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Biomedical subjects

S S Zakharenko

Publications and source records attributed to S S Zakharenko.

3 recordsLinked to original sources
PubMed2001

Visualization of changes in presynaptic function during long-term synaptic plasticity.

Controversy exists regarding the site of modification of synaptic transmission during long-term plasticity in the mammalian hippocampus. Here we used a fluorescent marker of presynaptic activity, FM 1-43, to directly image changes in presynaptic function during both short-term and long-term forms of plasticity at presynaptic boutons of CA3-CA1 excitatory synapses in acute hippocampal slices. We demonstrated enhanced presynaptic function during long-term potentiation (LTP) induced either chemically (with tetraethylammonium), or by high-frequency (200-Hz) electrical stimulation. Both of these forms of LTP required activation of L-type voltage-gated calcium channels and NMDA receptors in the postsynaptic CA1 neuron. These results thus implied that a long-lasting increase in the efficacy of synaptic transmission is likely to depend, at least in part, on enhanced transmitter release from the presynaptic neuron.

Animals↗
PubMed1998

Mechanisms of vascular wall calcium relaxation.

Using the method of isometric tension measurement in isolated blood vessels, we investigated some mechanisms of action of high calcium concentrations (>3 mM) on the mechanical activity of small branches of the rat mesenteric artery. Calcium in concentrations up to 30 mM caused relaxation of the arteries (calcium relaxation). The amplitude of the effect decreased in the presence of ouabain (10(-4) M), tetraethylammonium (10(-3) M), charibdotoxin (10(-7) M) and in the potassium-free external solution in intact and denuded rings. Glibenclamide (10(-6) M), 4-aminopyridine (10(-3) M), barium (10(-3) M) and cesium (2.10(-2) M) were inefficient. Calcium relaxation of intact vessels was impaired in the presence of N(omega)-nitro-L-arginine (10(-4) M) or methylene blue (10(-4) M) but not in the presence of indomethacin (10(-5) M). The attenuation of calcium relaxation to the same extent was observed in denuded mesenteric arteries. We conclude that calcium can cause relaxation of vascular smooth muscle cells by two mechanisms. The first is mediated via the cell membrane hyperpolarization due to the activation of Na+/K(+)-ATPase and Ca(2+)-activated potassium channels. The second mechanism is endothelium-mediated and depends on the nitrogen monoxide-guanylate cyclase pathway.

Animals↗