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Biomedical subjects

F Drago

Publications and source records attributed to F Drago.

At least 181 records · Page 10Linked to original sources

Phospholipid liposomes potentiate the inhibitory effect of antidepressant drugs on immobility of rats in a despair test (constrained swim).

Male rats forced to swim in a cylinder assumed an immobile posture. Immobility was reduced by antidepressant drugs, such as imipramine, desimipramine, iproniazid and mianserin injected 24, 5 and again 1 h prior to behavioral testing. Subchronic (4, 7 and 10 days) treatment with sonicated preparations of bovine hypothalamic phospholipid liposomes potentiated the inhibitory effect of all antidepressant drugs in the despair test. Acute administration of phospholipid liposomes failed to influence the drug effect. Furthermore, neither subchronic nor acute administration of phospholipid liposomes per se modified the immobility in the despair test. It is possible that the action of phospholipid liposomes on the inhibitory effect of antidepressant drugs on immobility of rats in the despair test may depend on potentiation of antidepressant-induced change in the sensitivity of monoamine receptors in the brain.

Animals↗

Effects of endogenous hyperprolactinaemia on opiate-induced behavioral changes in rats.

Endogenous hyperprolactinaemia, as induced by pituitary homografts under the kidney capsule, was followed by an inhibition of heroin self-administration in rats. This effect was mimicked by intracerebroventricular (i.c.v.) injection of rat prolactin (PRL) or peripheral administration of a hyperprolactinaemia-inducing drug, domperidone. I.c.v. injection of anti-PRL serum totally abolished the effect of hyperprolactinaemia on heroin self-administration behavior and facilitated it in rats with normal plasma PRL levels. The development of tolerance to morphine was facilitated in hyperprolactinaemic animals or in rats injected i.c.v. with rat PRL. This effect was abolished in hyperprolactinaemic animals by i.c.v. injection of anti-PRL serum. Furthermore, rats with normal plasma PRL levels showed an inhibited development of tolerance to morphine after i.c.v. injection of anti-PRL serum. Morphine-induced analgesia appeared to be potentiated in hyperprolactinaemic rats tested in the hot-plate test. It is concluded that endogenous hyperprolactinaemia can affect opiate-induced behavioral changes in rats, possibly through central mechanisms involving opioid transmission.

Analgesia↗

[Evaluation of the diagnostic role of the carcinoembryonic antigen in ascitic fluid].

The diagnostic role of carcinoembryonic antigen (CEA) in ascitic fluid was evaluated in order to assess whether or not ascitic haemorrhage is related to cancer. A total of 30 patients with ascitic haemorrhage were analysed (17 had cirrhosis, 5 non-metastasised cancers and 8 metastasised cancers). CEA radioimmunoassay was performed in serum and ascitic fluid. The results showed that CEA in the ascitic fluid highlighted a clear distinction between the average values of the 3 groups examined serum assay did not. Results were respectively: cirrhotic patients 6.11, non-metastasised cancers 38 and metastasised cancers 204.12. Ascitic fluid measurement revealed considerable variation, especially between the first and third groups examined (p = .00000004). Although CEA must be regarded as an aspecific laboratory test for malignancy, these results suggest that CEA determination in the ascitic fluid may be useful for screening patients with ascitic haemorrhage.

Aged↗

Ocular instillation of naloxone increases intraocular pressure in morphine-addicted patients: a possible test for detecting misuse of morphine.

The effect of conjunctival instillation of naloxone on intraocular pressure has been examined in morphine-addicted patients as compared to non-addicted healthy volunteers. Morphine-addicted subjects showed a lower basal value of intraocular pressure as compared to the control volunteers. The instillation of naloxone caused a normalization of intraocular pressure to a level similar to that of control volunteers. This test seems to be a useful screening method for detecting morphine addiction.

Adolescent↗

Prolactin inhibits the development of stress-induced ulcers in the rat.

Hyperprolactinaemia, as induced by pituitary homografts under the kidney capsule, was accompanied by an inhibition of development of gastric ulcers following the application of cold-plus-restraint stress in male rats. This effect was mimicked by intracisternal administration of a low dose of the hormone. Peripheral injection of the dopamine receptor antagonist, domperidone, also inhibited the development of stress-induced ulcers. However, no effect was found after peripheral injection of another dopamine receptor antagonist, haloperidol. This latter drug appeared to antagonize the cytoprotective effect of prolactin (PRL) on stress-induced ulcers. Furthermore, peripheral injection of the prostaglandin synthesis inhibitor, indomethacin, increased the incidence of gastric ulcers in hyperprolactinaemic rats subjected to cold -plus-restraint stress. These data suggest that the cytoprotective effect of PRL on development of gastric ulcers in stressed animals may involve both central (i.e. dopamine transmission) and peripheral (i.e. prostaglandin synthesis) mechanisms.

Animals↗

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↗

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↗

Intracameral administration of alpha-MSH increases intraocular pressure in rabbits.

A growing body of evidence suggests that neural peptides may induce important modulations on vegative and motor functions of the eye. The present study was designed to evaluate the effect of intracameral (I.C.) administration of alpha-melanocyte-stimulating hormone (alpha-MSH) and several other ocular peptides on intraocular pressure (IOP) in rabbits. alpha-MSH (5 micrograms) produced a significant and prolonged unilateral increase of IOP. This effect of I.C. alpha-MSH was dose-dependent (ED50 = 2.5 micrograms). Structure-activity studies revealed that equimolar doses of beta-MSH and gamma-MSH, unlike alpha-MSH, were totally ineffective. In addition, the structurally unrelated peptides beta-endorphin, thyrotropin-releasing hormone (TRH) and gonadotropin-releasing hormone (Gn-RH) did not affect IOP, when tested in a dose equimolar to 5 micrograms of alpha-MSH. These results confirm and extend previous observations, suggesting that alpha-MSH may be an important factor involved in regulation of IOP.

Animals↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗

Prolactin and sexual behavior: a review.

Despite the large body of evidence showing that prolactin (PRL) can suppress sexual behavior in humans and rodents, it is still unclear how this hormone affects sexual capacity of male subjects. Few studies have been performed on the effects of PRL on female sexual behavior. Short-term hyperprolactinaemia seems to facilitate some elements of sexual behavior in male rats. Furthermore, contrasting finding exist on the effects of drug-induced hyperprolactinaemia on sexual capacity of male animals. The possible mechanisms of action (on peripheral organs, endocrine, central) or PRL on male behavior are discussed in details.

Amenorrhea↗