Search PubMed⌕ Search

Biomedical subjects

C Netti

Publications and source records attributed to C Netti.

67 records · Page 4Linked to original sources
PubMed1977

Effect of halopredone acetate on rat liver tryptophan oxygenase and tyrosine aminotransferase activities.

The possible inductive effect of a new local antiinflammatory steroid, 17,21-bis(acetyloxy)-2-bromo-6beta,9-difluoro-11beta-hydroxypregna-1,4-diene-3,20-dione (halopredone acetate; Topicon), on the rat liver enzymes tryptophan oxygenase and tyrosine aminotransferase was evaluated. The new steroid, when present in the implanted cotton-pellets or when s.c. injected, unlike the reference compound, fluocinolone acetonide, which induced a large increase in both enzymes, did not modify either tryptophan oxygenase or tyrosine aminotransferase. The results confirm that halopredone acetate elicits potent local antiinflammatory activity in the absence of systemic effects.

Administration, Topical↗
PubMed1977

Hypersensititivity of rats to anorectic agents after lesions in the ventromedial hypothalamus.

Anorectic agents such as d-amphetamine and fenfluramine showed a remarkably higher effect in rats with hyperphagia after lesioning the ventromedial hypothalamus. A persistence and even a further increase of the hypersensitivity to anorectics was observed in animals which, eight months after ventromedial hypothalamus-lesioning, resumed almost normal eating patterns. The appearance of the hypersensitivity to anorectic agents after lesioning and its persistence or enhancement in long-term operated animals are interpreted in terms of the mechanisms contributing to the neural reorganization of the control of the feeding center after suppression of ventromedial inhibitory influences.

Animals↗
PubMedDate not supplied

Eel calcitonin binding site distribution and antinociceptive activity in rats.

The distribution of binding site for [125I]-eel-calcitonin (ECT) to rat central nervous system, studied by an autoradiographic technique, showed concentrations of binding in the diencephalon, the brain stem and the spinal cord. Large accumulations of grains were seen in the hypothalamus, the amygdala, in the fasciculus medialis prosencephali, in the fasciculus longitudinalis medialis, in the ventrolateral part of the periventricular gray matter, in the lemniscus medialis and in the raphe nuclei. The density of grains in the reticular formation and in the nucleus tractus spinalis nervi trigemini was more moderate. In the spinal cord, grains were scattered throughout the dorsal horns. Binding of the ligand was displaced equally by cold ECT and by salmon CT(sCT), indicating that both peptides bind to the same receptors. Human CT was much weaker than sCT in displacing [125I]-ECT binding. The administration of ECT into the brain ventricles of rats dose-dependently induced a significant and long-lasting enhancement of hot-plate latencies comparable with that obtained with sCT. The antinociceptive activity induced by ECT is compatible with the topographical distribution of binding sites for the peptide and is a further indication that fish CTs are active in the mammalian brain.

Animals↗
PubMedDate not supplied

Treatment with pertussis toxin does not prevent central effects of eel calcitonin.

To determine whether or not the CNS inhibitory activity of eel calcitonin (eCT) on adenylyl cyclase is the endocellular mechanism underlying the antinociceptive effect of the peptide, as shown for morphine analgesia, we administered Bordetella pertussis toxin (PTX) by intracerebroventricular (ICV) injection (0.5 microgram/rat) to block the receptor-mediated inhibition of adenylyl cyclase. In PTX-treated rats there was no change in eCT (2.5 micrograms/rat, ICV)-induced antinociceptive activity (hot-plate test) nor in eCT (100 ng/rat, ICV) inhibition of gastric acid secretion (Shay test) whereas morphine (5 micrograms/rat, ICV) analgesia was significantly reduced. In vitro studies showed no reduction of eCT binding in the CNS of rats treated with PTX in vivo. Moreover, PTX treatment did not change the inhibitory effect of eCT on adenylyl cyclase in isolated membranes from rat striatum in contrast with opiates (DAME and morphine) whose effects were lost. As PTX is known to inactivate the guanidine binding inhibitory protein Gi, these data suggest that a G protein, distinct from the Gi protein involved in the coupling of opiate receptors into a functional response, could be responsible for regulating the intracellular pathways resulting in eCT-induced antinociceptive effect and inhibition of gastric acid secretion.

Adenylate Cyclase Toxin↗
PubMedDate not supplied

Specific inhibition of basal gastric acid secretion by salmon calcitonin in rats does not necessarily involve a central pathway.

It is well established that salmon calcitonin (sCT), given either by central (intracerebroventricular) or peripheral (parenteral) injection is a potent inhibitor of gastric acid secretion. It is generally believed that this effect of sCT is mediated by the central nervous system based on reports that the effective peripheral dose is up to 1000 times greater than the effective dose administered centrally. We have reexamined this hypothesis by carrying out a number of independent experiments in two laboratories on the effect of sCT, given either by intracerebroventricular or by subcutaneous injection, on basal gastric acid secretion in unanaesthetized rats. Statistical evaluation of the data showed the reproducibility of the effective inhibitory dose ranges of sCT despite the inherent variability of the pylorus ligated rat system (Shay test). The effective dose range for sCT given centrally was between three- and ten-fold lower than that for peripherally administered sCT. There is no published evidence that a significant amount of peripherally administered sCT passes through the blood-brain barrier to relevant areas of the brain and this is confirmed in our study by autoradiography of serial sections of brain following intravenous administration of radioiodinated sCT. It therefore appears that the inhibitory effect of sCT, given centrally or peripherally, may not necessarily be mediated by a common pathway in the central nervous system. Our results also show that the inhibitory effect of peripherally administered sCT is lost when rats are treated with cysteamine to deplete somatostatin, thus implicating somatostatin as a peripheral mediator.

Analysis of Variance↗
PubMedDate not supplied

Effects of pyridoxine neurotoxicity on a distribution of calcitonin gene-related peptide binding sites.

The possibility of changes in binding sites for calcitonin gene-related peptide (CGRP) in response to sensorial denervation was studied in rats after pyridoxine-induced neurotoxicity. Changes in CGRP binding sites were evaluated by an in vitro autoradiographic technique using [125I]-Tyr-rat-CGRP as a ligand. A bidirectional binding response was obtained: an increased binding, in comparison with the respective control, was observed in spinal cord and cerebellar regions whereas a decreased binding was noted in cerebrum. CGRP binding in selective areas comparising the pathways that are responsible for transmitting sensory impulses have shown significant changes. These results suggest that CGRP plays a modulatory role in the central nervous system. This study has also proposed and evaluated pyridoxine toxicity as a model for studying sensory denervation.

Animals↗