Fast decrease of the peak current carried by barium ions through calcium channels in the somatic membrane of mollusc neurons

1985 ◽  
Vol 404 (1) ◽  
pp. 88-90 ◽  
Author(s):  
P. G. Kostyuk ◽  
P. A. Doroshenko ◽  
A. E. Martynyuk
Keyword(s):  
Calcium Channels ◽  
Somatic Membrane ◽  
Peak Current ◽  
Barium Ions ◽  
Fast Decrease ◽  
Mollusc Neurons

Two calcium currents in the somatic membrane of mollusc neurons

1986 ◽  
Vol 17 (5) ◽  
pp. 451-455
Author(s):  
S. L. Mironov ◽  
A. V. Tepikin ◽  
A. V. Grishchenko
Keyword(s):  
Calcium Currents ◽  
Somatic Membrane ◽  
Mollusc Neurons

scholarly journals Modulation of Recombinant Human T-type calcium Channels by Δ9-tetrahydrocannabinolic acid in vitro

2020 ◽  
Author(s):  
Somayeh Mirlohi ◽  
Chris Bladen ◽  
Marina Santiago ◽  
Mark Connor
Keyword(s):  
Calcium Channels ◽  
Low Voltage ◽  
Absence Epilepsy ◽  
Resting Membrane Potential ◽  
Peak Current ◽  
Negative Shift ◽  
Whole Cell Patch Clamp ◽  
Psychoactive Effects ◽  
Steady State Inactivation

AbstractIntroductionLow voltage-activated T-type calcium channels (T-type ICa), CaV3.1, CaV3.2, and CaV3.3 are opened by small depolarizations from the resting membrane potential in many cells and have been associated with neurological disorders including absence epilepsy and pain. Δ9-tetrahydrocannabinol (THC) is the principal psychoactive compound in Cannabis and also directly modulates T-type ICa, however, there is no information about functional activity of most phytocannabinoids on T-type calcium channels, including Δ9-tetrahydrocannabinol acid (THCA), the natural non-psychoactive precursor of THC. The aim of this work was to characterize THCA effects on T-type calcium channels.Materials and MethodsWe used HEK293 Flp-In-TREx cells stably expressing CaV3.1, 3.2 or 3.3. Whole-cell patch clamp recordings were made to investigate cannabinoid modulation of ICa.ResultsTHCA and THC inhibited the peak current amplitude CaV3.1 with a pEC50s of 6.0 ± 0.7 and 5.6 ± 0.4, respectively. 1μM THCA or THC produced a significant negative shift in half activation and inactivation of CaV3.1 and both drugs prolonged CaV3.1 deactivation kinetics. THCA (10 μM) inhibited CaV3.2 by 53% ± 4 and both THCA and THC produced a substantial negative shift in the voltage for half inactivation and modest negative shift in half activation of CaV3.2. THC prolonged the deactivation time of CaV3.2 while THCA did not. THCA inhibited the peak current of CaV3.3 by 43% ± 2 (10μM) but did not notably affect CaV3.3 channel activation or inactivation, however, THC caused significant hyperpolarizing shift in CaV3.3 steady state inactivation.DiscussionTHCA modulated T-type ICa currents in vitro, with significant modulation of kinetics and voltage dependence at low μM concentrations. This study suggests that THCA may have potential for therapeutic use in pain and epilepsy via T-type channel modulation without the unwanted psychoactive effects associated with THC.

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