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C Netti

Publications and source records attributed to C Netti.

At least 19 recordsLinked to original sources
PubMed1992

Electrophysiological correlates for antinociceptive effects of histamine after intracerebral administration to the rat.

Data have been collected indicating possible functions for histamine in brain but there are only a very few data, collected exclusively with behavioural tests, about the effects of histamine on the perception of the pain, an important aspect in the homeostasis of the human body. The purpose of the present study was to investigate the effects of histamine, injected directly into the lateral cerebral ventriculi on the firing of nociceptive thalamic neurones, detected by electrophysiological techniques in rats rendered arthritic by injection of Freund's adjuvant into the left hindfoot. The noxious test stimuli used were either extension or flexion of the ankle or mild lateral pressure on the heel. With increasing doses of histamine (5, 10, 20, 40 micrograms) it was possible to observe an increasing inhibitory and long-lasting effects of the evoked activity, with a significant dose-effect linear regression. The inhibitory responses, induced by histamine, probably by a hyperpolarization phenomenon that decreased excitatory postsynaptic potentials, were clues for the presence of a histaminergic pathway in parallel with and/or in connection with other adrenergic, gabaergic, serotoninergic and opioidoergic pathways that regulate the transmission and the modulation of algogenic electrophysiological messages.

Analgesics↗
PubMed1992

Decrease in rat brain calcitonin binding sites and adenylyl-cyclase activity during ageing.

In order to investigate the effects of ageing on the cerebral receptors for calcitonin (CT), we used an in vitro autoradiographic method to study the distribution of the binding sites for eel CT (eCT) in young and old rat brain. The inhibitory action of eCT on adenylyl-cyclase (AC) activity upon isolated brain cell membranes was also evaluated. The results show area-specific reduction of binding particularly in the hypothalamus and pons medulla of the old rat. The inhibitory action of eCT on AC activity was significantly reduced in the same areas, whereas in the striatum and mesencephalon no changes were observed. The parallel decrease of binding of eCT and of the inhibitory action of eCT on AC in ageing may represent a functional decline of neuronal activities during ageing.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Effects of selective histamine H3-receptor ligands on prolactin and growth hormone secretion in the rat.

The effects of intracarotid (i.a.) administration of the histamine (HA) H3-receptor agonist (R)-alpha-methyl-histamine (alpha MeHA) and of the H3-antagonist thioperamide, (THIO) on basal or morphine (M)-induced prolactin (PRL) and growth hormone (GH) secretion were studied in male rats. M was administered 3 h after the H3-drugs. Neither THIO (2.5 mg/kg) nor alpha MeHA (10 mg/kg) changed basal PRL levels and only THIO enhanced the PRL-releasing effect of M (6 mg/kg). Basal GH secretion was not modified by THIO. alpha MeHA slightly increased GH secretion. THIO significantly decreased M-stimulated GH secretion (1 mg/kg, i.a.) and alpha MeHA slightly increased it. These results, in agreement with previous evidence obtained after central HA administration, indicated that endogenous brain HA facilitates PRL and inhibits GH secretion.

Animals↗
PubMed1991

Antinociceptive activity of eel calcitonin, injected into the inflamed paw in rats.

This study examined the possible peripheral activity of eel calcitonin in the modulation of the response to noxious pressure on inflamed paws in rats (Randall and Selitto test). The intraplantar injection of eel calcitonin (20-200 ng/rat) but not the subcutaneous administration (200 ng and 2 micrograms/rat, s.c.), was able to significantly inhibit hyperalgesia induced by intraplantar injection of carrageenin. The development of oedema on the other hand was not inhibited. The intraplantar administration of eel calcitonin (200 ng/rat) in a non-inflamed paw did not modify paw pressure thresholds. Eel calcitonin (200 ng/rat, intraplantar, i.pl.) was also able to elicit an antinociceptive effect on formalin-induced hyperalgesia, both when the peptide was injected before or after (60 min) formalin. This effect, at difference with morphine (80 micrograms/rat, i.pl.), was not blocked by naloxone (10 micrograms/rat, i.pl.). These results demonstrate the local antinociceptive effect of eel calcitonin in inflammatory pain and might indicate a new way of using calcitonin in the control of pain.

Analgesics↗
PubMed1991

Stress-related changes in calcitonin gene-related peptide binding sites in the cat central nervous system.

The possibility of area-specific changes in binding sites for CGRP in response to stress was studied in cat CNS after repeated sleep-deprivation and restriction of movement. Brain sections were obtained from a cat placed under stressful conditions for 2 h the 1st day, 6 h the 2nd day and 24 h the 3rd day. Changes in CGRP binding sites were evaluated by an in vitro autoradiographic technique with 125I-Tyr-rat-CGRP as a ligand. The autoradiograms were then compared with those of control animals. The results show decreased labelling in the cortex prefrontalis and pyriformis and in some basal ganglia (n. caudatus, claustrum, n. entopedencularis). Increased CGRP binding site densities were seen in areas involved in the integration of sensory information, in the control of endocrine secretion and in those that participate in sleep-walking cycles. These changes in CGRP binding in selective CNS areas following stress suggests that CGRP plays a role in processes of adaptation.

