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1

Effects of intracortical microinjection of vitamin B12 on penicillin-induced epileptiform activity in rats

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Erfanparast A., Tamaddonfard E.
Acta Neurobiologiae Experimentalis
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2015
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tom 75
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nr 2
There are increasing studies indicating neuroprotective effects for vitamin B12. In the present study, the effect of intracortical microinjection of vitamin B12 was investigated on penicillin-induced epileptiform activity. We also examined the effects of intracortical microinjection of diazepam (a GABA-benzodiazepine receptor agonist) and flumazenil (a GABA- benzodiazepine receptor antagonist) to clarify the possible mechanism of vitamin B12. In urethane-anesthetized rats, epileptiform activity was induced by intracortical microinjection of penicillin (300 IU, 1.5 ^l), and the number and amplitude of spike waves were analyzed using electroencephalographs (EEG) recordings. Intracortical microinjections of vitamin B12 at doses of 100 and 200 ng/site, diazepam at a dose of 200 ng/site and their ineffective doses (50 ng/site of vitamin B12 with 50 ng/site of diazepam) co-microinjection treatment significantly (P<0.05) reduced both the number and amplitude of spike waves. In addition, combined microinjection of effective doses of vitamin B12 (100 ng/site) and diazepam (200 ng/site) produced more antiepileptiform effect in comparison with their alone used doses. The antiepileptic effects induced by microinjection of vitamin B12 and diazepam at a same dose of 200 ng/site were prevented by the same site microinjection of 50 ng/site of flumazenil. The results showed antiepileptiform activities for vitamin B12 and diazepam at the cerebral cortex level. A central GABA-benzodiazepine receptor complex-mediated mechanism might be involved in the antiepileptiform activity of vitamin B12.
2

Magnesium effects on nonsynaptic epileptiform activity in leech Retzius neurons

100%
Stanojevic M., Lopicic S., Jovanovic Z., Pathak D., Pavlovic D. V., Spasic S., Nedeljkov V., Prostran M.
Folia Biologica
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2015
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tom 63
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nr 4
3
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Different receptor subtypes are involved in the serotonin-induced modulation of epileptiform activity in rat frontal cortex in vitro

100%
Bobula B., Zahorodna A., Bijak M.
Journal of Physiology and Pharmacology
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2001
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tom 52
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nr 2
4
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Imipramine counteracts corticosterone-induced alterations in the effects of the activation of 5-HT7 receptors in rat hippocampus

84%
Tokarski K., Pitra P., Duszynska B., Hess G.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 2
83-88
Using extracellular recording we studied changes in the reactivity of rat hippocampal slices to an agonist of the 5-HT7 receptor, 5-carboxamidotryptamine (5-CT; 0.025-1 µM), induced by an earlier treatment of animals with corticosterone. Spontaneous bursting activity was recorded in ex vivo slices incubated in the presence of 2-[4-(2-methoxyphenyl)-1piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide (WAY 100635; 2 µM), an antagonist of the 5-HT1A receptor, in the medium devoid of Mg2+ ions. Saturation binding assays were performed using [3H]-(2R)-1-[(3-hydroxyphenyl)sulfonyl]-2-[2-(4-methyl-1-piperidinyl)ethyl]pyrrolidine hydrochloride (SB 269970), a specific antagonist of the 5-HT7 receptor. Repetitive, but not single, corticosterone administration lasting 7 and 21 days, resulted in an enhancement of the effect related to the 5-HT7 receptor activation without changes in its binding properties. In a separate set of experiments rats were treated with corticosterone for 3 weeks and additionally with imipramine, beginning on the eighth day of corticosterone administration. In the corticosterone plus imipramine group the excitatory effect of 5-CT was weaker than in the corticosterone group, indicating that corticosterone-induced functional modifications in the reactivity of the 5-HT7 receptor were reversed and further weakened by imipramine treatment. This effect was accompanied by a reduction in the density of [3H]-SB 269970 binding sites. Thus, imipramine treatment counteracts the corticosterone-induced increase in the reactivity of the hippocampal circuitry to the activation of the 5-HT7 receptor.
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