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Biomedical subjects

U Scapagnini

Publications and source records attributed to U Scapagnini.

At least 73 records · Page 4Linked to original sources
PubMed1985

Effects of haloperidol on morphine-induced antinociception morphine tolerance and withdrawal in hyperprolactinaemic rats.

Male rats with hyperprolactinaemia, induced by adenohypophyseal homografts under the kidney capsule, were injected with haloperidol for 3 days and then subjected to treatment with morphine, administered twice in a day at increasing doses for 12 days. At the first treatment, morphine induced an antinociceptive effect that was more prolonged in homografted rats than in sham-operated controls. The pretreatment with haloperidol did not change the prolongation of morphine-induced antinociception in homografted rats. After 12 days of treatment with morphine, all animals were tested for the development of tolerance to the antinociceptive effect of morphine. Pituitary homografts resulted in an inhibition of the development of tolerance, while this effect was absent in homografted rats pretreated with haloperidol. At the end of the treatment with morphine, the naloxone-precipitated abstinence syndrome was studied. Homografted rats shown an attenuation of the withdrawal syndrome and pretreatment with haloperidol did not change this response. These results suggest an involvement of dopaminergic transmission in prolactin-induced changes in the development of tolerance to morphine, but not in the antinociceptive effect following an acute injection of morphine and in naloxone-precipitated withdrawal syndrome of the rat.

Animals↗
PubMed1985

Effect of (Asu1,7)E-CT, synthetic analogue of eel-calcitonin, on nociceptive transmission.

The effect of (Asu1,7)E-CT a deaminodicarba-analogue of the synthetic eel-calcitonin on the nociceptive transmission has been studied in mice. The analogue was intracerebroventricularly (0.0.5-0.01-0.02 U.I./kg) or intravenously (0.02-0.04-0.05 -0.1 U.I./kg) injected. This synthetic derivative of eel-calcitonin increased the antinociceptive effect also after peripheral administration. Moreover, preliminary studies on the time-course of this analogue showed that the dose of 0.1 U.I./kg i.v. injected, was able to elicit antinociceptive effect, already 5 min after the administration.

Animals↗
PubMed1985

Quantitative alteration of grooming behavior in aged male rats.

Novelty-induced grooming was studied in aged male rats (24 months old) compared to young animals (3 months old). When put in a novel environment, aged rats exhibited a grooming activity markedly higher than that shown by young rats. Such an excessive grooming did not disappear over a 30 min observation. Furthermore, no significant difference between old and young rats was found in ambulation, rearing and defecation, as observed in an open field. It may be suggested that increased grooming activity in aged rats involves a disability to adapt to a novel environmental situation.

Adaptation, Psychological↗
PubMed1985

Neurotensin stimulates polyphosphoinositide breakdown and prolactin release in anterior pituitary cells in culture.

Biochemical events underlying neurotensin action at the pituitary were investigated in primary culture of anterior pituitary cells prelabeled with [3H]inositol. Incubation with the tridecapeptide produced a dose-dependent increase in the content of total [3H]inositol phosphates. The time-course showed that the effect was rapid and significant within 1 min. Fractionation of [3H]inositol phosphates revealed that inositol triphosphate (IP3) and inositol diphosphate (IP2) increased earlier than inositol monophosphate (IP1). Structure/activity correlation studies demonstrated the specificity of neurotensin effect, showing that acetylneurotensin(8-13) displayed an action similar to the natural peptide, while neurotensin(1-6) hexapeptide did not exhibit any effect. The neurotensin analog [D-Trp11]-neurotensin antagonized in a concentration-dependent manner the effect of neurotensin both on prolactin release and on [3H]inositol phosphate production. The loss of prelabeled phosphoinositides was also investigated. Phosphatidylinositol-4,5-bisphosphate (PtdIns-4,5-P2) and phosphatidylinositol-4-phosphate (PtdIns-4-P) decreased significantly within 15 s, while a slight decline in phosphatidylinositol (PtdIns) level appeared only 1 min after neurotensin addition. These results suggest that neurotensin action at the pituitary is mediated by the early hydrolysis of polyphosphoinositides, leading to the production of 1,2-diacylglycerol and inositol phosphates which may initiate intracellular processes responsible for hormonal release.

Animals↗
PubMed1985

Differential responses in prolactin levels induced by naloxone in humans.

