Tamara V. Kozyreva

In experiments on rats, the participation of co-mediators of the sympathetic nervous system in the suppressive effect of deep cooling on the antibody-forming function of the spleen was studied. Studied: 1) the effect of deep cooling (decrease in deep temperature by 3–4°С), 2) the introduction of the mediator of the sympathetic nervous system norepinephrine (NE, 1 mg/ml), 3) its co-transmitter ATP (0.01 mg/ml and 10 mg/ml) and 4) P2X-purinergic receptor blocker PPADS on the number of antibody-forming cells of the spleen in response to immunization with sheep erythrocytes. Deep cooling as well as ATP inhibited, while NE stimulated antibody formation in the spleen. Blockade of P2X-purinergic receptors by PPADS stimulated antibody formation in the norm. Against the background of blockade of P2X-purinergic receptors, the inhibitory effect of ATP and deep cooling on antibody formation was not manifested. The results obtained indicate the opposite effects of co-mediators of the sympathetic nervous system on antibody formation in the spleen and suggest that the inhibitory effect of cold on antibody formation in the spleen occurs with the participation of ATP through P2X-purinergic receptors.

The involvement of sympathetic nervous system (SNS) co-transmitters ATP and norepinephrine (NE) in the suppressive effect of deep cooling on antibody production in the spleen was studied in Wistar rats. Specifically, we analyzed the effects of deep cooling (rectal temperature decreased by 3–4°), iontophoretic administration of NE (1 mg/mL) and its SNS co-transmitter ATP (0.01 mg/mL), as well as intraperitoneal administration of the purinergic P2X receptor blocker PPADS, on the number of antibody-producing cells in the rat spleen in response to immunization with sheep red blood cells (RBCs). While deep cooling and ATP suppressed antibody production in the spleen by 43.2% and 53.5%, respectively, NE stimulated it by 93%. Normally, PPADS-induced blockade of P2X receptors stimulated antibody production by 100.3%. Against the background of P2X receptor blockade, the suppressive effects of ATP and deep cooling on antibody production was not manifested. Our results indicate opposite effects of NE and ATP on antibody production in the spleen, suggesting that deep cooling exerts its suppressive effect with the involvement of ATP through P2X receptors.

Analysis of the role of genomic regulation of systolic BP (SBP) in normal and hypertensive rats showed the presence of an inverse relationship between the

The present study is aimed to elucidate the possible involvement of the thermosensitive TRPM2 ion channel in changing of the temperature sensitivity of the hypothalamus after different cold exposures—long-term adaptation to cold and short-term cooling. Quantitative RT-PCR was used to study the expression of the gene of thermosensitive TRPM2 ion channel in the hypothalamus in the groups of control (kept for 5 weeks at +20 to +22 °C) and cold-adapted (5 weeks at +4 to +6 °C) rats, as well as in the groups of animals which were subjected to acute cooling (rapid or slow) with subsequent restoration of body temperature to the initial level. It has been shown that after long-term adaptation to cold, the decrease in the Trpm2 gene expression was observed in the hypothalamus, while a short-term cooling does not affect the expression of the gene of this ion channel. Thus, long-term adaptation to cold results in the decrease in the activity not only of the TRPV3 ion channel gene, as shown earlier, but also of the Trpm2 gene in the hypothalamus. The overlapping temperature ranges of the functioning of these ion channels and their unidirectional changes during the adaptation of the homoeothermic organism to cold suggest their functional interaction. The decrease in the Trpm2 gene expression may indicate the participation of this ion channel in adaptive changes in hypothalamic thermosensitivity, but only as a result of long-term cold exposure and not of a short-term cooling. These processes occurring at the genomic level are one of the molecular mechanisms of the adaptive changes.