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Biomedical subjects

U Scapagnini

Publications and source records attributed to U Scapagnini.

At least 91 records · Page 5Linked to original sources
PubMed1984

Effects of mastectomy and vagotomy on grooming behavior of the rat: possible involvement of prolactin.

Surgical interventions such as unilateral mastectomy or vagotomy affect plasma prolactin (PRL) levels. Right-side mastectomized rats exhibiting high levels of plasma PRL showed increased grooming behavior. Left-side mastectomized rats with low levels of plasma PRL performed poor grooming activity. Bilateral mastectomy that caused a slight increase in plasma PRL levels was followed by enhanced grooming behavior. Both left and right vagotomy resulted in a significant increase in plasma PRL levels. However, only left-side vagotomized rats exhibited increased levels of grooming behavior, while no difference between right-side vagotomized rats and controls occurred. It is possible that changes in plasma PRL levels induced by surgical interventions affect grooming activity of the rat. However, the hypothesis that the integrity of peripheral organs is important for the display of grooming behavior cannot be ruled out.

Animals↗
PubMed1984

Effects of calcitonin, parathyroid hormone and its related fragments on acquisition of active avoidance behavior.

The acquisition of active avoidance response was studied in rats injected intracerebroventricularly with calcitonin (CT), parathyroid hormone (PTH) or PTH-related fragments. PTH and PTH65-84 facilitated the acquisition of shuttle-box active avoidance behavior as indicated by the number of conditioned avoidance responses and the percentage of animals reaching the learning criterion. PTH1-34 and PTH44-68, on the contrary, inhibited the acquisition of active avoidance behavior, while CT totally suppressed this behavior in the rat. It is possible that the opposite effects of PTH and CT on learning ability of the rat depend on a different action on calcium metabolism.

Animals↗
PubMed1984

Behavioral activity of a short chain ACTH analog.

The behavioral activity of ACTH1-17 analog (beta-Ala1, Lys17) ACTH1-17-4 -amino-n-butilamide (Ala1-Lys17-ACTH1-17) has been studied in the rat. Acquisition of shuttle-box active avoidance behavior was facilitated by Ala1-Lys17-ACTH1-17 administered both subcutaneously (SC) and intracerebroventricularly (ICV), and this effect was suppressed by peripheral administration of haloperidol or naltrexone. Extinction of pole jumping active avoidance behavior was delayed by SC administration of the peptide in a dose-dependent manner. Retention of a step-through passive avoidance behavior was facilitated SC or ICV injection of Ala1-Lys17-ACTH1-17. Adrenalectomy failed to modify the effects of the peptide on the retention of passive avoidance behavior. Furthermore, ICV injection of graded doses of Ala1-Lys17-ACTH1-17 induced excessive grooming, and this effect was totally prevented by intraperitoneal (IP) injection of haloperidol or naltrexone SC administration of Ala1-Lys17-ACTH1-17 induced a slight but significant increase in negative responses in a test for behavioral responsiveness to electrical footshock. This effect was totally prevented by IP injection of naltrexone. It is concluded that Ala-Lys17-ACTH1-17 shares some of the behavioral effects of ACTH4-10 and some ACTH1-24, but it seems to be more potent than the latter peptides. Both dopamine and opioid transmission seem to be involved in the behavioral activity of Ala1-Lys17-ACTH1-17.

Adrenocorticotropic Hormone↗
PubMed1984

Effects of valproic acid derivatives on the acquisition of active avoidance behavior in the rat.

The effects of valproic acid derivatives on the acquisition of active avoidance behavior have been studied in the rat. Sodium valproate (50 and 100 mg/kg), magnesium valproate (100 mg/kg) and dipropylacetamide (100 mg/kg) were administered intraperitoneally 1 hr prior to the behavioral test (shuttle-box, single session). Acquisition of active avoidance behavior was facilitated by sodium valproate, unaffected by magnesium valproate, and inhibited by dipropylacetamide. These findings suggest that behavioral effects of valproic acid derivatives cannot be explained only in terms of a general inhibitory action on the central nervous system.

Animals↗
PubMed1984

Effect of calcitonin on ACTH secretion.

We have investigated the effects of salmon calcitonin injected intracerebroventricularly on adrenocorticotropic (ACTH) secretion in rats. Salmon calcitonin was able to increase significantly (p less than 0.05) ACTH secretion at the dose of 5 ng/rat and (p less than 0.01) at the doses of 12.5, 25 and 50 ng/rat; the effect (50 ng/rat) was maximal at 30 min and still present after 60 and 120 min. The maximal dose of calcitonin produced a significant (p less than 0.05) increase in serum ACTH concentration also in stressed animals. It is suggested that calcitonin may increase serum ACTH secretion by central norepinephrine and/or 5-hydroxytryptamine pathways that regulate corticotropic releasing factor activity.

