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C Netti

Publications and source records attributed to C Netti.

At least 55 records · Page 3Linked to original sources
PubMed1988

Central effects of histamine H2-receptor agonists and antagonists on nociception in the rat.

The effects of intracerebroventricular injection of histamine H2-receptor agonists (4-methylhistamine, 4-MeH; dimaprit, DIM), H2-antagonists (cimetidine, CIM; ranitidine, RAN; famotidine, FAM) and of the DIM chemical analogue SK&F 91487 on hot-plate latency in rats were examined. Both DIM (0.4-0.8 mumol/rat) and 4-MeH (0.4-0.8 mumol/rat) significantly enhanced the pain threshold, whereas SF&F 91487 (0.8 mumol/rat) had no effect, indicating that DIM antinociception is specifically due to its activity on histamine (HA) receptors. The H2-antagonists CIM (0.8 mumol/rat) and RAN (0.6 mumol/rat) also enhanced the pain threshold, while FAM (0.03 mumol/rat) did not modify pain latency. When injected before 4-MeH, FAM reduced the antinociceptive effect of 4-MeH. These findings suggest that the antinociceptive activity of CIM and RAN is not related to specific blockade of H2-receptors and that the activation of HA-H2-receptors is inhibitory to nociception.

Animals↗
PubMed1988

Further evidence that brain histamine H2 receptors are stimulatory in the control of prolactin in the rat.

The effects of administration into the brain ventricle of H2 receptor agonists (4-methylhistamine, 0.8 mumol/rat; dimaprit, 0.4-0.8 mumol/rat), H2 antagonists (cimetidine, 0.8 mumol/rat; ranitidine, 0.4-0.8 mumol/rat; famotidine, 0.03 mumol/rat) and of the dimaprit chemical analogue SK&F 91487 (0.4 mumol/rat) on unstimulated and histamine-stimulated prolactin secretion in normal male rats were studied. The H2 agonist 4-methylhistamine caused a significant increase in unstimulated blood PRL, whereas dimaprit, SK&F 91487, and the H2 antagonists tested did not change PRL levels. 4-Methylhistamine significantly enhanced the stimulatory effects of histamine on prolactin, whereas all the H2 antagonists inhibited histamine-induced prolactin release. The inhibition of histamine-induced prolactin secretion by the H2 agonist dimaprit is nonspecific, since its chemical analogue SK&F 91487, which has no H2 agonist activity, also inhibits it. These results indicate that stimulation of the H2 receptors in the central nervous system is facilitatory for PRL secretion, suggesting that the activation of H2 receptors may contribute to the PRL-releasing effects of histamine.

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 gene-related peptide: antinociceptive activity in rats, comparison with calcitonin.

The effects of synthetic human calcitonin gene-related peptide (CGRP) on nociceptive response were evaluated in rats by two behavioral tests (tail-flick and hot-plate) and by electrophysiological recording of the firing of thalamic neurons evoked by peripheral noxious mechanical stimuli. CGRP was administered intracerebroventricularly (i.c.v.) and its effects were compared with that of salmon calcitonin (sCT). In the tail-flick test, CGRP (0.25, 2.5 and 5 micrograms/rat) dose-dependently increased response latencies, whereas sCT (0.125, 2.5, 5 and 10 micrograms/rat) did not. Conversely, in the hot-plate test CGRP was effective in enhancing response latencies only at the highest dose of 10 micrograms/rat, while sCT (0.125, 0.25 and 2.5 micrograms/rat) inhibited the hot-plate response dose-dependently. In electrophysiological studies, CGRP (2.5 micrograms/rat, i.c.v.) completely inhibited the evoked neuronal thalamic firing and the same dose of sCT induced only a partial reduction. Furthermore, the antinociceptive effects of CGRP in the tail-flick test and in the electrophysiological studies were not prevented by naloxone. These results demonstrate that central administration of CGRP is effective in inhibiting nociceptive responses and its action like that of sCT does not involve an opioid mechanism. The differences in the antinociceptive profiles of CGRP and sCT suggest that the inhibitory effects of these peptides may involve different neuronal pathways.

Analgesics↗
PubMed1987

Involvement of brain histamine in basal and stress-induced release of prolactin in the rat.

