Search PubMed⌕ Search

Biomedical subjects

L Steardo

Publications and source records attributed to L Steardo.

At least 73 records · Page 4Linked to original sources
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

Failure of the GABAergic drug, sodium valproate, to reduce basal plasma prolactin secretion in chronic schizophrenia.

The psychoneuroendocrinology of schizophrenia derives from the presumption that neurotransmitter or receptor abnormalities in the limbic regions might extend to or influence the hypothalamus, which plays a role in the regulation of prolactin (PRL) secretion from the anterior pituitary gland. Since a GABA disturbance has been recently proposed in the pathogenesis of certain schizophrenic symptoms, and since a tuberoinfundibular-GABA (TI-GABA) system has been shown to modulate PRL secretion in humans, we tested the activity of this system both in controls and in chronic schizophrenic women. For this purpose the GABAergic drug sodium valproate (800 mg) was administered orally to 20 healthy women and 18 chronic schizophrenic women. Plasma PRL levels were measured before and after the drug administration. Sodium valproate decreased PRL concentrations only in the healthy women. Although the hypothesis of a GABA disturbance in schizophrenia at present is only speculative, these results might suggest a defect of the TI-GABA system in chronic schizophrenia.

Adult↗
PubMed1985

CCK26-33 degrading activity in brain and nonneural tissue: a metalloendopeptidase.

Cholecystokinin octapeptide (CCK26-33) is metabolized by neural membranes with an initial cleavage to CCK29-33 and subsequent breakdown to CCK31-33 and CCK32-33; this pattern of proteolysis occurs on incubation with either P2 or purified lysed synaptosomal membranes. To determine whether the pattern of CCK26-33 proteolysis is unique to the brain and whether regional brain differences in its pathway or rate exist, we analyzed the proteolysis of CCK by synaptic membranes of various brain areas and cellular membranes of peripheral tissue. The pattern of degradation in brain did not differ among the regions studied. The overall proteolysis rate, as measured by the formation of tryptophan, was higher in the striatum than in the cortex, although CCK29-33 was formed at the same rate in both areas. In nonneural tissue, the rate of degradation was highest in liver membranes and lowest in pancreatic acinar cell preparations. Thus, it appears that degradative peptidases are not necessarily colocalized with CCK receptors. The pattern of product formation is the same in peripheral compared with CNS membranes; thus, the degradative pathway does not appear to be unique to brain tissue. The enzyme present in synaptic membranes that is responsible for CCK29-33 formation requires a metal ion and sulfydryl groups for the catalysis and thus is a metalloendopeptidase. Furthermore, its activity is inhibited by Ac-Gly-Phe-Nle-al, a peptide aldehyde whose sequence bears some homology to the amino acid sequence in the region of CCK26-33 that is cleaved by this enzyme.

Animals↗
PubMed1985

[Effects of septal lesions on the response of vasopressin to angiotensin II].

Electrolytic lesion of the medio-ventral septal (MVS) area produces a sustained increase in daily water intake and urine output. This polyuria and hyperdipsia are associated with decreased levels of circulating radioimmunoassayable ADH. In addition, the usual ADH release to angiotensin II observed in normal controls and sham-lesioned rats was markedly blunted in MVS-lesioned animals.

Angiotensin II↗
PubMed1984

Vasopressin release to central and peripheral angiotensin II in rats with lesions of the subfornical organ.

Angiotensin II (Ang II), peripherally or centrally administered, increases plasma vasopressin concentrations in the rat. Peripherally injected Ang II was unable to effect the release of vasopressin in rats with subfornical organ (SFO) lesions. In contrast, a normal increase of plasma vasopressin levels was induced by centrally injected Ang II. These results suggest that peripherally administered Ang II elicits antidiuretic hormone (ADH) release by stimulating receptors in the SFO, whereas centrally administered Ang II acts at receptors outside the SFO.

Angiotensin II↗
PubMed1984

Cholecystokinin-octapeptide fragments: binding to brain cholecystokinin receptors.

Structural determinants of cholecystokinin octapeptide (CCK-8) binding to central nervous system receptors have been studied to assess the relative importance of the amino and the carboxyl end of the active peptide sequence, CCK-(26-33). The relative ability to inhibit equilibrium binding of [125I]CCK-33 to guinea pig cortical membranes was determined for a series of amino and carboxyl terminal fragments of CCK-8. While N-acetyl CCK-(26-29), N-acetyl CCK-(26-30) amide and N-acetyl CCK-(26-31) amide were inactive, the N-acetyl CCK-(26-32) amide fragment displayed binding to central receptors. Of the carboxyl terminal peptide fragments, both CCK-(29-33) and CCK-(30-33) bound less potently than CCK-8; CCK-(31-33) interacted more weakly than the tetra- and pentapeptide, but with a higher affinity to brain receptors than to peripheral receptors. The heptapeptide, CCK-(26-32) amide, and the tripeptide, CCK-(31-33), are known to antagonize CCK action at peripheral receptors. The heptapeptide bound to central receptors 25 times more potently than a known peripheral antagonist, dibutyryl cyclic GMP. Thus these peptides may act centrally to oppose CCK-8 mediated functions.

Amino Acid Sequence↗
PubMed1984

Efficacy of baclofen in trigeminal neuralgia and some other painful conditions. A clinical trial.

