Sodium channel heterologous expression in mammalian cells and the role of the endogenous beta1-subunits.

Journal article

Sodium currents in cell lines transfected with the sole alpha-subunit, or constitutively expressing sodium channels, have an inactivation that is always prevalently mono-exponential. Differently, expression of alpha-subunit in Xenopus oocytes exerts slow inactivating currents with biphasic decay, while simultaneous co-transfection of alpha and beta1 restores a mono-exponential (normal) inactivation. A hypothesis for such differences is that an endogenous presence of beta1 or beta1-alternative splicing, beta1A, in cells could account for the normal inactivation. To test this hypothesis and to evaluate the role for the beta1A, we inhibited the expression of beta1/beta1A by antisense oligonucleotides on Nav1.4-transfected human embryonic cell line 293 (HEK) cells. Reduction of beta1/beta1A produces no significant functional effects in Nav1.4-HEK. This result invalidates the hypothesis that the lack of slow-mode in cell lines is simply due to a constitutive expression of beta1/beta1A.

Authors: Moran, O; Conti, F; Tammaro, P

• Publication status: Published
• Journal: Neuroscience letters
• Volume: 336
• Issue: 3
• Pages: 175-179
• Publication date: 2003-01-01
• DOI: 10.1016/s0304-3940(02)01284-3
• EISSN: 1872-7972
• ISSN: 0304-3940
• Language: English
• Keywords: Oligonucleotides, Antisense; Alternative Splicing; Humans; Cell Line; Electrophysiology; Sodium Channels; Immunohistochemistry