Clomiphene citrate can mimic the augmentative (positive) but not the depressing (negative) effect of estradiol on the LHRH-stimulated release of LH and FSH by the pituitary gland of the long-term ovariectomized rat

Summary In the long-term ovariectomized rat, both estradiol benzoate (EB) and clomiphene citrate enhance the release of LH induced by luteinizing hormone-releasing hormone (LHRH). EB also enhances the release of FSH. In rats pretreated with LHRH, EB strongly depresses the LHRH-induced LH/FSH release, but clomiphene enhances this release, regardless of the presence of EB.     

Clomiphene citrate can mimic the augmentative (positive) but not the depressing (negative) effect of estradiol on the LHRH-stimulated release of LH and FSH by the pituitary gland of the long-term ovariectomized rat

In the long-term ovariectomized rat, both estradiol benzoate (EB) and clomiphene citrate enhance the release of LH induced by luteinizing hormone-releasing hormone (LHRH). EB also enhances the release of FSH. In rats pretreated with LHRH, EB strongly depresses the LHRH-induced LH/FSH release, but clomiphene enhances this release, regardless of the presence of EB.     

Depression of spontaneous and ionophore-induced neurotransmitter release by Salmonella.

Exposure of frog neuromuscular junctions to heat-killed, lyophilized Salmonella typhimurium (SR 11) produces an early increase in spontaneous transmitter release followed by depression of release and blockade of the obligatory release usually induced by ionophore X537A.     

Liberation of adenosine triphosphate after depolarization of the Torpedo electroplaque by potassium chloride]

The release of ATP after potassium depolarization was measured on fragments of electric tissue incubated in a solution containing the firefly extract. Light emission was proportional to the extracellular KCL concentration. In contrast to the release of ATP after single nerve impulses, the release after direct KCL depolarization was insensitive to curare of eserin.     

Colchicine inhibits stimulated release of gastric histamine but not activation of histidine decarboxylase

Summary In the rat, gastric mucosal histamine is mobilized and histidine decarboxylase activated by treatment with insulin or pentagastrin. Colchicine pretreatment prevented the histamine release without preventing the enzyme activation. The results suggest a) that histamine release and histidine decarboxylase activation are independent events, and b) that microtubules are involved in the release of histamine.     

Colchicine inhibits stimulated release of gastric histamine but not activation of histidine decarboxylase.

In the rat, gastric mucosal histamine is mobilized and histidine decarboxylase activated by treatment with insulin or pentagastrin. Colchicine pretreatment prevented the histamine release without preventing the enzyme activation. The results suggest a) that histamine release and histidine decarboxylase activation are independent events, and b) that microtubules are involved in the release of histamine.     

Sulfhydryl oxidation induces calcium release from fragmented sarcoplasmic reticulum even in the presence of glutathione

Alcian blue and plumbagin induced transient Ca²⁺ release from fragmented sarcoplasmic reticulum. Dithiothreitol (DTT) and glutathione (GSH) partially blocked Ca²⁺ release induced by these oxidizing compounds. Pretreatment of alcian blue and plumbagin with DTT or GSH for more than 1 min was required to abolish the ability of the oxidizing compounds to release Ca²⁺. Mg²⁺ and ruthenium red completely blocked alcian blue-and plumbagin-induced Ca²⁺ release. These results suggest that oxidation of sulfhydryls on Ca²⁺ release channels induces Ca²⁺ release even in the presence of GSH in situ.     

Tetanus toxin does not affect the release of noradrenaline and taurine from rat cerebral cortex slices evoked by high K+ and Na+-free media

Summary Noradrenaline and taurine release from superfused rat cerebral cortex slices was stimulated by potassium ions, veratrine, ouabain and omission of sodium ions. Tetanus toxin enhanced only the ouabain-evoked calcium-dependent noradrenaline release and the ouabain-evoked calcium-independent taurine release. The uptake of both was marginally affected.     

Light evoked release of radioactivity from rabbit retinas preloaded with (3H)-GABA

Summary Light flashes evoke an increased release of radioactivity in vitro from rabbit retinas preloaded with (³H)-GABA in vivo. Constant light does not affect the release. No light evoked release can be demonstrated from the glia. Pentobarbitone and AOAA depress the evoked release. The results are consistent with GABA being a retinal neurotransmitter, most likely in a class of amacrines.This work was supported by grants from the Swedish Medical Research Council (project 04X2321), The Faculty of Medicine, University of Lund, Royal Physiographic Society.     

Tetanus toxin does not affect the release of noradrenaline and taurine from rat cerebral cortex slices evoked by high K+ and Na+-free media

Noradrenaline and taurine release from superfused rat cerebral cortex slices was stimulated by potassium ions, veratrine, ouabain and omission of sodium ions. Tetanus toxin enhanced only the ouabain-evoked calcium-dependent noradrenaline release and the ouabain-evoked calcium-independent taurine release. The uptake of both was marginally affected.     

