New technologies for the digital recording of broadband complex signals have made it possible to develop and create laboratory autonomous multichannel equipment to record bioacoustic activity on a digital medium with low power consumption and the possibility of continuous recording for up to 4 h. The equipment operates under the control of a fit-PC computer with the Windows operating system and the PowerGraph program for digital recording in a frequency band of the analog path of up to 600 kHz. Equipment testing recorded paradoxical signals from toothed whales with a frequency band exceeding 200 kHz. Signals with an extended frequency band were recorded in a laboratory experiment in open water while solving the problem of target tracking and in an experiment with provocation of acoustic communication behavior.

Using Fura-2AM microfluorimetry, we have shown for the first time that sigma-1 receptor agonist, tricyclic antidepressant amitriptyline, significantly inhibits glutoxim- and molixan-induced Ca2+-responses in rat peritoneal macrophages. The results suggest possible involvement of sigma-1 receptors in the signaling cascade induced by glutoxim or molixan and leading to intracellular Ca2+ concentration increase in macrophages.

The influence of the neuroleptic trifluoperazine on the intracellular concentration of Ca2+ in macrophages of rats was studied using a Fura-2AM fluorescent Ca2+ probe. It was found that trifluoperazine causes a dose-dependent increase in the intracellular Ca2+ concentration associated with Ca2+ mobilization from intracellular Ca2+ stores and subsequent entry of Ca2+ into peritoneal macrophages of rats. It was also shown that inhibitors of phospholipase A2 (4-bromophenacyl bromide, prednisolone, and dexamethasone), cyclooxygenases (aspirin and indomethacin), and lipoxygenases (caffeic acid, zileuton, and baicalein) suppress Ca2+ responses induced by trifluoperazine in macrophages. The data obtained indicate the participation of enzymes and/or products of the cascade of arachidonic acid metabolism in the influence of trifluoperazine on the intracellular concentration of Ca2+ in peritoneal macrophages.

Using Fura-2AM microfluorimetry, it was shown for the first time that phospholipase A(2) inhibitors 4-bromophenacyl bromide and glucocorticosteroids prednisolone and dexamethasone attenuate Ca2+ responses induced by neuroleptic trifluoperazine in macrophages. The results suggest the involvement of phospholipase A(2) and arachidonic acid metabolism cascade in the effect of trifluoperazine on intracellular Ca2+ concentration in macrophages.

Using Fura-2AM microfluorimetry, we have shown for the first time that preincubation of macrophages with the calsequestrin inhibitor neuroleptic trifluoperazine leads to a significant inhibition of the store-dependent Ca2+ entry induced by endoplasmic Ca2+-ATPase inhibitors thapsigargin or cyclopiazonic acid in rat peritoneal macrophages. The results suggest calsequestrin involvement in the regulation of the store-dependent Ca2+ entry in macrophages.

С помощью флуоресцентного Са-зонда Fura-2AM впервые показано, что преинкубация макрофагов с метил- -циклодекстрином, вызывающим экстракцию мембранного холестерина и разрушение рафтов, приводит к значительному подавлению депозависимого входа Са, индуцируемого тапсигаргином в перитонеальных макрофагах крысы. Добавление метил- -циклодекстрина после того, как механизмы входа Са уже были активированы опустошением депо под влиянием тапсигаргина, напротив, вызывает усиление последующего депозависимого входа Са. Полученные результаты свидетельствуют о том, что целостность липидных рафтов необходима для активации, но не для поддержания депозависимого входа Са в макрофаги.

Using Fura-2AM microfluorimetry, we have shown for the first time that sigma-1 receptor antagonist, antipsychotic haloperidol, significantly inhibits glutoxim- and molixan-induced Ca2+-response in peritoneal macrophages. These results indicate possible involvement of sigma-1 receptors in the signal cascade induced by glutoxim or molixan and leading to intracellular Ca2+ concentration increase in macrophages.

Using Fura-2AM microfluorimetry, it was shown for the first time that neuroleptic chlorpromazine causes intracellular Ca2+ concentration increase in macrophages due to Ca2+ mobilization from intracellular Ca2+ stores and subsequent Ca2+ entry from the external medium. Chlorpromazine-induced Ca2+ entry is inhibited by La3+ and 2-aminoethoxydiphenyl borate and is associated with Ca2+ store depletion.

Using Fura-2AM microfluorimetry, we have shown for the first time that preincubation of macrophages with methyl-β-cyclodextrin, inducing cholesterol extraction from membranes and raft disruption, leads to significant inhibition of thapsigargin-induced store-dependent Ca2+ entry in rat peritoneal macrophages. In contrast, macrophage treatment with methyl-β-cyclodextrin after Ca2+ entry mechanisms were activated by store depletion by thapsigargin application leads to potentiation of subsequent store-dependent Ca2+ entry. The results suggest that intact lipid rafts are necessary for the activation but not the maintenance of store-dependent Ca2+ entry in macrophages.

Using Fura-2AM microfluorimetry, we have shown for the first time that methyl-β-cyclodextrin, inducing cholesterol extraction from membranes and raft disruption, significantly inhibits glutoxim- and molixan-induced Ca 2+ -responses in rat peritoneal macrophages. The results suggest that intact rafts are necessary for signaling cascade induced by glutoxim or molixan and leading to intracellular Ca 2+ concentration increase in macrophages.