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Purpose: This study attempted to clarify the role of histamine or histamine H1 receptors in the development of amygdaloid kindling by using histidine decarboxylase (HDC)-deficient and histamine H1 receptor (H1R)-deficient mice. Methods: Under pentobarbital anesthesia, mice were fixed to a stereotaxic apparatus, and bipolar electrodes were implanted into the right amygdala. Electrodes were connected to a miniature receptacle, which was embedded in the skull with dental cement. A bipolar electroencephalogram was recorded; bipolar stimulation of the amygdala was applied every day with a constant-current stimulator and continued until a generalized convulsion was obtained. Results: The development of amygdaloid kindling in HDC-deficient and H1R-deficient mice was significantly accelerated compared with that in their respective wild-type mice. In addition, the afterdischarge (AD) duration and generalized seizure duration in HDC-deficient and H1R-deficient mice were prolonged. Intraperitoneal injection of histidine resulted in an inhibition of amygdaloid kindled seizures in wild-type mice at doses that caused an increase in the histamine contents of the brain. However, no significant effect was observed with histidine in H1R-deficient mice at the same dose. Conclusions: These findings suggest that histaminergic mechanisms through H1 receptors play a crucial role not only in amygdaloid kindled seizures but also in the development of amygdaloid kindling. [ABSTRACT FROM AUTHOR]

The effect of histamine H3 antagonist, iodophenpropit on amygdaloid kindled seizures in rats was studied in comparison with those of other H3 antagonists. Under pentobarbital anesthesia, the rats were fixed to a stereotaxic apparatus and bipolar electrodes were implanted into the amygdala. Electrodes were connected to a miniature receptacle, which was embedded in the skull with dental cement. To cause kindled seizures, electrical stimulation was applied to the amygdala bipolarly every day by a constant current stimulator, and electroencephalogram and convulsive behavior were observed. Drug effects were estimated in rats showing generalized kindled seizures. Intraperitoneal injection of H3 antagonists, iodophenpropit, thioperamide, AQ0145 and clobenpropit, resulted in a dose-related inhibition of amygdaloid kindled seizures. The effect of iodophenpropit on amygdaloid kindled seizures was more potent than those of thioperamide, AQ0145 and clobenpropit. In conclusion, iodophenpropit may be useful for the treatment of partial epilepsy and/or secondary generalized seizures in humans. [Copyright &y& Elsevier]

The epileptogenic activities induced by histamine H1 antagonists in amygdala-kindled rats were studied in comparison with activities in nonkindled rats (sham rats). Intraperitoneal injection of pyrilamine, diphenhydramine and ketotifen resulted in behavioral and electroencephalogram (EEG)-detected seizures in amygdala-kindled rats at doses which caused no or negligible seizures in sham rats. On the other hand, loratadine and cetirizine caused no behavioral or EEG seizures in either amygdala-kindled or sham rats even at a dose of 40 mg/kg. In conclusion, first-generation H1 antagonists likely elicit epileptogenic activity in amygdala-kindled rats more potent than that in sham rats. [Copyright &y& Elsevier]

Abstract: Pyrite, a common gangue mineral in complex sulfide ores and coals, is rapidly oxidized in water by ferric ions and dissolved oxygen to form a very acidic and heavy metal-laden leachate called acid mine drainage (AMD). Carrier-microencapsulation (CME) using Ti4+, Si4+, and Al3+ was reported as a promising new approach to prevent pyrite oxidation by forming a passivating barrier on the pyrite surface. In CME, the presence of Fe3+-catecholate complexes is unavoidable but their effects on pyrite oxidation remain unclear. In this study, the effects of Fe3+-catecholate complexes on pyrite oxidation were investigated. Formations of mono-, bis-, and tris-catecholate complexes of Fe3+ were verified by UV–Vis spectrophotometry and their speciation with pH was consistent with thermodynamic considerations. Linear sweep voltammetry was conducted to evaluate the redox properties of Fe3+-catecholate complexes, and the results indicate that ligands in the three complexes were sequentially oxidized until Fe3+ is released. Coating formation on pyrite was confirmed after treatment with mono- and bis-catecholate complexes. Results of SEM-EDX and ATR-FTIR indicate that the coating is composed primarily of iron oxyhydroxide phases. The results of leaching experiments showed that pyrite oxidation was suppressed by Fe3+-catecholate complexes via two mechanisms: (1) electron donating effects of the complexes, and (2) formation of a protective coating on pyrite. The results provide not only a better understanding of the effects of Fe3+-catecholate complexes on pyrite oxidation but also some possible applications of Fe3+-based CME such as the suppression of pyrite oxidation to prevent AMD formation and depression of pyrite floatability in mineral processing. Graphical abstract Image 1 Highlights • Fe3+-catecholate complexes were oxidatively decomposed to release Fe3+ on pyrite surface. • Fe3+ was precipitated as an iron oxyhydroxide coating on pyrite surface. • Iron-based CME suppressed pyrite oxidation and could depress its floatability in mineral processing. [ABSTRACT FROM AUTHOR]