The Ca2+ channels selectivity was examined in hair cells isolated from the canals and patch-clamp recorded. As found previously, 60% of the cells exhibited in 4 mM extemal Ca2+ a steady Ca2+ current carried by L+R2 components, while the remaining ones exhibited also an R1 component showing Ca2+-dependent inactivation. In 10 nM external Ca2+ all cells displayed a steady Na+ current, 5-6 times larger than the control Ca2+ one, whose I-V peaked at —50 mV rather than at —20 mV. Nifedìpine 10 microM blocked the Ca2+ current by 60% in cells endowing the L+R2 components and by 78% in cells exhibiting also the R1 component; R1 inactivation was hastened 1.6 times owing to a partial block of the open R1 channel. The Ca2+ current activated monoexponentially (tauon=0.7 ms), whereas deactivation was bi¬exponential (tauoff1=1.2; tauoff2 = 9.1 ms): both Na+ current tauon and tauoff were accelerated by a factor 1.7. In cells displaying the L+R2 components, nifedipine affected also the open R2 channel, producing a sag in the Na+ current tracing, which was reduced by 65% at the peak and by 77% at the plateau with respect to the control. Nifedipine affected also the open R1 channel in cells exhibiting the L+R2+R1 components, reducing the control Na+ current by 77% at the peak and by 85% at the plateau, respectively. Blockade of R1 and R2 channels was more effettive at more negative potentials. Therefore, all three channel types lose their Ca2+ selectivity in low Ca2+ solution and are all affected by nifedipine, although to a different extent.
Na+ Current through voltage-gated Ca2+ channels of frog hair cell semicircular canals.
MARTINI, Marta;RISPOLI, Giorgio;FARINELLI, Federica;GONZALEZ, Edgardo Maximiliano;ROSSI, Marialisa
2003
Abstract
The Ca2+ channels selectivity was examined in hair cells isolated from the canals and patch-clamp recorded. As found previously, 60% of the cells exhibited in 4 mM extemal Ca2+ a steady Ca2+ current carried by L+R2 components, while the remaining ones exhibited also an R1 component showing Ca2+-dependent inactivation. In 10 nM external Ca2+ all cells displayed a steady Na+ current, 5-6 times larger than the control Ca2+ one, whose I-V peaked at —50 mV rather than at —20 mV. Nifedìpine 10 microM blocked the Ca2+ current by 60% in cells endowing the L+R2 components and by 78% in cells exhibiting also the R1 component; R1 inactivation was hastened 1.6 times owing to a partial block of the open R1 channel. The Ca2+ current activated monoexponentially (tauon=0.7 ms), whereas deactivation was bi¬exponential (tauoff1=1.2; tauoff2 = 9.1 ms): both Na+ current tauon and tauoff were accelerated by a factor 1.7. In cells displaying the L+R2 components, nifedipine affected also the open R2 channel, producing a sag in the Na+ current tracing, which was reduced by 65% at the peak and by 77% at the plateau with respect to the control. Nifedipine affected also the open R1 channel in cells exhibiting the L+R2+R1 components, reducing the control Na+ current by 77% at the peak and by 85% at the plateau, respectively. Blockade of R1 and R2 channels was more effettive at more negative potentials. Therefore, all three channel types lose their Ca2+ selectivity in low Ca2+ solution and are all affected by nifedipine, although to a different extent.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
