Induction by convulsant drugs of brain-derived neurotrophic factor in the rat brain: an involvement of voltage-dependent calcium channels

2000 ◽  
Vol 38 ◽  
pp. S138
Author(s):  
R Katoh-Semba
2004 ◽  
Vol 366 (3) ◽  
pp. 277-281 ◽  
Author(s):  
Machiko Iwamoto ◽  
Tairo Hagishita ◽  
Yoko Shoji-Kasai ◽  
Susumu Ando ◽  
Yasukazu Tanaka

1990 ◽  
Vol 68 (11) ◽  
pp. 1414-1418 ◽  
Author(s):  
P.-A. Lavoie ◽  
G. Beauchamp ◽  
R. Elie

We have used a resting (5 mM K+) or depolarizing (60 mM K+) choline-based medium, and a nondepolarizing sodium-based or choline-based medium, to characterize the inhibitory potential of tricyclic antidepressants against the voltage-dependent calcium channels or the Na+–Ca2+ exchange process, respectively, in synaptosomes from rat brain cortex. Imipramine, desipramine, amitriptyline, and clomipramine inhibited net K+-induced 45Ca uptake with similar IC50 values (26–31 μM), and this uptake was also inhibited by diltiazem with an IC50 of 36 μM; these results indicate an inhibition of voltage-dependent calcium channels by tricyclic antidepressants. The net uptake of 45Ca induced by Na+–Ca2+ exchange was also inhibited by the four tricyclic antidepressants tested, but not by diltiazem; imipramine (IC50 = 94 μM) was a more potent inhibitor of this process than desipramine (IC50 = 151 μM), and the IC50 values of amitriptyline (107 μM) and clomipramine (97 μM) were similar to that of imipramine. Some degree (~25%) of brain calcium channel blockade could be present at the steady-state concentrations of tricyclic antidepressants expected to occur during therapeutic use of these compounds to treat depression or panic disorder.Key words: voltage-dependent calcium channels, Na+–Ca2+ exchange, synaptosomes, tricyclic antidepressants, diltiazem.


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