Adrenocorticotropic Hormone↗
PubMed1984

Effect of CRF on the release of anterior pituitary hormones in normal subjects and patients with Cushing's disease.

Patterning of plasma ACTH, beta-EP/beta-LPH and cortisol in response to ovine CRF (1 microgram/kg b.w.t. injected i.v.), was studied in three normal subjects and in five patients with Cushing's disease, two of whom had undergone total bilateral adrenalectomy. CRF caused in all subjects a prompt and concurrent rise of plasma hormone levels. The hormonal response was of the same magnitude in normal controls and in the three untreated Cushing's patients, but was much greater in the two adrenalectomized subjects. No changes were noted, after CRF, in plasma levels of GH, PRL, TSH, LH and FSH. These findings indicate that CRF specifically promotes the pituitary release of ACTH and ACTH-related peptides both in normal subjects and patients with Cushing's disease. In view of the likely CRF hypersecretion of the adrenalectomized patients, their ACTH and beta-EP/beta-LPH hyperresponsiveness to exogenous CRF would denote that the peptide does not down regulate its own pituitary receptors.

Adolescent↗
PubMed1984

Gangliosides antinociceptive effects in rodents.

The present paper shows that a mixture of gangliosides (GA = GM1 + GD1a + GD1b + GT1b) is provided with a specific and powerful antinociceptive activity. The GA is active in reducing acetic acid and phenylquinone writhings, the acetic acid capillary-induced permeability and some acute inflammatory reactions. These actions seem to be mostly due to an anti-exudative property of the compounds which shows up right after the administration. The mixture of four gangliosides given in the proportion naturally occurring in the nervous system is more active than each single component in increasing the pain threshold, presenting therefore a synergistic effect. It is suggested that gangliosides can reduce the exudative phenomena interfering with the membrane permeability of the nerve-endings breaking interfering with the membrane permeability of the nerve-endings breaking the vicious circle of the neurogenic mechanisms of plasma extravasation.

Acetates↗
PubMed1983

Influence of sex steroids and prolactin on haloperidol-induced catalepsy.

The effects of sex steroids and prolactin on haloperidol-induced catalepsy were investigated in male rats. Repeated administration with estradiol benzoate (5 micrograms/rat, twice daily for 10 days) significantly potentiated catalepsy induced by 0.25 or 0.5 mg/kg haloperidol, but no effect was observed 10 min or 1 h after a single injection of estradiol benzoate (5 or 50 micrograms/rat). Conversely, a single administration with the catecholestrogen 2-hydroxyestradiol (50 micrograms/rat) significantly increased haloperidol-induced catalepsy, suggesting that catecholestrogens may directly interfere with nigrostriatal dopaminergic transmission. Haloperidol-induced catalepsy has been found to be attenuated in conditions of hyperprolactinaemia resulting from anterior pituitary isograft underneath the kidney capsule. This is consistent with the hypothesis that prolactin may stimulate nigro-striatal dopaminergic function. Results obtained also indicate that medroxy-acetate progesterone, a progesterone derivative, may influence haloperidol-induced catalepsy. Specifically, a single administration with medroxy-acetate progesterone (5 mg/kg, i.p.) enhanced catalepsy but opposite effects were observed after repeated administration of medroxy-acetate progesterone (5 mg/kg, i.p., once a day for 7 days).

Animals↗
PubMed1983

Prolactin-enhanced grooming behavior: interaction with ACTH.

The interaction between prolactin (PRL) and ACTH in enhancing grooming behavior after intracerebroventricular (i.c.v.) administration was investigated in intact and endogenously hyperprolactinaemic rats. In intact rats, 4 h after the i.c.v. injection of rat PRL or ACTH, a subsequent administration of ACTH or rat PRL did induce similar excessive grooming as observed after the first injections. In hyperprolactinaemic rats, which displayed excessive grooming 12 days after homografting adenopituitaries under the kidney capsule, i.c.v. injection of rat PRL failed to enhance further the grooming activity while this behavior was substantially enhanced by i.c.v. injection of ACTH1-24. Twenty-six days after surgery, when the grooming activity of hyperprolactinaemic rats was at the same level as control animals, the i.c.v. injection of rat PRL was effective in inducing excessive grooming in control but not in hyperprolactinaemic animals. In contrast, at this time the i.c.v. injection of ACTH1-24 induced again excessive grooming in both hyperprolactinaemic and control rats. Accordingly, there was no cross-tolerance between PRL and ACTH in inducing excessive grooming, but hyperprolactinaemic rats became hyposensitive to exogenous PRL. It is suggested that although PRL and ACTH may affect common neurotransmitter systems in the brain, the two hormones probably act on independent neural mechanisms in inducing excessive grooming in the rat.