Baclofen (beta-4-chlorophenyl-gamma-aminobutyric acid) shows analgesic properties in rats and resembles carbamazepine and phenytoin in its effects on the spinal trigeminal nucleus of cats. We have, therefore, conducted a clinical trial in 25 subjects, 16 suffering from trigeminal neuralgia, and 9 patients were affected by different painful conditions such as postherpetic neuralgia, tabes dorsalis, postarachnoid radiculitis. 5 of the former groups were refractory to or unable to tolerate carbamazepine. Baclofen has significantly exhibited analgesic efficacy: all groups, as a whole, were improved by 68.61%. These results substantiate that baclofen is useful in the treatment of trigeminal neuralgia and other painful conditions.

Adult↗
PubMed1983

Inhibition of septal hyperreactivity by testosterone and its reversion by an estrogen antagonist in weanling female rats.

Neonatal administration of testosterone inhibits emotional hyperreactivity to capture and tactile stimulation in female rats following septal lesions at 25 days of age. Testosterone, an aromatizable androgen, after metabolization to estrogen interacts with estrogen receptors in neonatal rat brain. In order to investigate whether the testosterone inhibited septal hyperreactivity via estrogen receptors rats were tested after pretreatment with the estrogen receptor antagonist tamoxifen. Weanling female rats pretreated with tamoxifen showed emotional hyperreactivity, while androgenized females showed no change. In addition, estradiol benzoate, neonatally administered, was able to inhibit emotional reactivity displayed after septal lesions. These results suggest that the action of testosterone on septal hyperreactivity might be mediated by estrogen receptors.

Animals↗
PubMed1983

Dexamethasone suppression test in major and minor depressive disorders.

The validity of the dexamethasone ofe suppression test was evaluated for the differential diagnosis of major and minor depressive disorders. Thirty-eight out-patients (14 major depressed, 14 minor depressed and 10 normal controls) were studied. The Research Diagnostic Criteria of Spitzer et al. (1978) were used to classify these patients. Six out of the 14 major depressed patients had an abnormally high plasma cortisol at 4 p.m. and at 11.00 p.m. after midnight 2 mg-dexamethasone. None of the 14 minor depressed patients and none of the 10 controls had an abnormal response to dexamethasone. Based on these results, the dexamethasone suppression test has a sensitivity of 43%, a specificity of 100% and a high predictive value.

Circadian Rhythm↗
PubMed1983

Evidence for a dose-dependent effect in the sex-specific plasma prolactin response to naloxone in humans.

In attempt to ascertain if the sex specific plasma PRL response to naloxone, that we suggested in previous studies, was a dose dependent effect, 26 healthy volunteers were studied. They received naloxone 2 mg and 4.8 mg or a volume matched of saline i.v. as a bolus. Blood samples were collected and plasma PRL was measured by double antibody RIA. Naloxone, at dose of 2 mg, was able to decrease significantly plasma PRL levels in normally menstruating women (p less than 0.05 at 60 min.; p less than 0.01 at 120 min.), but not in post-menopausal ones and in men. In addition, the dose of 4.8 mg of the drug did not change plasma PRL in any group. These results suggest a dose-dependent effect in the sex specific PRL response to naloxone in humans.

Adult↗
PubMed1983

Muscimol inhibits ADH release induced by hypertonic sodium chloride in rats.

The effect of the GABA-agonist muscimol on ADH release induced in rats by administration of hypertonic sodium chloride solutions was studied by means of intracerebroventricular and intraperitoneal injections of the drug. Injected by the intracerebroventricular route, muscimol produced a significant reduction of plasma ADH concentration not only in animals treated with hypertonic sodium chloride, but also in unstimulated animals. Following intraperitoneal administration larger doses were required to produce such an effect, thus suggesting a central site of action for the effect of muscimol on ADH release. Bicuculline, given intraperitoneally before muscimol injection, completely blocked ADH inhibition induced by muscimol, thus suggesting a specific involvement of GABAergic receptors. These findings indicate that GABAergic mechanisms may be involved in the regulation of body fluids in the rat by affecting ADH release.

Animals↗
PubMed1983

Timed-release dihydroergotamine in the prophylaxis of mixed headache. A study versus amitriptyline.

A pharmacological trial has been carried out on 41 out-patients suffering from mixed headache. The prophylactic effect of a timed-release dihydroergotamine formulation was tested versus amitriptyline. Patients reported daily, on appropriate cards, the hours of headache and the degree of pain during the month before therapy and on the following two months of treatment. Whereas amitriptyline was found to be more effective than dihydroergotamine in reducing headache intensity, timed-release dihydroergotamine was found significantly more effective than amitriptyline in reducing attacks of "migraine" type.

Adolescent↗
PubMed1982

Headache patients: different responses induced by naloxone during work-test.

The responses to work-test in ischemia (tourniquet technique), before and after I.V. injection of naloxone (2 mg) or saline, were investigated in healthy volunteers and patients suffering from various types of headache. The patients were examined during both painful and painless periods. We found that only the subjects suffering from migraine showed a significantly shortened pain tolerance at work-test in ischemia, after injection of naloxone, and only during painful periods. Psychogenic headache patients and migraine patients in painless periods showed responses during work-test similar to those in healthy volunteers, even after injection of naloxone. We believe that hyperalgesic effect of naloxone is due to involvement of beta-endorphin systems only during organic pain.

Adult↗