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P Falaschi

Publications and source records attributed to P Falaschi.

At least 37 records · Page 2Linked to original sources
PubMed1986

Role of arachidonate metabolism on the in vitro release of luteinizing hormone and prolactin from the anterior pituitary gland: possible involvement of lipoxygenase pathway.

The aim of the present study was to evaluate whether arachidonic acid metabolism may play a role on luteinizing hormone (LH) and prolactin (PRL) release directly at the pituitary level. To this purpose, exogenous arachidonic acid, alone or in presence of inhibitors of cyclooxygenase (indomethacin:IND) and lipoxygenase pathways (nordihydroguaiaretic acid:NDGA), was added to perfused rat anterior pituitary cells. PGE, PGF alpha, LH and PRL levels present in the eluate were assayed with specific RIA methods. Both PGE and PGF alpha show a dose-related response after the addition of increasing doses of arachidonic acid. The addition of 0.05 mM arachidonic acid induces an increase of LH and PRL. The addition of IND to the perfusion medium highly potentiates the stimulatory effects induced by arachidonic acid on LH and PRL release. On the contrary, the addition to the medium of either NDGA or IND plus NDGA completely reverses the stimulatory action induced by arachidonic acid alone. The present results suggest that: adenohypophyseal cells are able to metabolize exogenous arachidonic acid; arachidonic acid induces an elevation in LH and PRL levels; lipoxygenase pathway metabolite(s) are likely involved in these activities, and the site of action of arachidonic acid is at the pituitary level.

Animals↗
PubMed1986

Inhibitory effect of bromocriptine treatment on luteinizing hormone secretion in polycystic ovary syndrome.

In order to investigate a possible common role of central dopaminergic mechanisms in the release of PRL and LH in patients with the polycystic ovary syndrome (PCO), plasma LH pulsatile profiles and the response to GnRH were studied in a group of 12 PCO patients before and after 3 months of treatment with bromocriptine, 2.5 mg twice daily. They were divided into two groups of six patients according to the occurrence or not of hyperprolactinemia (plasma PRL, 30.3 +/- 2.7 (SE) ng/ml vs. 9.5 +/- 0.8 (SE) ng/ml). Integrated LH secretion significantly decreased in hyperprolactinemic [2537 +/- 371 (SE) vs. 907 +/- 102 mIU/ml X min] as well as in normoprolactinemic (2847 +/- 460 vs. 901 +/- 152 mIU/ml X min) patients, but there was no difference in the response of the two groups. The LH increment after a bolus injection of 100 micrograms GnRH was reduced (P less than 0.01) to the same extent in both groups. These results indicate a dopaminergic component in the control of LH release in PCO patients, independent of the mechanism governing PRL secretion. Since bromocriptine reduced LH secretion, it may be useful for the management of this condition.

Bromocriptine↗
PubMed1986

Neuroendocrine effects of setoperone: a new neuroleptic drug.

Setoperone (R 52245), a serotonin S2 and dopamine D2 receptor blocker, was tested on eight healthy male volunteers, receiving 5 or 40 mg orally, in order to assess the modifications of plasma prolactin levels, as an index of receptor blocking activity. Both doses significantly increased plasma levels, confirming the dopamine blocking activity. In vitro and in vivo studies have shown serotonin S2 receptor blockade and lysergic acid diethylamide antagonist activity. Setoperone is proposed as a possible new neuroleptic drug.

Adolescent↗
PubMed1985

Common migraine versus daily chronic headache: a study of the relationship between depression and anxiety scores, and dexamethasone suppression test.

To achieve a better understanding of CH and DCH, we used a multidisciplinary approach evaluating both the depression and anxiety scores and the ability of DEX to decrease plasma cortisol levels in patients with these two forms of headache. The Hamilton rating scale for depression, the Zung test for depression and Stai X2 for anxiety showed scores within the control range in both groups of patients without any statistically significant difference between the groups. The DEX test showed significant cortisol suppression in both groups of patients either at 8 a.m. or at 4 p.m. (after DEX administration, 1 mg orally at 11 p.m. the night before). The results obtained indicate that in CM and in DCH, normal depression and anxiety scores exist in the present of the apparent integrity of the hypothalamic-pituitary-adrenal axis.