The plasma prolactin (PRL) response to the opiate antagonist naloxone was tested in drug-free healthy volunteers (10 men, 18 regularly menstruating women who were in the late follicular phase of their ovarian cycles, and seven post-menopausal women). Naloxone hydrochloride (2 mg intravenous bolus) and placebo (normal saline) were administered on two different days in a double-blind fashion. Blood samples were collected at -15, 0, 30, 60, 120, 180 and 240 min after the injection. In the women of reproductive age, naloxone reduced plasma PRL concentrations, whereas in the post-menopausal women and the men, naloxone resulted in no significant change. However, in the post-menopausal women treated with estrogen (intramuscular 17-beta-estradiol), the opiate antagonist was able to lower plasma PRL concentrations. Thus, it appears that opiate effects on PRL secretion are influenced by the gonadal steroid environment and that estrogens may play a modulating role.

Adult↗
PubMed1985

Involvement of arachidonate metabolism in neurotensin-induced prolactin release in vitro.

Neurotensin increased in a concentration-dependent manner the level of hypophyseal [3H]arachidonic acid in vitro as well as prolactin release from hemipituitary glands. The effect of 1 microM neurotensin on arachidonate release was already present at 2.5 min, maximal at 5, and disappeared after a 10-min incubation. Neurotensin analogues produced an enhancement of hypophyseal arachidonate similar to their relative potencies in other cellular systems, whereas other peptides (somatostatin and vasoactive intestinal peptide) were devoid of any effect on the concentration of the fatty acid in the pituitary. Seventy micromoles RHC 80267, a rather selective inhibitor of diacylglycerol lipase, completely prevented the neurotensin-stimulated prolactin release and decreased arachidonate release both in basal or in neurotensin-induced conditions. Similar results were obtained with 50 microM quinacrine, a phospholipase A2 inhibitor. To clarify whether arachidonate released by neurotensin requires a further metabolism through specific pathways to stimulate prolactin release, we used indomethacin and BW 755c, two blockers of cyclooxygenase and lipoxygenase pathways. Thirty micromoles indomethacin, a dose active to inhibit cyclooxygenase, did not affect unesterified arachidonate levels either in basal or in neurotensin-induced conditions; moreover, the drug did not modify basal prolactin release but slightly potentiated the stimulatory effect of neurotensin on the release of the hormone. On the other hand, 250 microM BW 755c, an inhibitor of both cyclooxygenase and lipoxygenase pathways, significantly inhibited both basal and neurotensin-stimulated prolactin release and further potentiated the increase of the fatty acid concentrations produced by 1 microM neurotensin.(ABSTRACT TRUNCATED AT 250 WORDS)

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1985

Ovarian LHRH receptors increase following lesions of the major LHRH structures in the rat brain: involvement of a direct neural pathway.

Specific lesions of different brain structures known to contain or to be coursed by LHRH neurons have been carried out in intact cycling female rats in order to investigate the role played by central LHRH and neuronal systems in the regulation of ovarian and hypophyseal LHRH receptor (LHRH-R) levels, using the stable LHRH analog [D-Ser (TBU)6] Des-Gly10, LHRH ethylamide, buserelin. Radiofrequency lesions were placed bilaterally or unilaterally into female rats showing at least two consecutive estrous cycles, under pentobarbital anesthesia, while groups of animals were sham-operated. Bilateral lesions placed into the septal area and into the nucleus and tract of the diagonal band of Broca (DBB) resulted in a nearly 25-40% stimulation of LHRH binding activity within the ovaries and a 30% inhibition of LHRH analog binding to pituitary homogenate, while lesions placed into the medial preoptic area (MPO), where the majority of LHRH neurons are found, produced a doubling of ovarian LHRH-R accompanied by a 60% decrease of pituitary binding sites. Lesions involving the median eminence and arcuate hypothalamic nucleus, where the most conspicuous convergence of LHRH fibers occurs, produced a twofold increase in ovarian LHRH-R levels and an almost complete loss of pituitary LHRH-R binding capacity, with no change in affinity. In order to clarify the importance of direct neural signals modulating the ovarian LHRH-R concentration, lesions were placed in the right or left MPO and DBB, and the content of LHRH-R measured in right and left ovaries. Lesions placed unilaterally (right or left) produced a significant increase of LHRH-R binding activity within the ovary ipsilateral to the lesion, while a reduction or no effect was observed in the contralateral gland. Data show a marked stimulation of ovarian LHRH-R number following bilateral lesions placed in the major LHRH-containing structures, while pituitary LHRH binding sites are significantly inhibited, indicating impairment in the rate and/or amplitude of endogenous hypothalamic LHRH release. Furthermore results obtained following unilateral lesions indicate that a neural mechanism is involved in ovarian LHRH receptor induction and further reinforce our view that a direct neural connection links the brain and the ovaries.

