Literature DB >> 7719708

Distinctive functional properties of the neuronal BII (class E) calcium channel.

M Wakamori1, T Niidome, D Furutama, T Furuichi, K Mikoshiba, Y Fujita, I Tanaka, K Katayama, A Yatani, A Schwartz.   

Abstract

Functional diversity of voltage-dependent calcium channels (VDCC) is primarily due to the existence of six distinct genes of the channel-forming subunit alpha 1, which can be further classified into the L-type and neuronal non-L-type subfamilies. We have examined functional properties of the calcium channel BII expressed from the cloned cDNA, in Xenopus oocytes, and compared the results with the other members of the non-L-type subfamily, the BI and BIII channels. The BII channel is a high voltage-activated calcium channel pharmacologically features by its unique sensitivity to the inorganic blocker Ni2. The decaying component of the BII current shows high sensitivity to Ni2+ similar to that of the low voltage-activated channels and the R-type channel in cerebellar granule cells, whereas the sustained component is relatively resistant to Ni2+ as are the other high voltage-activated calcium channels. Dihydropyridines, omega-CgTx-GVIA, and omega-Aga-IVA, which have been used to discriminate L-, N-, and P-types, do not affect the BII current. The mode of modulation of the BII channel by auxiliary subunits is strikingly different from that observed in the L-type channels. Both activation and inactivation rates of the BII current are decelerated by coexpression of the beta subunit, and this effect is cancelled by further coexpression of the alpha 2 subunit. In situ tissue distribution studies indicate a higher level of BII mRNA expression in the hippocamus compared to other brain regions, revealing important difference in the relative abundance of BI, BII, and BIII channels in brain tissues. Overall, the results suggest that the BII channel forms a novel functional category of VDCC that is different from T-, L-, N-, and P-type.

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Year:  1994        PMID: 7719708

Source DB:  PubMed          Journal:  Receptors Channels        ISSN: 1060-6823


  20 in total

1.  Biphasic, opposing modulation of cloned neuronal alpha1E Ca channels by distinct signaling pathways coupled to M2 muscarinic acetylcholine receptors.

Authors:  U Meza; R Bannister; K Melliti; B Adams
Journal:  J Neurosci       Date:  1999-08-15       Impact factor: 6.167

2.  Auxiliary subunits operate as a molecular switch in determining gating behaviour of the unitary N-type Ca2+ channel current in Xenopus oocytes.

Authors:  M Wakamori; G Mikala; Y Mori
Journal:  J Physiol       Date:  1999-06-15       Impact factor: 5.182

3.  T-channel-like pharmacological properties of high voltage-activated, nifedipine-insensitive Ca2+ currents in the rat terminal mesenteric artery.

Authors:  Hiromitsu Morita; Juan Shi; Yushi Ito; Ryuji Inoue
Journal:  Br J Pharmacol       Date:  2002-10       Impact factor: 8.739

Review 4.  Targeting mechanisms of high voltage-activated Ca2+ channels.

Authors:  Stefan Herlitze; Mian Xie; Jing Han; Alexander Hümmer; Katya V Melnik-Martinez; Rosa L Moreno; Melanie D Mark
Journal:  J Bioenerg Biomembr       Date:  2003-12       Impact factor: 2.945

Review 5.  The ß subunit of voltage-gated Ca2+ channels.

Authors:  Zafir Buraei; Jian Yang
Journal:  Physiol Rev       Date:  2010-10       Impact factor: 37.312

Review 6.  Molecular characterization of a novel family of low voltage-activated, T-type, calcium channels.

Authors:  E Perez-Reyes
Journal:  J Bioenerg Biomembr       Date:  1998-08       Impact factor: 2.945

7.  G-Protein-dependent facilitation of neuronal alpha1A, alpha1B, and alpha1E Ca channels.

Authors:  U Meza; B Adams
Journal:  J Neurosci       Date:  1998-07-15       Impact factor: 6.167

8.  T-type Ca2+ current properties are not modified by Ca2+ channel beta subunit depletion in nodosus ganglion neurons.

Authors:  R C Lambert; Y Maulet; J Mouton; R Beattie; S Volsen; M De Waard; A Feltz
Journal:  J Neurosci       Date:  1997-09-01       Impact factor: 6.167

9.  Altered pain responses in mice lacking alpha 1E subunit of the voltage-dependent Ca2+ channel.

Authors:  H Saegusa; T Kurihara; S Zong; O Minowa; A Kazuno; W Han; Y Matsuda; H Yamanaka; M Osanai; T Noda; T Tanabe
Journal:  Proc Natl Acad Sci U S A       Date:  2000-05-23       Impact factor: 11.205

10.  Nickel block of three cloned T-type calcium channels: low concentrations selectively block alpha1H.

Authors:  J H Lee; J C Gomora; L L Cribbs; E Perez-Reyes
Journal:  Biophys J       Date:  1999-12       Impact factor: 4.033

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