A short-term trial of an analogue of eel-calcitonin in headache.
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Adult↗
Biomedical subjects
U Scapagnini
Publications and source records attributed to U Scapagnini.
Cholinergic stimulation of inositol phosphate production in cultured anterior pituitary cells.
The effects of acetylcholine and of the muscarinic receptor agonist carbachol on inositol phosphate production were studied in cultured rat anterior pituitary cells. In the presence of the cholinesterase inhibitor physostigmine, acetylcholine significantly (p less than 0.05-p less than 0.01) stimulated inositol phosphate formation in a concentration-related fashion: carbachol, but not oxotremorine, produced similar effects. The increase in the amount of inositol phosphates (primarily inositol trisphosphate and inositol bisphosphate) was very rapid, an effect potently antagonized by the muscarinic receptor antagonist atropine. This agent significantly attenuated the stimulatory effect of carbachol on growth hormone (GH) release. These results indicate that the effects exerted by acetylcholine on anterior pituitary function (i.e. GH release) may be mediated, at least in part, by receptor-activated polyphosphoinositide hydrolysis. In addition, acetylcholine and carbachol's relation with other intracellular pathways and with hormone release is discussed.
Acetylcholine↗
Effect of dihydroergocryptine and dihydroergocristine on cyclic AMP accumulation and prolactin release in vitro: evidence for a dopaminomimetic action.
Dihydroergocryptine and dihydroergocristine, two C-9, 10-hydrogenated ergot alkaloids, inhibited in a concentration-dependent manner prolactin release and cyclic AMP accumulation in cultured anterior pituitary cells. The inhibitory effect of dihydroergocryptine was more potent and started at lower concentrations than that of dihydroergocristine. Haloperidol and pimozide, two dopamine receptor antagonists, completely abolished the inhibitory activity of the ergot alkaloids. The involvement of the adenylate cyclase-cyclic AMP system in the inhibitory action of the two compounds was demonstrated by the antagonism by pertussis toxin of the reduction of both prolactin release and cyclic AMP accumulation produced by dihydroergocryptine and dihydroergocristine.
Animals↗
Clinical and neuropsychological study with oxiracetam versus placebo in patients with mild to moderate dementia.
40 out-patients with a mild to moderate degree of dementia (11 less than or equal to MMSE less than 24) participated in a between-subjects (n = 20 + 20) double-blind placebo-controlled randomized trial comparing the effects of oxiracetam 800 mg bid and placebo during 90 days of treatment. At the end of therapy, statistical analysis (ANOVA) detected significant differences between groups: after oxiracetam treatment, improvements were observed on Mini Mental State Examination, Auditory Continuous Performance Test, Block Tapping Test, Word Fluency and Instrumental Activities of Daily Living. No side effects were observed. In conclusion, in the present population of patients with mild to moderate degree dementia, 1600 mg/day of oxiracetam was effective in enhancing both attentional activities and other, more complex, neuropsychological functions.
Aged↗
Effects of salmon calcitonin on plasma renin activity and systolic blood pressure in the rat.
Salmon calcitonin, centrally injected, increased plasma renin activity and blood pressure in rats. It is possible that the peptide through an action on the central serotonergic tone stimulated plasma renin activity with subsequent enhancement of blood pressure. Conversely, peripheral administration of the peptide increased plasma renin activity but did not cause changes in blood pressure. Probably, the enhancement of renin may be a physiological response to the renal activity of calcitonin; however, this activity does not seem to involve urinary prostaglandins.
Animals↗
Growth hormone releasing factor (GRF) increases free arachidonate levels in the pituitary: a role for lipoxygenase products.
GRF, a specific stimulator of GH release, increased in a concentration- and time-dependent manner pituitary [3H]-arachidonate levels in vitro. This effect was antagonized by 100 nM somatostatin. Exogenous arachidonate also stimulated GH release in vitro. Quinacrine, a phospholipase A2 inhibitor, reduced both basal and GRF-stimulated free arachidonate levels as well as GH release. The cyclooxygenase inhibitor indomethacin was ineffective, while BW755c, which also inhibits the lipoxygenase pathway, produced a further increase in the levels of the fatty acid stimulated by GRF and potently reduced GH release. These results provide additional evidence for the involvement of arachidonate metabolism in the hormone-releasing effect of GRF at the somatotroph.
4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
Dopamine neurotransmission in the nucleus accumbens may be involved in oxytocin-enhanced grooming behavior of the rat.
Intracerebroventricular (ICV) infusion of a low dose of oxytocin enhanced novelty-induced grooming in male rats. The present experiments were undertaken to investigate whether dopamine neurotransmission in the nucleus accumbens is involved in this effect. Bilateral lesions of the nucleus accumbens by microinjections of 6-hydroxydopamine (6-OHDA) totally prevented the enhancement of grooming behavior after subsequent ICV infusion of oxytocin. Furthermore, bilateral injections of the dopamine receptor antagonist, haloperidol, into the nucleus accumbens completely suppressed grooming behavior of rats infused ICV with oxytocin. These results suggest that dopamine neurotransmission in the nucleus accumbens is involved in the behavioral response enhanced by the peptide.
Animals↗
Behavioral effects of acetyl-l-carnitine in the male rat.
