[Variations of some physiological and biochemical indices in the population of red-backed vole (Clethrionomys rutilus)].

We studied the changes in the population density of the red-backed vole (Clethrionomys rutilus Pall.) on the northern coast of the Sea of Okhotsk (60 degrees N) during three population cycles (1980-1990). A total of 3111 animals were studied, including 1006 alive voles.

[Specificity of morphological changes and DNA degradation in the Ehrlich ascite carcinoma cells exposed to various damaging agents].

Using the Ehrlich ascite carcinoma cells, exposed to oxidative stress, heat shock, cytochalasin B, vinblastine, Triton X-100 and energy starvation, morphological changes, DNA degradation, and form of cell death were investigated. A rather clear specificity of cell morphology, characteristic of apoptosis, was revealed for the most of treatments, including membrane blebs, chromatin condensation and apoptotic body formation. Karyorhexis was not common for the examined cells.

[The effect of calcium channel blockers on anxiety evoked by amputation of the vibrissae in rats].

The effect of diazepam (0.5 mg/kg) and calcium channel blockers on the behavior of rats in an "open field" was studied on a model of incomplete amputation of vibrissae. Diazepam, diltiazem (1 mg/kg), fendiline (1 mg/kg), and cinnarizine (1 mg/kg) stimulated motor activity of animals with amputated vibrissae.

[The effect of the subchronic administration of calcium-channel blockers on CNS excitability].

The effect of a single day administration of nifedipine (10 mg/kg), cinnarizine (25 mg/kg), verapamile (25 mg/kg), fendiline (10 mg/kg), dilthiazem (10 mg/kg), and diazepam (0.5 mg/kg) on the dynamics of changing a convulsive dose of convulsant was studied on a model of intermittent intracutaneous administration of Corazole (10 mg/kg until convulsions) during 5 days. Repeated intermittent Corazole administrations were found to increase the sensitivity of animals with respect to convulsive effect of the drug.

Resistance of Ehrlich tumor cells to apoptosis can be due to accumulation of heat shock proteins.

Previously we have found that stationary Ehrlich ascites carcinoma (EAC) cells in vivo accumulated heat shock proteins (HSPs) and became resistant to necrotic death induced by prolonged energy deprivation of hyperthermia. Here we report that apoptotic death induced by nutrient starvation, transient ATP depletion, heat shock and a microtubule-disrupting drug, vinblastine, was also suppressed in stationary EAC cells comparing with exponential cells. When exponential (sensitive) cells were subjected to short-term heating with recovery to accumulate inducible form of HSP70, they also became resistant to all of the employed apoptosis-inducing exposures, and an inhibitor of cytosolic protein synthesis, cycloheximide, prevented acquisition of the resistance.