Effect of agonists and antagonists of cholinergic neurotransmission on growth hormone release in the dog

1983 ◽  
Vol 103 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Felipe F. Casanueva ◽  
Roberto Betti ◽  
Silvano G. Cella ◽  
Eugenio E. Müller ◽  
Paolo Mantegazza
Keyword(s):  
Growth Hormone ◽  
Muscarinic Receptors ◽  
Nicotinic Receptors ◽  
Anticholinergic Drug ◽  
Complete Suppression ◽  
Butyl Bromide ◽  
Clear Cut ◽  
The Central Nervous System ◽  
Pre Treatment ◽  
Releasing Effect

Abstract. In unanaesthetized dogs iv administration of the cholinesterase inhibitor eserine (0.5 mg) or the cholinergic muscarinic receptor agonist oxotremorine (0.25 mg) induced a clear-cut rise in plasma canine growth hormone (cGH) levels. Complete suppression of the GH-releasing effect of eserine and oxotremorine was induced by blockade of cholinergic muscarinic receptors by atropine (80 or 20 μg/kg, 30 min before) but not by scopolamine-N-butyl bromide (0.8 mg/dog, 30 min before), an anticholinergic drug which does not cross the blood brain barrier (BBB). In contrast, activation of cholinergic nicotinic receptors by nicotine (6 mg) failed to alter resting cGH concentrations, and pre-treatment with the nicotinic receptor blocker mecamylamine (5 mg, 30 min before) did not counteract the GH-releasing effect of eserine. Other cholinomimetic drugs, e.g. pilocarpine, 4-aminopyridine, carbachol and bethanechol failed to induce a rise in plasma cGH concentrations. These data indicate that: 1) cholinergic muscarinic but not nicotinic receptors located in the central nervous system (CNS) inside the BBB play a facilitatory role in tonic cGH release; 2) pharmacologically distinct muscarinic receptors may exist in the CNS.

scholarly journals Mechanism and Clinical Importance of Respiratory Failure Induced by Anticholinesterases

2017 ◽  
Vol 18 (4) ◽  
pp. 349-355
Author(s):  
Anita Ivosevic ◽  
Natasa Miletic ◽  
Maja Vulovic ◽  
Zoran Vujkovic ◽  
Snjezana Novakovic Bursac ◽  
...  
Keyword(s):  
Respiratory Failure ◽  
Respiratory Depression ◽  
Muscarinic Receptors ◽  
Nicotinic Receptors ◽  
Neuromuscular Synapse ◽  
Clinical Importance ◽  
Respiratory Muscles ◽  
Respiratory Drive ◽  
The Central Nervous System ◽  
Central Nicotinic Receptors

AbstractRespiratory failure is the predominant cause of death in humans and animals poisoned with anticholinesterases. Organophosphorus and carbamate anticholinesterases inhibit acetylcholinesterase irreversibly and reversibly, respectively. Some of them contain a quaternary atom that makes them lipophobic, limiting their action at the periphery, i.e. outside the central nervous system. They impair respiratory function primarily by inducing a desensitization block of nicotinic receptors in the neuromuscular synapse. Lipophilic anticholinesterases inhibit the acetylcholinesterase both in the brain and in other tissues, including respiratory muscles. Their doses needed for cessation of central respiratory drive are significantly less than doses needed for paralysis of the neuromuscular transmission. Antagonist of muscarinic receptors atropine blocks both the central and peripheral muscarinic receptors and effectively antagonizes the central respiratory depression produced by anticholinesterases. To manage the peripheral nicotinic receptor hyperstimulation phenomena, oximes as acetylcholinesterase reactivators are used. Addition of diazepam is useful for treatment of seizures, since they are cholinergic only in their initial phase and can contribute to the occurrence of central respiratory depression. Possible involvement of central nicotinic receptors as well as the other neurotransmitter systems – glutamatergic, opioidergic – necessitates further research of additional antidotes.