The behavioral activity of carnitine acetylate derivative, acetyl-l-carnitine has been studied in the male rat. Intraperitoneal (IP) injection of acetyl-l-carnitine was followed by an increase in ambulation and rearing items in the open field behavior. Both the number of conditioned avoidance response (CARs) and the percentage of learners in the acquisition of shuttle-box active avoidance behavior appeared to be increased by IP or intracerebroventricular (ICV) injection of the drug at different doses. Subchronic administration of the drug mimicked the effects found after acute injection. The number of CARs in the extinction of shuttle-box active avoidance behavior appeared to be increased after acute IP or ICV injection, and after subchronic administration of acetyl-l-carnitine. The retention of passive avoidance behavior was facilitated by IP injection of the substance. The behavioral effects of acetyl-l-carnitine may involve central mechanisms, e.g., cholinergic neurotransmission in the brain.
Acetylcarnitine↗
Intracerebroventricular injection of anti-prolactin serum suppresses excessive grooming of pituitary homografted rats.
Rats with endogenous hyperprolactinaemia, as induced by pituitary homografts under the kidney capsule, displayed increased grooming behavior as compared to that of sham-operated animals. Twelve days after surgery, intracerebroventricular injection of anti-prolactin serum (dilution 1:100, 1 microliter) suppressed the excessive grooming of homografted rats. These observations suggest that prolactin from a peripheral source may reach the central nervous system to affect brain mechanisms involved in grooming behavior.
Adrenocorticotropic Hormone↗
Effect of sulpiride on chronic abstinence syndrome in addicted patients.
A total of 410 patients (342 men and 68 women) addicted to heroin for at least 38 months, with or without previous methadone treatment experience, were treated with sulpiride before the appearance of withdrawal syndrome. The drug was injected intramuscularly in a single administration at a dosage of 600 mg. Successively, sulpiride was injected intramuscularly at a dosage of 200 mg 3 times per day from days 2-21 of hospitalization, and then at a dosage of 100 and 50 mg 3 times per day (days 22-25 and 26-29, respectively). All patients showed a suppression of withdrawal signs and symptoms within 6 days of treatment, as assessed by subjective and objective scores. The effect of sulpiride was compared with that of placebo administered to a control group of 10 heroin addicts. Because prolactin has been shown to reduce the dependence of rats to heroin and the naloxone-precipitated withdrawal syndrome in morphine-addicted animals, the effects of sulpiride on heroin addiction may be related to the hyperprolactinemic action of this drug.
Adolescent↗
Hormonal modulation of central dopaminergic transmission.
Central dopaminergic transmission is subjected to influences of various hormones of hypophyseal and extra-hypophyseal origin. Ablation of hypophysis prevents the supersensitivity of central dopamine receptors induced by chronic treatment with the dopamine receptor antagonist, haloperidol. Furthermore, hypophysectomized rats show a potentiation of hypomotility induced by low doses of the dopamine receptor agonist, apomorphine. Among the hypophyseal hormones, prolactin (PRL) seems to exert a modulatory activity on central dopamine transmission. Exogenous administration of PRL increases the density of dopamine receptors in intact and hypophysectomized rats. Furthermore, hyperprolactinaemic rats show alterations of the concentration and turnover of dopamine in various brain areas, and a potentiation of apomorphine-induced stereotypies. Endorphins related to gamma-endorphin also modulate central dopamine transmission. In particular, des-enkephalin-gamma-endorphin seems to interfere specifically with apomorphine-sensitive dopamine receptors. The administration of this endorphin is followed by a potentiation of hypomotility induced by low doses of apomorphine, and restores the sensitivity of hypophysectomized rats to these doses. The administration of estrogens also influences the sensitivity of central dopamine receptors. Depending on the doses, these hormones can potentiate or inhibit the dopaminergic neurotransmission in the brain.
Animals↗
[Certain central effects of calcitonin and parathormone].
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Calcitonin↗
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↗
The analgesic activity of calcitonin and the central serotonergic system.
The effect of peripherally administered cyproheptadine or reserpine and the administration of 5,7-dihydroxytryptamine (5,7-DHT) in the nucleus raphe dorsalis on the analgesic activity of salmon calcitonin (sCT) injected into the lateral ventricle were investigated in male rats. Cyproheptadine or reserpine, given respectively 30 min or 24 h before the peptide, completely abolished the analgesic activity at all the times studied. However, when reserpine was given before the peptide it increased the effect of sCT at 30 (P less than 0.01), 60 (P less than 0.001), 120 (P less than 0.01) and 180 (P less than 0.01) min. 5,7-DHT injected in the nucleus raphe dorsalis 15 days before the peptide led to complete abolition of the analgesic activity. If neurotoxin was injected 4 days before sCT, the effect of the peptide was significant (P less than 0.05) only at 60 min. The results obtained confirm that the analgesic activity of sCT may involve central serotonergic pathway(s), and that the midbrain raphe nuclei 5-HT content is an important focus for this activity.
5,7-Dihydroxytryptamine↗
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↗
Inhibition of restraint stress by systemic (Asu1,7) eel-calcitonin.
The effects of different doses of (Asu1,7) eel-calcitonin, iv injected, on gastric secretion were studied in conscious rats with pyloric occlusion. Moreover, we evaluated the activity of this analogue on gastric ulcer formation by restraint stress. It was found that 2.5 or 5 Ul/kg (Asu1,7) eel-calcitonin decreased gastric acid secretion and inhibited the development of stress-induced ulcers in rats. In the isolated rat stomach the peptide at the concentrations of 1 nM to 1 microM did not modify acetylcholine, histamine or 5-hydroxytriptamine-induced contractions. These results suggest that this peripheral activity of (Asu1,7) eel-calcitonin does not involve a direct interference with cholinergic, histaminergic or serotonergic pathways at gastric level.
Animals↗