Adrenocorticotropic Hormone↗
PubMed1983

Effects of calcitonin on the brain of aged rats.

We have recently demonstrated that calcitonin, a putative neuromodulator, may influence extrapyramidal motor system by decreasing nigro-striatal dopaminergic function. Since calcitonin is extensively used in aged patients, we have investigated whether calcitonin might influence extrapyramidal motor behavior (haloperidol-induced catalepsy and apomorphine-induced hyperactivity) in rats of different ages. Intracerebroventricular injection of salmon calcitonin (1 micrograms/kg) prevented apomorphine-induced hyperactivity in 2, 7, 18 or 21 month old rats, but potentiated haloperidol-induced catalepsy only in 2 or 7 month old rats. In addition, in all the animals salmon calcitonin significantly decreased the secretion of prolactin, an anterior pituitary hormone that may act at central level enhancing nigro-striatal dopaminergic activity.

Age Factors↗
PubMed1983

Hypoprolactinemic action of calcitonin and the tuberoinfundibular dopaminergic system.

The effects of calcitonin on neurochemical parameters related to the tuberoinfundibular dopaminergic system have been investigated in an attempt to elucidate how calcitonin decreases serum prolactin levels. Intracerebroventricular human or salmon calcitonin injection decreases serum prolactin, medial basal hypothalamic dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) and hypophysial DA and increases hypophysial DOPAC. Results suggest that calcitonin may decrease prolactin secretion via the tuberoinfundibular dopaminergic system.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Effects of dopaminergic drugs on cerebellar prostaglandin concentrations.

Previous data indicate that the injection of dopaminergic drugs induces changes in cerebellar 3',5'-guanosine monophosphate (cGMP) content. Accordingly, we have investigated the effects of haloperidol, sulpiride, or apomorphine on cerebellar prostaglandin (PG) concentration, a parameter related to cGMP content. Results obtained show that dopamine receptor blocking agents, such as haloperidol and sulpiride, significantly decrease cerebellar PGE2 and PGF2 alpha concentrations, while opposite changes are induced by apomorphine, a dopamine receptor agonist.

Animals↗
PubMed1983

Effects of hyper- and hypoprolactinemia on glutamate decarboxylase activity in medial basal hypothalamus of male rat.

Haloperidol, sulpiride, domperidone and apomorphine, drugs which influence dopamine (DA) receptors and in turn prolactin (PRL) secretion have been shown to induce parallel changes in medial basal hypothalamic (MBH) glutamate decarboxylase (GAD) activity and serum PRL levels. The possibility that PRL may be involved in the effects of the drugs on MBH GAD activity is suggested in view of the evidence that hypophysectomy completely prevents drug-induced MBH GAD activity changes and that hyperprolactinemia by anterior pituitary homograft results in a significant, although small, change in the enzymatic activity.

Animals↗
PubMed1983

Role of prolactin-opiate interactions in the central regulation of pain threshold.

Endogenous hyperprolactinaemia induced by anterior pituitary transplantation under the kidney capsule has been found to reduce the behavioural responsiveness to electrical footshock and to increase morphine-induced analgesia. The apparent analgesic effect of prolactin has been related to the stimulation of nigro-striatal dopaminergic transmission, as suggested by the increase in striatal dopamine turnover observed in hyperprolactinaemic rats. It seems likely that central opiate system is involved in the behavioural effects of prolactin. Thus, naloxone prevents the effects of hyperprolactinaemia on footshock responsiveness and heroin self-administration is decreased in hyperprolactinaemic rats.

Animals↗
PubMed1983

Down-regulation of prolactin secretion in men during continuous thyrotropin-releasing hormone infusion: evidence for induction of pituitary desensitization by continuous TRH administration.

TRH was administered as a 5-h constant rate iv infusion (5 micrograms/min) to seven healthy adult men. Serum samples were collected at regular intervals for measurement of PRL, TSH, and T3. Serum levels of PRL during TRH infusion increased sharply to maximum level by 40 min, and then, despite continued TRH stimulation, PRL levels declined gradually to a plateau value after 100 min. No further rise in serum PRL was observed when a bolus of 200 micrograms TRH was administered to three subjects after 240 min of infusion. Conversely, an iv bolus of sulpiride (25 mg), a dopaminergic antagonist, given to four subjects after 240 min, brought about a marked increase in serum PRL values above the plateau level. These results are consistent with the interpretation that down-regulation in PRL secretion which follows the initial peak of response most likely represents pituitary desensitization to TRH. During the infusion serum TSH increases in two phases. A first phase of secretion was observed by 40 min followed by a plateau, with a second phase of increase occurring between 80-180 min.

Adolescent↗