Animals↗
PubMed1991

Effect of unmodified eel calcitonin on gastric acid secretion and gastric ulcers in the rat.

A new peptide, eel calcitonin (eCT), synthesized to the sequence of calcitonin (CT) extracted from the ultimo branchial bodies of eels, is now on the market in some countries for clinical use in the treatment of Paget's disease of bone and in the prophylaxis or treatment of certain osteoporoses. We have now studied the effect of eCT on the inhibition of gastric acid secretion and protection against experimentally induced gastric ulcers in rats as other CTs have previously been shown to have such effects. EelCT shows a dose dependent inhibition of gastric acid secretion, both volume and concentration of acid - dose range 100-900 ng/Kg injected subcutaneously. Central administration is also effective at a dose of 100 ng/rat. There is no published evidence for a direct effect of CTs in the stomach and there is considerable speculation on possible mediating pathways. Somatostatin may be involved in the inhibitory effect of eCT on gastric acid secretion because when administered both centrally or peripherally eCT is ineffective in rats depleted of somatostatin by pretreatment with cysteamine. However, other mechanisms must also be involved as eCT has no preventive effect against gastric ulcers induced by ethanol but has a high index of protection against ulcers induced by cold restraint stress or indomethacin.

Animals↗
PubMed1990

A selective role for brain histamine in prolactin release induced by opiates.

We studied the effects of histamine (HA) antagonists on the facilitatory action of morphine (M) and beta-endorphin (beta E) on prolactin (PRL) release and the effect of alpha-fluoromethylhistidine (alpha-FMH, inhibitor of HA synthesis) on beta E-induced PRL secretion. Male rats were injected intracerebroventricularly (i.c.v.) with mepyramine (MEP, H1-antagonist, 0.8 mumol/rat) or ranitidine (RAN, H2-antagonist, 0.4 mumol/rat) 10 min before M (6 mg/kg, intracarotid, i.a.) or beta E (0.25 micrograms/rat, i.c.v.). alpha-FMH (200 micrograms/rat, i.c.v.) was administered 3 h before beta E. Plasma PRL levels were measured at various times before and after drug treatment. RAN but not MEP significantly reduced PRL release induced by M whereas neither HA-antagonists nor alpha-FMH modified beta E-induced PRL release. The results obtained show that brain HA contributes through activation of H2-receptors to the PRL facilitatory action of M but not of beta E.

Animals↗
PubMed1990

Inhibitory effects of centrally administered /ASU1-7/eel calcitonin on basal and stimulated prolactin release in rats.

We investigated the effects of /ASU1-7/eel calcitonin (ASU1-7eelCT) on basal and stimulated prolactin (PRL) release in male rats. /ASU1-7/eelCT was administered intracerebroventricularly (icv) into freely moving rats with indwelling catheters. The administration of /ASU1-7/eelCT (2.5 micrograms/rat, icv) significantly inhibited basal PRL secretion. When PRL secretion was stimulated by exposing rats to restraint stress, /ASU1-7/eelCT (250 ng; 800 ng; 2.5 micrograms/rat, icv) dose-relatedly inhibited the PRL surges at 10 min after stress. The same doses of icv /ASU1-7/eelCT were effective in inhibiting morphine (6 mg/kg, intracarotid, ia-induced PRL release. No effect on stress-induced PRL secretion was observed when the peptide was administered intracarotid at the dose of 10 micrograms/rat. These results demonstrate that /ASU1-7/eelCT, as we previously observed with salmon calcitonin (sCT), has central inhibitory activity on PRL secretion, probably through enhancement of hypothalamic inhibitory pathways involved in the control of PRL.

Analysis of Variance↗
PubMed1989

Effects of age on binding sites for calcitonin gene-related peptide in the rat central nervous system.

The binding site distribution of calcitonin gene-related peptide (CGRP) was studied in the central nervous system of aged rats (22 months old) and compared with that of young rats (2 months). The regional distribution of [125I]Tyr-rat CGRP binding in coronal sections of young and old rat CNS was examined by an in vitro autoradiographic technique. The results, showed that in aged rats there was a marked reduction in CGRP binding, without any change in binding affinity, in the hippocampus, the nucleus rhomboideus, the nucleus arcuatus, the colliculus superior, the substantia grisea centralis and the spinal cord. In the cortical areas, the amygdala, the caudatus putamen and the accumbens binding was not modified. In the cortex cerebellaris CGRP binding was strikingly greater in the aged rats. The increase in binding might be a consequence of an adaptive process due to a decline of the peptide synthesis with age and is suggestive of a role for CGRP in the cerebellum functions.

Aging↗
PubMed1989

Effects of brain histamine depletion on stimulated prolactin release in rats.

