We report here the results obtained from comparative analysis of learning and the dynamics of extinction of a conditioned passive avoidance response in mice with genetic knockout of monoamine oxidase A (MAO A) and the progenitor line C3H. Mice of both lines acquired the conditioned passive avoidance reaction efficiently. Mice with genetic knockout of MAO A were characterized by prolonged retention of reproduction of the memory trace, as compared with rapid extinction in C3H mice. Smaller numbers of transfers, and vertical rearings on days 7-13 and the numbers of glances into and rom the dark sector on days 11-13 of extinction in MAO A-knockout mice appear to reflect their more marked fear reactions when confronted with the "dangerous" sector, along with increased anxiety, these facilitating longer-lasting retention of the memory trace.

Experiments were performed on knockout Tg8 mice lacking monoamine oxidase A gene that plays a major role in dopamine catabolism. The study by the method of high-performance liquid chromatography revealed considerable regional differences in the contents of dopamine and its metabolite dihydroxyphenylacetic acid in brain structures of these animals. Tg8 mice differed from the parent C3H/HeJ strain by low level of dihydroxyphenylacetic acid in the striatum, midbrain, hypothalamus, and hippocampus and high concentration of dopamine in the striatum. No differences were revealed in the contents of dopamine and dihydroxyphenylacetic acid in the frontal cortex and amygdala. The 2.4-4.8-fold decrease in the content of dihydroxyphenylacetic acid in various brain structures was not accompanied by changes in dopamine concentration. These data reflect the effective compensation for deficiency of dopamine metabolism. Our results suggest that monoamine oxidases A and B and catechol-O-methyltransferase play different roles in dopamine metabolism in various brain structures.

NISAG rats with stress-induced arterial hypertension are characterized by hyperactivity of the sympathoadrenal system under rest conditions and during stress exposure.

The effects of the NO donor sodium nitroprusside and the NO synthase blocker L-omega-N-nitroarginine (LNA) on body temperature, hypothalamic monoamines, and plasma corticosterone in conditions of cooling were studied in Male Wistar rats. Reductions in body temperature on cooling, both after administration of sodium nitroprusside and LNA, were no different from those seen without treatment. The basal corticosterone level after treatment with sodium nitroprusside increased from 5.3 +/- 2.2 to 29.1 +/- 1.8 microg%. Cooling led to a multiple increase in corticosterone levels in all animals, both in control conditions and after treatment with sodium nitroprusside and LNA. Sodium nitroprusside significantly decreased the basal hypothalamic noradrenaline level, by 37%. Cooling of the animals in these conditions led to an additional drop in the noradrenaline level. Noradrenaline levels 48 h after cold stress applied to animals cooled after treatment with LNA or sodium nitroprusside were significantly higher than in those cooled without treatment. No changes in serotonin and 5-hydroxyindoleacetic acid levels were seen in these experiments. The basal dihydroxyphenylacetic acid and dopamine levels increased after treatment with sodium nitroprusside, by 379% and 239% respectively. No dopamine response to cold was observed, though the dihydroxyphenylacetic acid level in the control group and animals treated with LNA increased. Thus, cold stress did not reveal differently directed directions for the actions of the NO donor and the NO synthase blocker, as seen with other types of stress.

Experiments on rats showed that blockade of norepinephrine reuptake in the early reperfusion period after focal myocardial ischemia aggravates myocardial injury and abolishes the protective effect of ischemic preconditioning.

We studied the dynamics of interstitial serotonin during local myocardial ischemia under conditions of ischemic preconditioning in Wistar rats. Ischemic preconditioning increased serotonin content in the dialysate (p=0.003). During 30-min ischemia, ischemic preconditioning delayed serotonin increase just before the 20th min of ischemia. Ischemic preconditioning promoted short-term increase in the serotonin level in the myocardial interstitium but followed by prolonged ischemia, it delayed the accumulation of serotonin in the myocardial interstitium.

No abstract

The relationships between serum corticosterone content, intensity of lipid peroxidation (LPO) and the concentration of tocopherol in tissues, and the transmembrane potential in thymocytes were studied in rats exposed to two consecutive coolings. Both exposures increased serum corticosterone. The first exposure activated LPO in the serum, while the second stimulated LPO in thymocytes. The second cooling lowered body temperature to a lesser extent than the first one. Body temperature did not depend on the content of LPO products or corticosterone, but negatively correlated with the content of tocopherol in the brain hemispheres and adrenal glands. The rats exhibiting high-level thermoregulation after the first exposure to cold showed a higher thymocyte transmembrane potential after the second cooling. The second exposure potentiated the negative relationship between the brain and serum content of corticosterone and LPO products, which indicates that the content of LPO products cannot be used as an index of stress intensity.Key Words: cold; stress; corticosterone; lipid peroxidation; tocopherol Activation of lipid peroxidation (LPO) is the most important pathogenic event in stress causing disruption of biological membranes and uncoupling of oxidative phosphorylation. Along with the adrenal cortical hormones, LPO products are widely used as a measure of stress-response. It is currently accepted that the content of LPO products is directly proportional to the intensity of stress. However, the relationship between LPO activity and the duration and intensity of stress is not linear, and the content of LPO products can decrease during the initial phase of organism's response to stress. Such a decrease was observed at some periods of the emotional pain stress [2], during physical exercises [12] and cold exposure [5,10,11], The data indicate that the periods during which the content of LPO products in diverse organs and tissues is decreased are not synchronized [10], but coincided with an increase in the serum content of corticosteroids. The total effect of steroids is probably deterInstitute of Physiology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk mined by their antioxidant properties [9] and the modulating effects on the antioxidant system, the key stress-protecting system controlled by a variety of hormones, including corticosteroids [6,15]. Therefore, it remains unclear what is reflected by LPO changes at different stress-response periods and how these changes correlate with adrenal cortex activation.To answer these questions we used the model of repeated cooling (two 1.5-h exposures with a 48-h interval). Correlation analysis was applied to assess the relations between serum concentration of corticosterone (CS) and the content of LPO products and tocopherol in tissues. Additionally, we measured the transmembrane potential of thymocytes (Aw), which is the sum of A~ on the plasma and mitochondrial membrane. Thymocytes represent an adequate model for the assessment of the intensity of bioe...