Animals↗
PubMed1985

Phospholipid metabolism and prolactin secretion in vitro.

The possible mechanisms by which phospholipid metabolism may be involved in the biochemical events underlying pituitary hormone secretion in basal and stimulated conditions were examined. Particular emphasis was given to the role of changes in the turnover of specific membrane phospholipids, the polyphosphoinositides, in the stimulatory effect of TRH and neurotensin on prolactin release in vitro. Finally, some comments on the involvement of arachidonate and/or its metabolites in the mechanisms of release of the hormone have been reported. In this respect, the possibility that a specific diacylglycerol lipase may represent a link between the 'phosphatidylinositol effect' and the production of arachidonate from mammotroph membranal phospholipids was examined using the rather selective inhibitor of diacylglycerol lipase RHC80267.

Animals↗
PubMed1985

Neuroendocrine and behavioral effects of flunarizine in young and old rats.

Neuroendocrine and behavioral effects following an acute or chronic treatment with the calcium antagonist, flunarizine, have been studied in young and old rats. Both in young and old rats, acute administration of flunarizine (2 mg/kg) failed to modify plasma prolactin (PRL) levels, as measured at 8.00 a.m., 4.00 p.m. and 12.00 p.m. A chronic treatment with flunarizine (0.5 mg/kg/day, for 20 days) in young rats was followed by a relevant, albeit statistically not significant, increase in plasma PRL levels, as measured at 8.00 a.m. and 4.00 p.m., and by a significant decrease at 12.00 p.m. A shift of nocturnal peak of plasma PRL levels from 12.00 p.m. to 4.00 a.m. was observed in these animals. A chronic treatment with flunarizine in old rats was followed by a significant increase in plasma PRL levels, as measured at 12.00 p.m. The acquisition of active avoidance behavior was studied in a shuttle-box test. Acute administration of flunarizine failed to change the performance of young and old rats in acquiring the behavioral response, as measured by the total number of conditioned avoidance responses (CARs) and the percentage of learners. When flunarizine was administered chronically, a decrease in CARs and learners was observed both in young and old rats. This was accompanied by a significant increase in the percentage of animals that froze during the acquisition session. No significant effect was found in young and old rats tested in a "despair" test after a chronic treatment with flunarizine.

Age Factors↗
PubMed1985

Side effects of drugs stimulating prolactin secretion on the behavior of male rats.

The behavioral effects of drugs stimulating prolactin (PRL) secretion have been studied in male rats. Acquisition of active avoidance behavior was facilitated by short- (SHPRL) and long-term hyperprolactinaemia (LHPRL) induced by pituitary homografts under the kidney capsule. Dopamine antagonists, such as haloperidol and bromperidol, though causing hyperprolactinaemia, suppressed the acquisition of active avoidance behavior. Sulpiride was not effective in this respect. SHPRL facilitated and LHPRL inhibited sexual behavior of male rats. Haloperidol, but not sulpiride, suppressed sexual capacity of these animals. Sulpiride and domperidone, but not haloperidol, increased locomotor activity of male rats. These data suggest that differences in the behavioral effects of dopamine antagonists may depend on their capacity to compete with PRL at the central level.

Animals↗
PubMed1984

Catecholamine utilization in specific rat brain nuclei after short-term hyperprolactinaemia.

Endogenous hyperprolactinaemia was induced in intact male rats by transplantation of pituitaries under the kidney capsule. Five days later the utilization of noradrenaline (NA) and dopamine (DA) in individual brain nuclei and changes of plasma prolaction (PRL) were measured. Inhibition of catecholamine synthesis by alpha-methyl-p-tyrosine (alpha-MPT) was used to measure utilization. Hyperprolactinaemia increased the utilization of NA in the locus coeruleus, the cell-body region of the dorsal noradrenergic bundle (DNB), but decreased it in some terminal projections of the same pathway (e.g. the cingulate gyrus). DA utilization was increased by hyperprolactinaemia in the eminentia mediana. In the nigrostriatal DA-ergic projection, hyperprolactinaemia decreased the utilization of DA in the cell-body region (substantia nigra) and increased it in the terminal projection (nucleus caudatus). In the ventral tegmental area (mesolimbic DA-ergic projection), hyperprolactinaemia decreased the utilization of DA. It is concluded that hyperprolactinaemia affects neurotransmission in the hypothalamus and also in specific extrahypothalamic pathways (e.g. DNB, nigrostriatal and mesolimbic DA-ergic projections) and that these changes may correlate with some behavioural effects of the pituitary hormone.

