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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


A POSSIBLE MECHANISM OF THE REGULATION OF CA2+RELEASE
Abstract number: PW01-2

Fedorenko1 O., Marchenko1 S.

1Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, Ukraine [email protected]

Aims: 

We have reported previously that the nuclear envelope of pyramidal neurons of hippocampus contained multiple IP3-activated Ca2+channels (IP3Rs) and large conductance cationic channels (LCC). The aim of this study was to investigate effects of membrane potential on properties of these channels.

Methods: 

Single ion channels were recorded with the patch – clamp technique from the inner membrane of nuclei isolated from pyramidal neurons of CA1 region of rat hippocampus. Results:

Channel activity of the IP3Rs was potential – dependent. The probability of the open state (Po) was much higher at positive potentials in the perinuclear space and decreased at negative potentials with the complete blockage at potentials below – 80 mV. Po of the LCC channels depended on the membrane potential too. At positive potentials they were almost all time open (Po > 0.8). At negative potentials the activity of these channels significantly decreased with complete block of the channels by potentials <= -40 mV.

Conclusion: 

These results demonstrate that the activity of IP3Rs and LCC is inhibited by negative potential in the perinuclear space. Ca2+release from intracellular stores is accompanied by large transfer of electric charge which results in development of negative potential in its lumen. This may prevent any further Ca2+release by the voltage – dependent inhibition of IP3 receptors. The voltage – dependent inhibition of LCC channels may enhance this effect by facilitating the negative shift of the potential. So we suggest that these two types of ion channels operate in concert to take part in the regulation of Ca2+signal duration.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :PW01-2

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