Binding site of salsolinol: its properties in different regions of the brain and the pituitary gland of the rat.


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Binding site of salsolinol: its properties in different regions of the brain and the pituitary gland of the rat.
Neurochemistry international
Homicskó K.G., Kertész I., Radnai B., Tóth B.E., Tóth G., Fülöp F., Fekete M.I., Nagy G.M.
0197-0186 (Print)
Statut éditorial
Date de publication
Publication types: Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
It has been recently shown that salsolinol (SAL) is present in the hypothalamic neuroendocrine dopaminergic (NEDA) system and appears to be a selective and potent stimulator of prolactin (PRL) secretion in the rat. Furthermore, the lack of interference of SAL with 3H-spiperone binding in the striatum and the anterior lobe (AL) of the pituitary gland has been also demonstrated. These data clearly indicate that SAL does not act at the dopamine (DA) D(2) receptors, and suggest that SAL supposedly has a binding site through which the secretion of PRL may be affected. Therefore, binding of 3H-SAL to different regions of the central nervous system (CNS) has been investigated. Specific and saturable binding has been detected in the striatum, cortex, median eminence and in the hypothalamus as well as in the AL and the neuro-intermediate lobe (NIL) of the pituitary gland. K(D) values of the bindings were in the nanomolar range in all tissue tested. 3H-SAL displacing activity of several agonists and antagonists of known DA receptors have also been tested. It has been found that DA and in a lesser extent, apomorphine could displace 3H-SAL, but other DA receptor specific ligands have not been able to affect it. Furthermore, several pharmacologically active compounds, selected on the basis of their influence on DA synthesis, transport mechanisms and signal transduction, have also been tested. Neither mazindol (a selective DA transporter inhibitor) nor clonidine (an alpha(2)-adrenoreceptor agonist) could alter SAL binding. At the same time, L-dopa, carbidopa, benserazide and alpha-methyldopa were able to displace 3H-SAL. The possible changes in SAL binding due to physiological and pharmacological stimuli, like suckling stimulus and reserpine pretreatment (that blocks vesicular monoamine transport in DA terminals), respectively, have also been investigated. In the NIL of the pituitary gland and in the median eminence of the hypothalamus the binding decreased following 10 min of suckling stimulus compared to the binding detected in the same tissues obtained from mothers separated from their pups for 4h and not allowed to be suckled. At the same time, there were no changes in the binding at the AL and striatum. Following reserpine pretreatment that has completely prevented PRL releasing effect of SAL, the binding was significantly augmented. These results support our assumption that SAL should have specific binding sites through which it can affect PRL secretion. Furthermore, it clearly suggests that it may regulate DAergic neurotransmission of NEDA neurons by an altered intracellular or intraterminal synthesis and/or distribution of hypophysiotropic DA.
Animals, Aromatic Amino Acid Decarboxylase Inhibitors, Aromatic-L-Amino-Acid Decarboxylases/metabolism, Benserazide/pharmacology, Binding Sites, Binding, Competitive, Brain/metabolism, Carbidopa/pharmacology, Clonidine/pharmacology, Corpus Striatum/drug effects, Corpus Striatum/metabolism, Dopamine/physiology, Dopamine Agonists/pharmacology, Dopamine Antagonists/pharmacology, Enzyme Inhibitors/pharmacology, Female, Isoquinolines/metabolism, Kinetics, Lactation/physiology, Levodopa/pharmacology, Male, Mazindol/pharmacology, Median Eminence/drug effects, Median Eminence/metabolism, Methyldopa/pharmacology, Pituitary Gland/metabolism, Pituitary Gland, Posterior/drug effects, Pituitary Gland, Posterior/metabolism, Prolactin/metabolism, Rats, Rats, Sprague-Dawley, Receptors, Dopamine/drug effects, Reserpine/pharmacology
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Création de la notice
02/06/2022 9:58
Dernière modification de la notice
03/06/2022 6:37
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