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Ion Channels and Excitable Membranes

開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Effects of Calmodulin in Modulating the Cav2.2

  • P2-004
  • Chih-Hung Chi:1 Chien-Yuan Pan:1 
  • 1:Dept LS, Nat Taiwan Univ, Taipei, Taiwan(R.O.C.) 

The influx of Ca2+ through the voltage-gated calcium channels (Cav) triggers the fusion of synaptic vesicle with the plasma membrane to release neurotransmitters at the nerve terminals. The binding of calmodulin (CaM) on the IQ motifs at the C-terminals of Cav1.1 and Cav2.1 is responsible for the Ca2+-dependent inactivation (CDI). The Cav2.2 is present in the both central and peripheral nervous system, and it has a major presynaptic role in regulation of transmitter release. The Cav2.2 has a similar IQ motif with IF as the central amino acids; however, its interaction with CaM has not been well investigated. In this report, Cav2.2 and CaM were co-expressed in 293T cells and the Ca2+ currents were recorded by patch-clamp technique in whole-cell mode. The inward Ca2+ currents inactivated quickly to 15.5 ± 5.8% of the peak current at 250 ms when co-expressed with CaM. This inactivation was blocked by the co-expressed Ca2+-binding deficient mutation CaM1234 to 44.1 ± 5.4%. CaM12 and CaM34 also decreased the Ca2+ dependent inactivation (CDI) to 40%. IF mutations caused a lower current density and shifted the activation curve Vh from 18.5 ± 3.1 mV to 30.5 ± 5.3mV, but had no significant effect on the CDI (19.1 ± 4.2%). When co-expressed with IF mutations, CaM mutations did not affect the gating kinetics of the channels. Although CaM34 and CaM1234 did not change CDI (22.5 ± 5.3/ 23.2 ± 5.8%), CaM12 decreases CDI to 46.6 ± 5.7%. In addition, CaM12 co-expression increased the current density of wild type and IF mutations. Therefore, the N- and C-lobes of CaM play distinct roles in modulating the Cav2.2 activities.

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