Adult↗
PubMed1984

Dermorphin stimulates prolactin secretion in the rat.

The effect of dermorphin, a new opioid peptide originally isolated from amphibian skin, on the release of prolactin (Prl) was studied in vivo and in vitro. In vivo experiments: subcutaneous administrations of different doses of dermorphin ranging from 0.1 to 5 mg/kg body weight to normal male rats induce a statistically significant, dose-related increase in serum Prl levels. Pretreatment with the specific opioid antagonist, naloxone (2 mg/kg i.p.) completely prevents the rise in serum Prl, induced by 2 mg/kg of dermorphin. In normal male rats, the intraventricular injection of 0.25 micrograms/kg of dermorphin is not able to induce any significant changes in serum Prl levels 10 min after injection. Serum Prl levels show a significant enhancement 30 min after the administration of this dose of dermorphin, and return to control values at 60 min. On the contrary, 1 microgram/kg of dermorphin significantly elevates Prl concentrations 10 min after injection, leaving serum Prl levels unchanged 30 and 60 min after the administration. Naloxone (25 and 100 micrograms/kg) alone does not substantially modify serum Prl concentrations at any time interval considered. Treatment with either dose of naloxone performed together with either 0.25 or 1 microgram/kg of dermorphin completely counteracts the stimulatory effect of the peptide at all time intervals in which dermorphin was active when given alone. In orchidectomized (3 weeks) rats, the intraventricular administration of dermorphin at the dose of 0.25 micrograms/kg appears effective in enhancing Prl levels only 30 min after treatment. No statistically significant modifications are observed at 10 and 60 min with this dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Sauvagine induces release of adrenocorticotropin, beta-endorphin and corticosterone in rats.

The effect of sauvagine, a frog skin peptide, on ACTH, beta-endorphin and corticosterone secretion, was studied in rats. A subcutaneous injection of 5 micrograms kg-1 of sauvagine in rats produced a prompt increase in immunoreactive plasma concentration of ACTH and beta-endorphin, which reached a peak value 15-30 min after the peptide injection. The stimulatory action of sauvagine on ACTH and beta-endorphin secretion was dose related. Intensity and duration of corticosterone secretion, produced by sauvagine mediated ACTH release, was dose-dependent, the threshold dose being 0,5 microgram kg-1 s.c. Pretreatment of rats with dexamethasone-21-phosphate, prevented the corticosterone releasing effect of sauvagine. Sauvagine perfusion (2,1 nM/h) of biogel columns containing isolated and dispersed anterior pituitary cells induced a sharp increase of ACTH levels in the eluate. Considering the high corticotropin releasing potency of sauvagine and its chemical similarity to ovine CRF, it is interesting to hypothesize whether this peptide may represent, in lower vertebrates, an ancestral form of the mammalian hypothalamic releasing factor.

Adrenocorticotropic Hormone↗
PubMed1983

Chrononeuroendocrine perspectives of ACTH and related peptides.

The mechanism of the circadian hormonal secretions is still obscure. The cyclic activity of the hypothalamus-ACTH-adrenal (H-A-A) axis is perhaps the most studied. ACTH derives with other peptides from a common precursor, proopiomelanocortin. ACTH secretion is under inhibitory and stimulatory influences. The inhibitory influence is mediated by the negative feed-back of adrenal corticosteroids and by the short loop feed-back of ACTH on its own secretion. The stimulatory influence is exerted by the hypothalamic corticotropin releasing factor (CRF), recently isolated in the ovine hypothalamus. CRF is regulated by various neurotransmitttttorial activities. Serotonin and acetylcholine play a stimulatory role, while dopamine and norepinephrine, in particular, seem to exert an inhibitory tonic control. The increased ACTH secretion in stress-response seems to be mediated by a reduction of this tone. However, the neurotransmitorial modifications involved in the rhythmic secretion of the H-A-A axis are still obscure. So chrononeuroendocrine study of the H-A-A axis in various psychoneuroendocrine diseases is of great interest in clearing up the neurotransmitorial mechanisms of this rhythm. Primary depression represents an interesting model being characterized by monoaminergic neurotransmitorial alterations. We have observed in this pathology an increase of the H-A-A axis activity and an alteration of the circadian cortisol profile characterized by an increase both in numeric and quantitative secretory bursts.