Growth hormone and prolactin secretion in liver cirrhosis: evidence for dopaminergic dysfunction

1981 ◽  
Vol 97 (4) ◽  
pp. 441-447 ◽  
Author(s):  
Mauro Borzio ◽  
Roberto Caldara ◽  
Carlo Ferrari ◽  
Cristiano Barbieri ◽  
Franco Borzio ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Liver Cirrhosis ◽  
Liver Disease ◽  
Clinical Improvement ◽  
Prolactin Secretion ◽  
Serum Growth Hormone ◽  
Dopaminergic Dysfunction ◽  
The Central Nervous System ◽  
Pre Treatment ◽  
Serum Gh

Abstract. Increased serum growth hormone (GH) and prolactin (Prl) levels and abnormal responses to some stimuli have been reported in patients with chronic liver disease. Serum GH and Prl concentrations were measured in 11 cirrhotic patients and in sex and age matched healthy controls in basal conditions and after administration of L-dopa alone (500 mg), and L-dopa (100 mg) with carbidopa (35 mg) following pre-treatment with carbidopa (50 mg every 6 h for one day), a regimen which results in selective activation of brain dopaminergic pathways. Basal GH and Prl levels were significantly higher in cirrhotics than in controls; serum GH did not increase significantly and serum Prl was subnormally inhibited in patients after both tests. A patient with clearcut hyperprolactinaemia unresponsive to dopaminergic stimulation showed normal basal Prl levels and suppression by L-dopa following clinical improvement, while her elevated GH levels remained unchanged and did not increase after L-dopa. These data confirm the existence of abnormalities in the regulation of GH and Prl release in liver cirrhosis and suggest that dopaminergic dysfunction may be responsible. The subnormal Prl suppression induced by L-dopa, which stimulates both brain and peripheral dopaminergic receptors, suggests that dopaminergic dysfunction is not confined to the central nervous system in liver cirrhosis. It appears that serum Prl concentration may be of value in monitoring decompensated liver disease and that abnormalities of Prl secretion are reversible with clinical improvement.

Activation of the cholinergic system and growth hormone release in the dog: functional interactions with other neurotransmitters

1985 ◽  
Vol 108 (1) ◽  
pp. 36-43 ◽  
Author(s):  
R. Betti ◽  
F. F. Casanueva ◽  
S. G. Cella ◽  
E. E. Müller
Keyword(s):  
Growth Hormone ◽  
Receptor Antagonist ◽  
Opiate Receptors ◽  
Gh Secretion ◽  
Clear Cut ◽  
Adrenergic Antagonist ◽  
Releasing Effect ◽  
Long Acting ◽  
Do So

Abstract. In unanaesthetized dogs iv administration of the cholinesterase inhibitor eserine (0.5 mg) induced a clear-cut rise in plasma canine growth hormone (cGH) levels. Diphenhydramine and meclastine, two antagonists of histamine (H) H1 receptors completely suppressed the GH-releasing effect of eserine, while cimetidine, an H2 receptor antagonist, only blunted and delayed it. Two long-lasting serotonin (5-HT) receptor antagonists, metergoline and pizotifen, partially or completely suppressed, respectively, GH release evoked by eserine, whereas fenfluramine, a releaser of neuronal stores of 5-HT and hence a functional activator of 5-HT neurotransmission, was ineffective in this context. Pimozide, a long-acting dopamine receptor antagonist, abolished the effect of eserine, whereas domperidone, which has the same pharmacological properties but does not cross the blood brain barrier, failed to do so. Finally, phentolamine, an antagonist of α-adrenoceptors, and propranolol, a β-adrenergic antagonist, were completely ineffective in preventing the rise in plasma cGH levels induced by eserine, as was naloxone, an antagonist of opiate receptors. All these data demonstrate that, although cholinergic mechanisms are involved in the mechanism(s) underlying cGH release, the final common pathway for GH secretion is not cholinergic. Preservation of dopaminergic and H1 neurotransmission, probably within the blood barrier, is needed to allow the neuroendocrine transduction of cholinergic inputs, whereas the role of 5-HT neurotransmission remains uncertain.

