Initiation of the phosphoinositide cycle by parathyroid hormone in synaptosomes.

We studied the effects of parathyroid hormone 10(-9) M) on the contents of mono-, di-, and triglycerides, total phospholipids, and free arachidonic acid in rat brain cortex synaptosomes using [1-(14)C]arachidonic acid at 2, 5, and 10 sec after addition of the hormone. Our data demonstrated the changes in lipid metabolism in synaptosomal membranes which were especially pronounced at 5 sec after addition of parathyroid hormone. Incorporation of 70% of [1-(14)C]arachidonic acid into the phosphoinositide fraction and the progress of changes in lipid metabolite composition suggest that the phosphoinositide cycle is initiated by parathyroid hormone, and the hormonal signal may be subsequently mediated in nerve cells by 1,2-diacylglycerol, a product of the phosphoinositide cycle.

[Parathyroid hormone stimulation of nerve cell calcium conduction]. / Stimuliatsiia paratireoidnym gormonom kal'tsievoi provodimosti nervnykh kletok.

Parathyroid hormone (PTH) has been studied for its effect on the voltage-sensitive calcium channels in voltage-clamp experiments on intracellularly perfused snail neurons. A two-stage action of the hormone on the calcium current (Ica) was shown. An initial stage was a short-term one and consisted in an increase of ICa by 7-10%. The second stage developed slowly for 60-70 min, ICa increased twice. The exogenous cAMP and cGMP did not produce such an effect as PTH did. It is suggested that the phosphoinositide pathway mediates the PTH effect.

[45Ca2+ and 3H-GABA transport in nerve endings separated from the cerebral cortex of rats with hypoparathyroidism]. / Transport 45Ca2+ i 3H-GAMK v nervnykh okonchaniiakh, vydelennykh iz kory golovnogo mozga krys s gipoparatireozom.

Ca2+ blood serum level was reduced by 34.5% in rats with hypoparathyroidism (HPT) on the 7th-12th day after the damage of parathyroid glands. Synaptosomes isolated from the brain cortex of rats during this period accumulated in a normal medium more 45Ca2+ than synaptosomes from healthy animals. In potassium depolarization, control and experimental synaptosomes accumulated more 45Ca2+, however in HPT the increment in 45Ca2+ uptake in high potassium medium was less temperature-dependent. In normal medium 3H-GABA uptake and release by synaptosomes from the brain of rats with HPT slightly differed from those in the control. On the contrary, 3H-GABA release induced by synaptosome depolarization was depressed in HPT. It is suggested that nerve terminal excretory function disturbances contribute to increased excitability of the central nervous system in hypoparathyroidism.

[Effect of parathyroid hormone on the transport of 45Ca2+ and 3H-GABA in nerve endings isolated from the rat cerebral cortex]. / Vliianie paratireoidnogo gormona na transport 45Ca2+ i 3H-GAMK v nervnykh okonchaniiakh, vydelennykh iz kory golovnogo mozga krys.

Parathyroid hormone (PTH) (0.1-10 ng/ml) evokes a dose-dependent increase in 45Ca2+ accumulation in synaptosomes isolated from the rat brain cortex. In the presence of PTH the fast (I sec) potential-dependent 45Ca2+ uptake was less than in the control. PTH had no effect on 3H-GABA uptake by synaptosomes (P2 fraction). Synaptosomes preincubated in the presence of PTH in Ca2+-free medium and transferred into Ca2+-containing normal medium released more 3H-GABA than control synaptosomes. In this case depolarization-evoked 3H-GABA release was diminished.

[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.