Ionic basis of the caesium-induced depolarisation in rat supraoptic nucleus neurones
The effects of external Cs + on magnocellular neurosecretory cells were studied during intracellular recordings from 93 supraoptic nucleus neurones in superfused explants of rat hypothalamus. Bath application of 3â5 m m Cs + provoked reversible membrane depolarisation and increased firing rate in...
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Veröffentlicht in: | The Journal of physiology 2001-11, Vol.536 (3), p.797-808 |
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Sprache: | eng |
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Zusammenfassung: | The effects of external Cs + on magnocellular neurosecretory cells were studied during intracellular recordings from 93 supraoptic nucleus neurones in
superfused explants of rat hypothalamus.
Bath application of 3â5 m m Cs + provoked reversible membrane depolarisation and increased firing rate in all of the neurones tested. Voltage-current analysis
revealed an increase in membrane resistance between â120 and â55 mV. The increase in resistance was greater below â85 mV than
at more positive potentials.
Voltage-clamp analysis showed that external Cs + blocked the hyperpolarisation-activated inward current, I H . Under current clamp, application of ZD 7288, a selective blocker of I H , caused an increase in membrane resistance at voltages â¤â65 mV. Voltage-current analysis further revealed that blockade of
I H caused hyperpolarisation when the initial voltage was < â60 mV but had no effect at more positive values.
Current- and voltage-clamp analysis of the effects of Cs + in the presence of ZD 7288, or ZD 7288 and tetraethyl ammonium (TEA), revealed an increase in membrane resistance throughout
the range of voltages tested (â120 to â45 mV). The current blocked by Cs + in the absence of I H was essentially voltage independent and reversed at â100 mV. The reversal potential shifted by +22.7 mV when external [K + ] was increased from 3 to 9 m m . We conclude that, in addition to blocking I H , external Cs + blocks a leakage K + current that contributes significantly to the resting potential of rat magnocellular neurosecretory cells. |
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ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1111/j.1469-7793.2001.00797.x |