We examined the effects of an irreversible inhibitor of brain histamine (HA) synthesis, alpha-fluoromethyl-histidine (alpha-FMH), on prolactin (PRL) release induced by an opiate agonist (morphine, M) or by a serotonergic agonist (MK212). alpha-FMH was administered intracerebroventricularly (i.c.v., 200 micrograms/rat) into freely moving rats with indwelling catheters in the carotid. M (6 mg/kg, intracarotid, i.a.) was administered simultaneously with or 3 h after alpha-FMH. MK212 (2.5 mg/kg, i.a.) was administered 3 h after alpha-FMH. Blood samples for assay for PRL were drawn at 0, 10, 20, 40 min after M or MK212 administration. alpha-FMH (3 h before) significantly reduced the PRL-releasing effect of M and MK212 but did not modify PRL release by M when administered simultaneously. The present results showing that the facilitatory actions of the opiate and serotonergic systems on PRL are impaired when brain HA synthesis is reduced, suggest that there is an HA-dependent step in opiate and serotonergic control of PRL.

Animals↗
PubMed1989

Evidence of a central inhibition of growth hormone secretion by calcitonin gene-related peptide.

The effects of intracerebroventricular or intracarotid injection of synthetic rat calcitonin gene-related peptide (CGRP) on growth hormone (GH) secretion induced by various stimuli in male rats were examined. CGRP (2.5 or 5 micrograms/rat intracerebroventricularly, i.c.v.) was administered 10 min before beta-endorphin (0.5 microgram/rat i.c.v.) or morphine (1 mg/kg intracarotidly, i.a.) or clonidine (0.25 mg/kg i.a.) or GH-releasing hormone (GHRH1-40; 2 micrograms/kg i.a.). When injected peripherally, CGRP (10 micrograms/rat, i.a.) was administered 5 min before morphine or GHRH. To investigate the possible involvement of somatostatin (SRIF) in the inhibition of GH secretion by CGRP, the effect of the peptide on GHRH-induced GH release was also examined in rats with hypothalamic SRIF depletion obtained by pretreatment (4 h before) with cysteamine (300 mg/kg subcutaneously). Blood samples for hormone determination were drawn from freely moving rats at various times before and after drug treatment. The intracerebroventricular administration of CGRP (5 micrograms/rat) significantly inhibited GH secretion induced by all the stimuli used. In rats with SRIF depletion CGRP did not modify the stimulation of GH by GHRH. When CGRP was administered intracarotidly, even the dose of 10 micrograms/rat did not reduce the GH release induced by GHRH or morphine. The effects of intracerebroventricular CGRP on basal or beta-endorphin-induced prolactin release were also examined. When given intracerebroventricularly, the peptide did not modify prolactin secretion. The present results indicate that CGRP has a central inhibitory role in the control of GH secretion, probably through a stimulation of SRIF release.

Animals↗
PubMed1987

Evidence for different classes of calcitonin binding sites in rat CNS: an autoradiographic study with carbo-calcitonin.

The distribution of binding sites in the rat CNS for a synthetic analogue of eel calcitonin, [Asu1-7]eel calcitonin (carboCT) was investigated. This distribution was compared to that for the natural peptide to see whether a modified molecule would also reveal different classes of binding sites for CT. The regional distribution of 125I-carboCT binding in coronal sections of rat CNS was examined by an in vitro autoradiographic technique. Non-specific binding was assessed after addition of excess cold carboCT or eel CT and the results showed that carboCT binding is specific and that it is displaced equally by cold carboCT and by eel CT. There was dense labelling in the nucleus accumbens, in the tractus striohypothalamicus, in the anterior and posterior part of the hypothalamus except for the nucleus ventromedialis, in the amygdala, in the pars medialis of the reticular formation, in the nucleus ruber, in the periventricular gray and in the raphe magnus. Grains were less dense in the hypothalamus lateralis, in the substantia nigra and in the nucleus interpeduncularis. In contrast to eel CT, carboCT did not bind in the spinal cord, nor did carboCT prevent eel CT binding in this area, whereas it was able to prevent it in the brain. These results are consistent with the existence of different classes of binding sites for CT in rat brain and in spinal cord, and indicate that the substitution of the S-S bond with a C-C bond in the eel CT molecule makes the peptide more selective for one class of binding sites.

Animals↗
PubMed1987

Calcitonin binding site distribution in the cat central nervous system: a wider insight of the peptide involvement in brain functions.

Calcitonin (CT) binding site distribution has been studied in the cat CNS. The autoradiographic analyses of [125I]-eelCT (ECT) binding showed high density of silver grains in the mesencephalic PAG, in the raphe nuclei and in the dorsal horns, laminae I, IV, V, and VI, where ECT may act to inhibit nociceptive transmission. Other binding-rich areas included the caudatus, the amygdala, the hypothalamus, the substantia nigra, the locus coeruleus and the formatio reticularis mesencephalica. Medium to low density was seen, amongst other areas in the cortex piriformis, the hippocampus, the medial and intralaminar thalamus and the tractus spino-thalamicus. ECT binding site distribution revealed essentially homologous locations in the cat and rat CNS. At difference, the presence of binding in the piriform cortex and in discrete thalamic nuclei suggests a widespread involvement of ECT in a variety of central functions in addition to what already demonstrated.

Animals↗
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

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↗