[Changes in transmitter release processes in the rat neuromuscular junction as affected by calcium metabolic disorders]. / Perestroika protsessa sekretsii peredatchika v nervno-myshechnom soedinenii krysy v usloviiakh narusheniia kal'tsievogo obmena.

Spontaneous synaptic activity, miniature end plate potentials (MEPP), was recorded intracellularly in rat phrenic diaphragmatic preparations isolated 8-10 days after removal of the external lobes of the parathyroid glands, with the total blood serum calcium being decreased from 2.75 +/- 0.07 to 1.50 +/- 0.09 mM. The frequency of MEPP was high in both normocalcium (2 mM) and hypocalcium (1 mM) media and complete removal (1 mM EGTA) of Ca2+ from the preparation-washing solution. In the latter case one could observe two synaptical population with different levels of secretion activation. Besides, if judged from the distribution of MEPP amplitudes and the appearance of "spontaneous EPP", the pattern of transmitter exocytosis also experiences changes. It is assumed that under experimental endogenous hypocalcemia there develop functional restitutions in the axonal terminal, leading to the accumulation in them of the transmitter and (or) Ca2+.

[Ca2+ content of rat liver and brain mitochondria in hypoparathyroidism]. / Soderzhanie Ca2+ v mitokhondriiakh pecheni i golovnogo mozga u krys pri gipoparatireoze.

Rats with experimental hypoparathyrosis showed an increase in the content of Ca2+ in liver and brain mitochondria, discovered by fluorescent testing with chlorotetracycline. That increase correlated with the degree of hypofunction of the parathyroid glands.

[Functional activity of mitochondria in experimental hypoparathyroidism]. / Funktsional'naia aktivnosti' mitokhondrii pri éksperimental'nom gipoparatireoze.

Respiration and oxidative phosphorylation of the brain and hepatic mitochondria, as well as the activity of succinate dehydrogenase, succinate-cytochrome-c-reductase and cytochrome oxydase were studied in experimental hypoparathyrosis. Activated respiration and decreased effectiveness of the brain and hepatic mitochondrial phosphorylation and enhanced succinate dehydrogenase activity are seen during hypoparathyrosis development. It is suggested that alterations in mitochondrial functional activity are caused not only by the changed blood calcium ion number, but also by hypoxia, developing in experimental hypoparathyrosis.