We investigated whether inhibition of brain histamine (HA) synthesis by alpha-fluoromethylhistidine (alpha-FMH) can influence basal or stimulated prolactin (PRL) release in male rats. alpha-FMH was administered either into the carotid (i.a., 20 and 100 mg/kg) or intracerebroventricularly (i.c.v., 200 micrograms/rat) into freely moving rats with indwelling catheters. Plasma PRL levels were measured 90, 120, 180 min later. Both i.a. and i.c.v. administration of alpha-FMH significantly inhibited basal PRL secretion at 120 and 180 min. When PRL secretion was stimulated by exposing rats to restraint stress, alpha-FMH administered 3 h before the stress (20 and 100 mg/kg, i.a.; 200 micrograms/rat, i.c.v.) was able to prevent the PRL surges at 10 and 20 min after stress. These results suggest that endogenous brain HA has a facilitatory role in the control of PRL secretion in rats.

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↗
PubMed1986

Relationship of analgesia induced by centrally injected calcitonin to the CNS serotonergic system.

The role of the serotonergic system in the antinociceptive effect of centrally administered salmon calcitonin (sCT) was studied in rats. The animals were given sCT either intracerebroventricularly (i.c.v.) or intrathecally (i.t.). I.c.v. administration of sCT (2,5 micrograms/rat) to animals depleted in CNS serotonin (5-HT) either by treatment with 25 mg/kg desmethylimipramine (DMI) i.p. plus 100 micrograms/rat 5,7 dihydroxytryptamine (5,7 DHT) i.c.v., ten days before or by 150 mg/kg p-chlorophenylalanine (pCPA) i.p., 72 and 24 h before, still significantly increased the hot-plate latencies comparable to those of non-depleted animals. The same result was obtained when the 5-HT receptors were blocked with metergoline. The i.t. administration of sCT (2 micrograms/rat) to animals with spinal cord 5-HT depleted by treatment with DMI plus 5,7 DHT, i.t., delayed but did not abolish the antinociceptive activity of i.t. injected sCT, which was of the same intensity as in non depleted animals. When 5,7 DHT was administered alone, either i.c.v. or i.t., without protection of the catecholaminergic neurons so that noradrenaline (NA) was greatly reduced, the antinociceptive effect of sCT was completely abolished even when NA had been depleted only in the spinal cord. We conclude that it is the catecholaminergic system, not the serotonergic, that plays a fundamental role in the anti-nociceptive effect of centrally administered sCT.

5,7-Dihydroxytryptamine↗
PubMed1985

Cimetidine-induced prolactin release: possible involvement of the GABA-ergic system.

The mechanism of cimetidine-induced prolactin (PRL) release was studied. Intracarotid (i.a.) administration of 1 mg/kg of impromidine, the most specific H2 histamine agonist known, did not counteract the cimetidine-induced hypersecretion of PRL. Pre-treatment with benzodiazepines (diazepam or lorazepam, 3 mg/kg/i.a.) completely suppressed it. Administration of gamma-aminobutyric acid (GABA 5 mg/kg/i.a.) was also able to prevent it, but to a lesser extent than benzodiazepines. Simultaneous administration of doses of diazepam (1.5 mg/kg/i.a.) and GABA (3 mg/kg/i.a.) ineffective per se markedly blunted the increase of PRL by cimetidine. We conclude that cimetidine does not induce hypersecretion of PRL by its action on histamine H2 receptors, but through other pharmacological activities of the drug, such as perhaps interaction with the GABA-ergic system in the pituitary.

Animals↗
PubMed1985

Role of catecholamines in calcitonin-induced analgesia.

The possibility that the catecholaminergic (CA) system might be involved in calcitonin (CT)-induced analgesia was examined. The administration of the neurotoxin for CA neurons, 6-hydroxydopamine (6-OHDA) significantly reduced salmon CT (sCT) analgesia as measured in rats by the hot-plate test. Pretreatment with an alpha- and beta-blocker (phentolamine and propranolol) was also effective in lowering significantly the activity of sCT. When the two drugs were administered alone, propranolol, but not phentolamine, reduced the analgesic effect of sCT. A more pronounced and long-lasting inhibitory effect on sCT-analgesia was obtained using atenolol (selective beta 1-receptor blocker). The present data support the role of the CA system in sCT-induced analgesic activity.