Adrenocorticotropic Hormone↗
PubMed1983

Effect of long term administration of ovine prolactin on hypothalamic-pituitary testicular axis in rat.

The effect of hyperprolactinaemia on testicular morphology and on hypothalamic-pituitary-testicular axis was studied in adult male Wistar rats. Animals received ovine prolactin (oPRL) 200 micrograms twice daily s.c.) for 24 and 36 days and were killed by exanguination. Blood was collected for hormonal determinations and sex accessory glands were removed for histological studies. Circulating testosterone (T) and luteinizing hormone (LH) levels showed a significant reduction after 36 days of treatment whereas plasma follicle-stimulating hormone (FSH) levels were unchanged in all animals. No macroscopic or light microscopic histological modifications were observed in the testes. The present results, while excluding a direct effect of hyperprolactinaemia on seminiferous tubules, suggest that LH suppression is the consequence of a central effect of the ovine PRL long-term administration. The increased DA turnover in the hypothalamus suggested as inhibitory on GnRH neurons could account for this effect. The reduction of T levels seems to be mediated by the LH suppression, even though a direct effect of oPRL on Leydig cell receptors could be hypothesized.

Animals↗
PubMed1983

Reproductive parameters in prolactinaemic men.

The sexual behavior, hypothalamic-pituitary-testicular axis and seminal fluid parameters in three different models of hyperprolactinaemia were studied: patients with prolactin secreting pituitary adenomas, normal volunteers before and during metoclopramide, and psychotic patients on chronic neuroleptic therapy. Hyperprolactinaemia is always accompanied by a reduced seminal volume but there is no clearcut evidence that it can induce spermatogenesis modifications. Impotence is constantly present in the hyperprolactinaemic syndromes. The mildly impaired androgen production by the Leydig cells during hyperprolactinaemia does not seem to explain the impotence. Hypotheses on the pathogenesis of this symptom are suggested.

Adenoma↗
PubMed1982

Phospholipid liposomes and prolactin secretion: effects on spontaneous and drug-induced hyperprolactinaemia.

Bovine brain phospholipid liposomes (BC-PL) reduce plasma prolactin (PRL) levels in humans after acute administration and counteract the metoclopramide- and sulpiride-induced hyperprolactinaemia. However, BC-PL, like nomifensine, a dopamine (DA) reuptake inhibitor and therefore an indirect dopaminergic compound, does not influence TRH-induced hyperprolactinaemia. Moreover, BC-PL and nomifensine reduce plasma PRL levels in hyperprolactinaemic PCO syndromes but not in PRL secreting pituitary adenomas. The results obtained indicate that BC-PL antagonizes the DA blockade-induced hyperprolactinaemia and that the main site of action of BC-PL seems to be at the hypothalamic level; however a concomitant pituitary effect cannot be ruled out.

Adult↗
PubMed1982

Prolactin response to acute administration of different L-dopa plus decarboxylase inhibitors in Parkinson's disease.