Effect of thyroid hormone on somatomedin-C release from perfused rat liver

The effect of thyroid hormone on plasma somatomedin-C (SmC) level and on SmC release from perfused rat liver was investigated. Plasma SmC levels and liver tissue SmC were significantly increased in thyroxine-treated rats. Physiological doses of triiodothyronine increased SmC release and SmC concentration in the perfused rat liver. These results indicate that thyroid hormone directly enhances the synthesis and release of SmC in the rat.     

Impaired amylase release from the parotid gland of rats treated with reserpine.

Using an automated system for the analysis of amylase, the release of this enzyme was compared in superfused parotid gland segments from control and reserpine treated rats. Stimulant-evoked amylase release was delayed and of smaller magnitude in the glands of the treated animals and a reduction of the transmembrane K+ gradient caused a smaller and short lasting reduction in Ach-evoked release of amylase in the glands from these animals.     

Regulation of calcitonin release from the 6.23 rat C-cell line by cyclic nucleotide analogues and pharmacological mediators.

Calcitonin release from 6.23 rat medullary thyroid carcinoma C-cells was stimulated by dibutyryl cyclic AMP and inhibited by dibutyryl cyclic GMP in concentration dependent fashion. Histamine, isoproterenol, prostaglandin E2 and Bay K 8644 stimulated calcitonin release, while acetylcholine and serotonin had no significant effect on CT release.     

Inhibition of TSH-stimulated thyroid hormone release and potentiation of TRH-stimulated TSH release by indomethacin in perifusion systems of rat thyroids and pituitaries

Using indomethacin (Ind), a prostaglandin synthesis inhibitor, in vivo experiments in rats and in vitro experiments with perifusion systems of rat thyroids and pituitaries were conducted. After 35 days of intragastric infusion of Ind, serum TSH levels were markedly increased, the thyroid was swollen and, as a consequence, T3 and T4 levels were normal. The T3 release from perifused rat thyroids under continuous stimulation with 10 mU/ml TSH was inhibited significantly (p less than 0.01) by 1.0 X 10(-6) M Ind. On the other hand, the TSH release from perifused rat pituitaries under TRH stimulation was enhanced conspicuously by Ind. It was concluded that Ind decelerated thyroid hormone release from the thyroid and accelerated TSH release from the pituitary in perifusion systems.     

Inhibition of LH-RH induced release of gonadotropins by substance P in cultured rat anterior pituitary cells]

Using anterior pituitary cells cultured for 7 days and then incubated for 4 hrs, substance P, an undecapeptide, inhibited the stimulatory effect of LH-RH on the release of LH-RH on the release of LH and FSH. This inhibitory effect, which was similar for both gonadotropins was only observed when the adenopituitary cells were put in culture at DI and Proestrus stages of the oestrous cycle. Furthermore substance P partly inhibited the basal release of FSH at DI and DII stages but did never affected that of LH.     

In vitro stimulation of chicken pituitary growth hormone and prolactin secretion by chicken hypothalamic extract

Summary The effect of an acid extract of chicken hypothalami on the in vitro secretion of prolactin and growth hormone (GH) by dispersed chicken pituitary cells has been investigated. Both prolactin and GH release were stimulated in a dose related manner in the presence of the hypothalamic extract (HE). Somatostatin had no effect on the basal or HE stimulated release of prolactin although it did inhibit the HE induced release of GH.     

Regulation of calcitonin release from the 6.23 rat C-cell line by cyclic nucleotide analogues and pharmacological mediators

Calcitonin release from 6.23 rat medullary thyroid carcinoma C-cells was stimulated by dibutyryl cyclic AMP and inhibited by dibutyryl cyclic GMP in concentration dependent fashion. Histamine, isoproterenol, prostaglandin E₂ and Bay K 8644 stimulated calcitonin release, while acetylcholine and serotonin had no significant effect on CT release.     

In vitro stimulation of chicken pituitary growth hormone and prolactin secretion by chicken hypothalamic extract.

The effect of an acid extract of chicken hypothalami on the in vitro secretion of prolactin and growth hormone (GH) by dispersed chicken pituitary cells has been investigated. Both prolactin and GH release were stimulated in a dose related manner in the presence of the hypothalamic extract (HE). Somatostatin had no effect on the basal or HE stimulated release of prolactin although it did inhibit the HE induced release of GH.     

Inhibition of platelet ADP and serotonin release by carbon monoxide and in cigarette smokers

Summary The release of¹⁴C-serotonin by ADP, epinephrine and arachidonic acid and the release of ADP by kaolin were measured in normal platelets in the presence and absence of carbon monoxide and in smokers' platelets. It is shown that carbon monoxide inhibits significantly the platelet release reaction. This function is also decreased in platelets obtained from heavy cigarette smokers.This work was supported by Veterans Administration Research Fund 8073-01.