Analgesics↗
PubMed1984

Antinociceptive effect of centrally administered cimetidine and dimaprit in the rat.

Cimetidine, an H2 receptor antagonist, administered into a lateral ventricle of the rat brain caused a significant increase in tail flick latency. Dimaprit, a specific H2 agonist, failed to counteract the analgesic effect of cimetidine. In contrast, it enhanced the effect of cimetidine and per se had marked analgesic activity. The specific opioid antagonist naloxone was without effect. Pretreatment with CaCl2 completely prevented the action of cimetidine. These findings suggest that the analgesic action of cimetidine and dimaprit is not due to specific effects on H2 receptors.

Analgesia↗
PubMed1984

Failure of somatostatin antiserum to reverse histamine-induced inhibition of pulsatile growth hormone secretion.

We attempted to determine whether the suppression by histamine of spontaneous episodic growth hormone (GH) secretion is mediated by an augmented release of somatostatin (SS). Adult male rats were passively immunized against SS by the injection of a specific goat anti-SS antibody. Plasma GH levels in rats bearing indwelling catheters were measured at 15-min intervals for 4 h. Histamine (0.1 mumol/rat) was administered intracerebroventricularly (i.c.v.) 1 h after the start of the experiment and once an hour for the next 2 h. Anti-SS serum (2 ml) was injected 2 h after the beginning of the experiment to two groups of rats, one given saline i.c.v. and the other histamine i.c.v. Histamine was able to suppress not only spontaneous GH secretion but also the antiserum-stimulated GH release. These data suggest that histamine inhibiton of GH is not mediated by SS but probably by a reduction of GH-releasing hormone or some other stimulatory signal.

Animals↗
PubMed1983

Localization of calcitonin binding sites in rat central nervous system: evidence of its neuroactivity.

The distribution of calcitonin (CT) binding sites in serial sections of the rat brain and spinal cord has been examined by an 'in vitro' autoradiographic technique using a radioisotope-sensitive sheet film and [125]salmon CT. Autoradiograms of the diencephalic region had the highest grain density throughout the entire hypothalamus, with the exception of the nuclei ventromedialis, posterior and mammillaris, which were not labeled at all. In the brainstem, large amounts of grains were found in the ventrolateral division of the periaqueductal gray, in the locus coeruleus, in the nucleus tractus spinalis nervi trigemini and in the raphe obscurus, pallidus and magnus, while a widespread and lower grain density was observed in the reticular formation. In the spinal cord the labeling was discretely localized in laminae IV, V and VI of the dorsal horn. The observed distribution of CT binding sites is closely related to the neuroendocrine and analgesic effects of exogenous CT and reinforces the concept of a possible neuromodulatory role proposed for the peptide at brain level.

Animals↗
PubMed1983

Comparison of the effects of histamine H2-receptor antagonists on prolactin secretion in the rat.

Various compounds with different blocking potencies on histamine H2-receptors were administered to rats both into the carotid (ia) and into the brain ventricles (icv) and their effects on PRL release were evaluated. The drugs were cimetidine, as reference compound, ranitidine, 5 to 7 times as potent, and oxmetidine, 8 to 10 times as potent. PRL was measured in blood samples collected at -15, 0 and +5, +10, +20 and +40 min after treatment. Cimetidine (80 mg/kg) and ranitidine (30 mg/kg), when injected ia as a single bolus, induced prompt increases (P less than 0.01) in PRL. On the contrary, oxmetidine (the most potent H2 antagonist), even at the high dose of 80 mg/kg ia, had no effect on PRL release. When the drugs were given icv (0.2 mumol/rat or 0.8 mumol/rat), none of them caused any significant PRL release. These results suggest that histamine H2-blocking potency is not correlated with PRL release. Furthermore, the PRL-releasing activity of the drugs seems not to be due to any action on the central neural control of PRL secretion. This comparative study shows that it is possible (as with oxmetidine) to achieve complete dissociation of the H2-receptor blocking action from the unwanted PRL-release stimulating effect.