Plasma prolactin (PRL) levels modifications after acute administration of L-dopa, L-dopa plus carbidopa and L-dopa plus benserazide were studied in parkinsonian patients. PRL increase after benserazide was compared with PRL response after carbidopa at the same dosage in untreated parkinsonian patients. A further study of the hyperprolactinemic effect of benserazide was performed in vitro on isolated and dispersed rat pituitary cells. The data gathered indicate that benserazide-induced hyperprolactinemia in parkinsonian patients could be due to a direct effect of the drug at the hypothalamic level and consequently to an inhibition of dopamine decarboxylation in the tuberoinfundibular dopaminergic system. It is not possible to exclude, however, that benserazide could exert its biological activity through the production of active metabolites in vivo.

Aged↗
PubMed1982

Potent in vivo and in vitro prolactin inhibiting activity of sauvagine, a frog skin peptide.

The effect of sauvagine (SAU), a frog skin peptide, on prolactin (PRL) levels was studied in vivo and in vitro. Subcutaneous administration of SAU (20 micrograms/kg) reduced plasma PRL levels in normal adult male rats and suppressed the suckling-induced rise of PRL in lactating rats even at doses of 1 and 5 micrograms/kg. Perfusion of isolated and dispersed rat pituitary cells in vitro with increasing doses of SAU (from 5 x 10(-10) to 1.7 x 10(-8)M) induced a significant dose-related decrease of PRL secretion in the eluate. These results indicate that SAU is a potent PRL inhibiting factor and that its action is exerted at the pituitary level. If SAU or a SAU-related peptide is present in the mammalian brain, it can be tentatively hypothesized that this peptide plays an important role in the control of PRL secretion.

Amphibian Proteins↗
PubMed1981

Prolactin response as an index of dopaminergic receptor function in Parkinson's disease. Correlation with clinical findings and therapeutic response.

Circadian rhythms of prolactin have been evaluated in thirteen untreated parkinsonian patients before and after 15 days of treatment with L-Dopa + carbidopa. The 24th secretory pattern was not significatively different from that observed in controls. The L-Dopa + carbidopa therapy does not change the basal circadian prolactin (PRL) rhythm. These results suggest that the tubero-infundibular dopaminergic system (TIDA) and the PRL secretion are conserved in untreated parkinsonian patients (PP). During chronic L-Dopa + carbidopa therapy, the basal PRL levels, evaluated in 21 PP, showed a correlation with the severity of clinical features. The effects of single doses of apomorphine, bromocriptine, lisuride and haloperidol, were studied on serum levels of PRL in 21 PP divided in two groups of "responders" and "non-responders". Haloperidol induced an enhancement of serum PRL; the dopaminergic drugs, apomorphine, bromocriptine and lisuride inhibited basal PRL secretion. It seems that the TIDA system, in Parkinson disease is not significatively altered, even though presenting a remarkable slower response in "non-responders" to L-Dopa therapy. We also evaluated the effect of L-Dopa, L-Dopa + carbidopa, bromocriptine, lisuride, nomifensine and deprenyl on growth hormone secretion in six PP. The endocrine effects of dopaminergic drugs show a mild rise in comparison with controls suggesting an important alteration in the dopamine (DA) control of growth hormone (GH).

Adult↗
PubMed1981

The brain-gut-skin triangle: new peptides.

New data on tachykinins and bombesins are displayed and the present situation of research on the novel amphibian skin peptides sauvagine and dermorphin is illustrated. The potent stimulant effect of sauvagine on ACTH and beta-endorphin release has been confirmed both in vivo and on columns of isolated and dispersed rat pituitary cells, and similarly the potent inhibitory effect on PRL and GH release, both in the rat and man. Particular emphasis is laid on the occurrence of sauvagine-like immunoreactivity in fish urophysis and in amphibian nervous structures, including the retina. It is suggested that the long-searched corticotropin releasing factor and PRL release-inhibiting factor may be a sauvagine-like peptide. Dermorphin, in its turn, has been found to cause, by intracerebroventricular injection, not only analgesia and catalepsy, but also conspicuous EEG and behavioral changes in the rabbit and chick, as well as a sharp reduction in gastric emptying time and gastric acid output in the rat, together with marked stimulation of PRL release.

Adrenocorticotropic Hormone↗