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Effects of caffeine on NMDA-evoked 45Ca2+ release in the rat dentate gyrus in vivo

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Alaraj M., Kosinska I., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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1998
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vol. 58
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issue 4
239-246
EN
Caffeine in 10-2 M concentration per se activates ryanodine receptors (RyR) in vitro, thereby increasing the intracellular concentration of Ca2+ ([Ca2+]i). In general opinion, caffeine applied in vivo in much lower doses does not affect [Ca2+]i in neurones. However, it was recently demonstrated that caffeine in low concentrations in vitro potentiates evoked Ca2+ release in neurones via RyR. Microdialysis of the rat dentate gyrus (DG), combined with measurement of 45Ca2+ efflux, has been used in our laboratory to study in vivo NMDA-evoked calcium induced calcium release (CICR) via RyR. The aim of the present microdialysis study was to investigate in vivo effects of caffeine, applied systemically in a pharmacologically-relevant dose, and locally in the dialysis medium in very high concentration, on the NMDA-evoked CICR in DG neurones. To ensure steady brain concentration of caffeine, its systemic (i.p.) administration in a dose of 40 mg/kg was followed by a continuous i.p. infusion of 80 mg/kg/min and application of 0.4 mM caffeine in the dialysis medium. The results demonstrated that in the rat DG, local administration of 50 mM caffeine significantly stimulates a spontaneous 45Ca2+ efflux and its release induced by 5 mM NMDA. However, systemic administration of caffeine had no effect on spontaneous and NMDA-induced 45Ca2+ release in the rat DG, which supports the view that caffeine, applied in vivo, even in high doses, does not influence CICR in brain neurones.
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Insulin impairs the anticonvulsive activity of carbamazepine against maximal electroshock-induced seizures in mice

100%
Alaraj M., Pieniak M., Kowalczyk M., Kosinska I.
Acta Neurobiologiae Experimentalis
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1998
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vol. 58
|
issue 4
283-286
EN
In view of the data indicating that insulin can modify penetration of some drugs across cell membranes and tissue barriers, particularly the blood-brain barrier, the aim of the present study was to evaluate the effect of insulin on both the anticonvulsant activity and the brain concentration of carbamazepine in mice suffering from seizures induced by maximal electroshock. The antiepileptic drug was administered per os in single doses either alone or in combination with insulin given as single intraperitoneal injections. To assess the anticonvulsant activity of carbamazepine the ED50 values were calculated. The results indicate that insulin given in doses up to 2 units/kg did not affect the convulsive threshold, whereas insulin applied at 2 units/kg led to a significant reduction in the anticonvulsant activity of carbamazepine, as judged by an increase in the ED50 value from 16.2 to 41.3 mg/kg. This effect was accompanied by the marked reduction in both the brain and blood concentrations of the drug. It is likely, therefore, that the inhibitory activity of insulin on the anticonvulsive function of carbamazepine is related not only to the effect of the former on the blood-brain transport of the latter, but also to insulin-induced modulation of the serum concentration of the drug.
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