Animals↗
PubMed1982

Influence of brain histaminergic system on episodic growth hormone secretion in the rat.

The effects of histamine and amodiaquine (a drug known to inhibit histamine-N-methyltransferase) on pulsatile growth hormone (GH) secretion were determined in unanaesthetized male rats. Intracerebroventricular (i.c.v.) administration of histamine (0.01, 0.05, 0.1 mumol/rat) caused a dose-related suppression of spontaneous pulses of rat GH (rGH) secretion. Amodiaquine (0.16 mumol/rat i.c.v.) also inhibited the pulses, but to a lesser degree. The results, which show the inhibitory effects of both exogenous histamine and increased levels of endogenous histamine on pulsatile rGH secretion, support the hypothesis that the histaminergic system also plays a role in physiological CNS control of rGH secretion.

Amodiaquine↗
PubMed1982

High sensitivity to calcitonin of prolactin-secreting control in lactating rats.

The effects of intracerebroventricular (icv;25ng/rat) or iv (10 micrograms/kg) salmon calcitonin (sCT) on PRL secretion were determined in lactating rats and compared to the effects in intact or ovariectomized-estrogen-treated female rats. The icv or iv injections of sCT 9 days after estrogen treatment did not significantly lower the PRL levels in intact rats. In ovariectomized-estrogen-primed animals, sCT (icv or iv) did not modify the afternoon surge of PRL secretion when injected during the surge, nor did it delay or attenuate the increasing secretory activity when administered (iv) before the afternoon surge had begun. On the contrary, 30 or 60 min after the icv or iv administration of sCT to lactating rats, suckling-induced PRL secretion was prevented. These results and our previous evidence that a greater dose of sCT is needed to decrease the less intense morphine- or stress-induced PRL secretion indicate differential hypoprolactinemic properties of sCT, which are particularly striking during lactation. While the mechanisms underlying these selective activities deserve further investigation, the proposed participation of PRL in the regulation of calcium metabolism during lactation suggests that the potent PRL inhibitory effect of CT in this condition should be regarded as one factor in the complex mechanism that prevents bone loss and protects the maternal skeleton.

Animals↗
PubMed1981

Histamine agonist and antagonist drugs: interference with CNS control of GH release in rats.

The effects of the administration into the brain ventricle of histamine, selective H1- and H2-receptor agonists and antagonists and chemically similar substances with nonspecific activity on basal and morphine-stimulated growth hormone (GH) secretion in normal male rats were studied. None of the drugs had any significant effect on baseline rat GH levels, but histamine and H1 agonists were able to decrease the rat GH release evoked by morphine. Mepyramine (H1 antagonist) had no consistent effect by itself but was effective in preventing the inhibitory action of 2-methylhistamine (H1 agonist). H2 agonists and antagonists and their chemical analogues were all inhibitory, but by a mechanism which is nonspecific and must be interpreted cautiously. These results confirm the inhibitory effect of histamine on rat GH release and indicate that H1 receptors in the CNS are responsible for this effect.

Animals↗
PubMed1980

The central GABAergic system and control of food intake under different experimental conditions.

Intracerebroventricular injections of gamma-aminobutyric acid (GABA) and of the GABA-transaminase inhibitor, ethanolamine-O-sulphate (EOS), decreased the food intake of freely-fed (GABA and EOS) and food-deprived rats (EOS). The effect, still evident 24 h after treatment, was not decreased by the GABA receptor-blocker bicuculline. In contrast, intracerebroventricular injections of the GABA receptor-agonist, muscimol, caused an increase in food intake of freely-fed rats that was antagonized by bicuculline. The eating of animals receiving only bicuculline was stimulated in free-feeding and depressed in food-deprived conditions. These opposite results suggest that muscimol binds preferentially to some GABA receptors, probably those within the satiety-controlling areas (i.e. ventromedial hypothalamus), and that bicuculline influences mainly those postsynaptic neurons where GABAergic inputs prevail. These observations and the data from EOS- and GABA-treated rats provide evidence for involvement of GABA neurons in the regulation of feeding behaviour. The balance of the different effects produced in each of these areas by this modulation appears to be a decrease in feeding behaviour.

Animals↗