Abstract
Aim:
To investigate the effect of aluminum (Al) on high voltage-dependent calcium current (I HVA) and its modulation by ginkgolide B (Gin B).
Methods:
The whole-cell, patch-clamp technique was used to record I HVA from acutely isolated hippocampal CA1 pyramydal neurons in rats.
Results:
Al 0.1 mmol/L (low concentration) reduced I HVA; Al 0.75 and 1.0 mmol/L (high concentrations) increased I HVA, and Al decreased and increased I HVA at intermediate concentrations of 0.25 and 0.5 mmol/L. The increase of I HVA by Al 1.0 mmol/L was enhanced by the adenylyl cyclase (AC) agonist forskolin and was partly abolished by the cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) antagonist H-89, whereas the decrease observed with Al 0.1 mmol/L was neither reversed by forskolin nor affected by H-89. Gin B had no effect on I HVA in normal neurons, but canceled the increase in I HVA by 1.0 mmol/L Al.
Conclusion:
The results indicate that the mechanism of Al affecting I HVA differs at different concentrations, and this may be attributed to its complex actions. Gin B could prevent neurons from injury by inhibiting calcium influx.
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Chen, L., Liu, Cj., Tang, M. et al. Action of aluminum on high voltage-dependent calcium current and its modulation by ginkgolide B. Acta Pharmacol Sin 26, 539–545 (2005). https://doi.org/10.1111/j.1745-7254.2005.00073.x
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DOI: https://doi.org/10.1111/j.1745-7254.2005.00073.x
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