^* This work was supported by the National Honor Scientist Program of Korea, grants from Korea Institute of Science and Technology, the National Creative Research Initiatives of the Ministry of Science and Technology of Korea, and Virginia Commonwealth University Medical Center Grant NEI EY12716. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1 and S2.

¹ To whom correspondence may be addressed. Tel.: 82-2-880-7854; Fax: 82-2-872-0596; E-mail: utoh{at}plaza.snu.ac.kr. ² To whom correspondence may be addressed. Tel.: 82-2-958-6931; Fax: 82-2-958-6937; E-mail: shin{at}kist.re.kr.

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