Increased thyrotrophin and prolactin secretion induced by domperidone in hypothyroid subjects

1981 ◽  
Vol 97 (1) ◽  
pp. 48-53 ◽  
Author(s):  
F. Massara ◽  
F. Camanni ◽  
A. Amoroso ◽  
G. M. Molinatti ◽  
E. E. Müller
Keyword(s):  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Primary Hypothyroidism ◽  
Post Injection ◽  
Clear Cut ◽  
Tsh Secretion ◽  
The Central Nervous System ◽  
Releasing Effect ◽  
Peripheral Site ◽  
Plasma Prl

Abstract. The thyrotrophin (TSH) and prolactin (Prl) releasing effects of domperidone, a recently developed antidopaminergic drug which does not cross the blood-brain barrier, were investigated in 8 women affected by primary hypothyroidism, and were compared to those elicited by another antidopaminergic drug, sulpiride. Domperidone (4 mg iv) induced a clear-cut and sustained rise in both plasma TSH and Prl, with peak levels occurring 15 and 30 min post-injection, respectively. The increments in plasma Prl after domperidone were significantly higher than those in plasma TSH. The TSH and Prl responses induced by domperidone were almost superimposable to those provoked in the same subjects by sulpiride (100 mg im). In view of the inability of domperidone to penetrate into the central nervous system (CNS), these findings imply a 'peripheral' site(s) of action (i.e., anterior pituitary and/or median eminence) for the effect of antidopaminergic drugs on TSH secretion, and, re-iterate the notion that the same 'peripheral' sites are involved in the Prl-releasing effect of these compounds.

scholarly journals Scopolamine fatal outcome in an inmate after buscopan® smoking

2021 ◽  
Author(s):  
Sabina Strano-Rossi ◽  
Serena Mestria ◽  
Giorgio Bolino ◽  
Matteo Polacco ◽  
Simone Grassi ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Drug Abuse ◽  
Muscarinic Receptors ◽  
Histopathological Examination ◽  
Fatal Outcome ◽  
Post Mortem ◽  
Butyl Bromide ◽  
Cannabis Abuse ◽  
Toxic Concentration ◽  
History Of

AbstractScopolamine is an alkaloid which acts as competitive antagonists to acetylcholine at central and peripheral muscarinic receptors. We report the case of a 41-year-old male convict with a 27-year history of cannabis abuse who suddenly died in the bed of his cell after having smoked buscopan® tablets. Since both abuse of substances and recent physical assaults had been reported, we opted for a comprehensive approach (post-mortem computed tomography CT (PMCT), full forensic autopsy, and toxicology testing) to determine which was the cause of the death. Virtopsy found significant cerebral edema and lungs edema that were confirmed at the autopsy and at the histopathological examination. Scopolamine was detected in peripheral blood at the toxic concentration of 14 ng/mL in blood and at 263 ng/mL in urine, and scopolamine butyl bromide at 17 ng/mL in blood and 90 ng/mL in urine. Quetiapine, mirtazapine, lorazepam, diazepam, and metabolites and valproate were also detected (at therapeutic concentrations). Inmates, especially when they have a history of drug abuse, are at risk to use any substance they can find for recreational purposes. In prisons, active surveillance on the management and assumption of prescribed drugs could avoid fatal acute intoxication.

THYROTROPHIN RELEASING HORMONE-INDUCED GROWTH HORMONE AND PROLACTIN RELEASE: PHYSIOLOGICAL STUDIES IN INTACT RATS AND IN HYPOPHYSECTOMIZED RATS BEARING AN ECTOPIC PITUITARY GLAND

1977 ◽  
Vol 72 (3) ◽  
pp. 301-311 ◽  
Author(s):  
A. E. PANERAI ◽  
IRIT GIL-AD ◽  
DANIELA COCCHI ◽  
V. LOCATELLI ◽  
G. L. ROSSI ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Time Lapse ◽  
Anterior Pituitary Gland ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Clear Cut ◽  
Urethane Anaesthesia ◽  
Releasing Effect

