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Gohar Madoyan, Arevik Azizyan, Gohar Museghyan and Sinerik Ayrapetyan*


Previously, we have suggested the metabolic controlling of cell hydration as a common quantum mechanical sensitive target through which different factors could modulate membrane excitability and impairment of metabolic driving of water efflux from the cells being a key mechanism, which inhibits inward Na+ currents (INa), considering as a primary mechanism for generation of membrane excitation. The Na+/K+ pump dysfunction, which is consequence of cell pathology, has a central role in generation of water efflux from the cells and controls membrane excitability for Na+ ions. It is known that the dysfunction of Na+/K+ pump leads to the increase of intracellular Ca2+ ([Ca2+]i) as a result of activation of Na+/Ca2+ exchange in the reverse (R) mode. Our previous study has shown that RNa+/Ca2+ exchange can be activated also through the activation of G-proteins in the membrane leading to elevation of intracellular cAMP, which activated by different weak chemical and physical factors is unable to activate ionic channels in the membrane and modulate Na+/K+ pump activity but is able to stimulate synaptic transmitters‟ release from presynaptic ending. The fact that the increase of [Ca2+]i leads to contraction of muscle and to nerve ending hydration suggests that the mechanical deformation of junction between nerve ending and endplate could serve as sources for pain signal generation. To check this hypothesis, the comparative study of the effects of intraperitoneal injections with PS containing 40Ca2+ and PS containing 45Ca2+ on pain threshold and tissue hydration depending on Na+/K+ pump and Na+/Ca2+ exchange activities have been performed. The obtained data bring to suggestion that the activation of Na+/Ca2+ exchange has quantum mechanical sensitive mechanism serving as a primary mechanism for pain signal generation.

Keywords: Rat, Thermal Sensitivity, Brain Cortex, Cerebellum, Heart Muscle.

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