Animals↗
PubMed1984

Altered time course of changes in the hippocampal concentration of excitatory and inhibitory amino acids during kainate-induced epilepsy.

The temporal sequence of electrophysiological and biochemical correlates of epilepsy induced by systemic injection of kainic acid (15 mg/kg i.p.) was investigated in male rats. A significant decrease in the hippocampal concentration of glutamate and aspartate was observed 20 min after the injection. These decreases preceded both electrographic and behavioral manifestations of epilepsy, thus suggesting a causal relationship between acidic amino acid changes and the genesis of kainate-induced hyperactivity. About 30-45 min after kainate injection, a decrease in glutamate, aspartate, glycine and taurine and no change in GABA concentration were observed. Bioelectrical activity, recorded in the regio inferior (CA3) of the hippocampus or in the fascia dentata revealed the presence of high frequency bursts separated by a long-lasting depression of discharge. About 55-75 min after the injection, the number of spikes in each burst increased and the duration and frequency of interictal pauses decreased. This stage was characterized by a decrease in glutamate and aspartate, restoration to normal of glutamine, glycine and taurine and a decrease in GABA.

Amino Acids↗
PubMed1984

Amphetamine-induced analgesia does not involve brain opioids.

The intrinsic analgesic properties of amphetamine were studied in rats. Subcutaneous injection of amphetamine exerted an additive effect on morphine-induced analgesia in the hot-plate test. Amphetamine itself showed intrinsic analgesic activity in a dose-dependent manner. Administration of naloxone failed to affect the analgesia induced by amphetamine. However, injection of haloperidol totally suppressed the amphetamine-induced change in pain response latency. Both naloxone and haloperidol failed to affect the pain threshold when injected alone, but inhibited morphine-induced analgesia. It is concluded that amphetamine possesses intrinsic analgesic properties which involve catecholamine but not opioid transmission in the brain.

Amphetamine↗
PubMed1984

Hyperalgesic activity of parathyroid hormone and its fragments in male rats.

Results presented in this paper indicate that intracerebroventricular injection of parathyroid hormone reduces pain threshold in male rats. This effect is induced by whole molecule (84 amino acids) or by fragments 1-34 and 44-68 of PTH. The fragment 65-84 of PTH does not induce any change in pain threshold.

Animals↗
PubMed1984

Fastigial influences on postural tonus as studied by kainate lesions and by local infusion of GABAergic drugs in the rat.

Localized lesions with kainic acid (KA) and local infusion of GABAergic drugs were used to study the role of the nucleus fastigii (NF) in postural tonus. Unilateral axon-sparing KA lesions of NF resulted in ipsilateral limb extensor atonia and contralateral limb extensor hypertonus and abduction. This effect lasted for 3-8 days depending on the dose of KA. Lesions of sites adjacent to the NF failed to produce postural asymmetries. Local infusion of the GABA agonist muscimol (10-50 ng) in the NF produced a reversible postural asymmetry fenomenologically similar to that produced by KA lesions of NF. Infusion of agents blocking GABAergic transmission in the NF (bicuculline, picrotoxin) resulted in a postural asymmetry of inverted laterality in respect to that produced by muscimol. Bilateral KA lesions of NF or bilateral infusion of muscimol resulted in bilateral hyperextension-abduction of the limbs. Infusion of GABAergic drugs in areas adjacent to the NF failed to produce postural changes. The results are interpreted to indicate that the NF exerts a crossed inhibitory and a direct excitatory influence on limb postural tonus.

Animals↗
PubMed1984

Role of serotonin in the analgesic activity of calcitonin.

The acute effects of peripherally administered methysergide or phentolamine on the analgesic activity of salmon calcitonin (sCT) injected into the lateral ventricle were investigated in male rats. Methysergide, but not phentolamine, significantly (P less than 0.05) antagonized the analgesic activity of sCT at 60 and 120 min after the administration of the peptide. The results obtained suggest that the analgesic activity of sCT may involve central serotonergic system(s), while the central noradrenergic system does not seem to be needed for this activity.

Analgesics↗