SUMMARY To determine how the sensitivity of the ectopic anterior pituitary gland to the GH-releasing effect of thyrotrophin releasing hormone (TRH) might be affected by the time lapse from transplantation, TRH (0·15 and 0·6 μg) was injected i.v. into hypophysectomized (hypox)-transplanted rats under urethane anaesthesia 1,3, 8,15, 30 and 60 days after transplantation, and plasma samples were taken 5 and 10 min later. Baseline GH values gradually decreased with time from about 16·0 ng/ml (1 day) to about 3·0 ng/ml (30 and 60 days). The TRH-induced GH release was absent 1 day after transplantation, present only with the higher TRH dose 3 and 8 days after transplantation, and clearly elicitable, also with the lower TRH dose (0·15 μg), from 15 up to 60 days. Determination of plasma prolactin concentrations showed a decline from about 85·0 ng/ml (1 day) to about 32·0 ng/ml (8 days); subsequently (15–60 days) prolactin values stabilized. Plasma prolactin levels increased 15 and 60 days after transplantation only when a dose of 0·6 μg TRH was given. In intact weight-matched rats, TRH induced a GH response only at the dose of 1·2 μg while a short-lived but clear-cut prolactin response could be obtained even with the 0·3 μg dose. The present results indicate that: (1) disconnexion between the central nervous system and the anterior pituitary gland greatly enhances GH responsiveness while blunting prolactin responsiveness to TRH; (2) the sensitivity of the anterior pituitary gland to the GH-releasing effect of TRH increases with time from transplantation; (3) TRH is a more effective prolactin-than GH-releaser on the pituitary gland in situ.

Some Aspects of the Psychopharmacological Activity of Maprotiline (Ludiomil®): Effects of Single and Repeated Treatments

1978 ◽  
Vol 6 (6) ◽  
pp. 421-429 ◽  
Author(s):  
A Delini-Stula ◽  
E Radeke ◽  
A Vassout
Keyword(s):  
Nervous System ◽  
Chronic Treatment ◽  
Conditioned Fear ◽  
Conditioned Avoidance ◽  
Repeated Treatment ◽  
Antidepressant Effects ◽  
The Central Nervous System ◽  
Pre Treatment ◽  
High Doses ◽  
Psychopharmacological Activity

Three different aspects of the psychopharmacological activity of the antidepressant maprotiline were investigated: its influence on serotoninergic functions the effects produced by chronic treatment its central nervous depressant and anxiolytic properties. Study of the effects of maprotiline on 5-HTP-induced head-twitch in mice pre-treated with pargyline or on hyperpyrexia in rats provided no evidence that the drug interferes with serotonin-mediated functions in the central nervous system even after quite high doses. These findings corroborate the results of extensive neurobiochemical investigations, which failed to demonstrate any influence of maprotiline on the metabolism of serotonin. Chronic studies showed that classical effects of maprotiline such as antagonism against reserpine-induced ptosis or tetrabenazine-induced catalepsy do not change in their intensity after daily administration of the drugs in a dose of 30 mg/kg p.o.for 11 days. A new component of the action of the compound, not detectable after one single dose, seems to appear, however, after repeated treatment (8 days). This effect is manifested in the restoration of conditioned avoidance behaviour after its suppression by pre-treatment with reserpine. The same effect is produced by imipramine. It is suggested that this restorative effect may be due to an additional activation of the dopaminergic nervous system and may have a bearing on the appearance of clinical antidepressant effects. Maprotiline was found to potentiate central nervous depressant effects of drugs like chlorpromazine, phenobarbitone and propranolol. This affords further confirmation that, in addition to its antidepressant qualities, it possesses sedative actions. An anxiolytic component was also demonstrated in rats in which maprotiline suppressed the conditioned, fear-induced rise in body-temperature.

Myelin Basic Protein inhibits the calcium response to phytohaemagglutinin in human lymphocytes

1990 ◽  
Vol 10 (1) ◽  
pp. 55-59
Author(s):  
Tiziana Bellini ◽  
Diana Degani ◽  
Maurizio Matteuzzi ◽  
Franco Dallocchio
Keyword(s):  
Myelin Basic Protein ◽  
Protein Concentration ◽  
Basic Protein ◽  
Human Lymphocytes ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Cellular Activation ◽  
The Central Nervous System ◽  
Pre Treatment ◽  
Preincubation Time

Myelin Basic Protein, one of the major membrane protein component of the central nervous system, was used to probe the molecular mechanism of cellular activation by phytohaemagglutinin. Pre-treatment of human lymphocytes with myelin basic protein results in a lower rising of cytosolic concentration of free calcium after stimulation with phytohaemagglutinin. This effect is dependent on myelin basic protein concentration and on the preincubation time of the protein with the cells. It is not due to a interaction between myelin basic protein and phytohaemagglutinin, but appears to be a consequence of the binding of the protein to the cell surface. The reduction of the rise of cytosolic calcium induced by phytohaemagglutinin is specific for the myelin basic protein because other proteins like albumin and protamine have no effect.

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