μ-Opioid receptor-regulated adenylate cyclase activity in primary cultures of rat striatal neurons upon chronic morphine exposure

1991 ◽  
Vol 208 (2) ◽  
pp. 105-111 ◽  
Author(s):  
Bernard J. Van Vliet ◽  
Taco J. De Vries ◽  
George Wardeh ◽  
Arie H. Mulder ◽  
Anton N.M. Schoffelmeer
1990 ◽  
Vol 5 (1) ◽  
pp. 69-76 ◽  
Author(s):  
G. Schettini ◽  
E. Landolfi ◽  
O. Meucci ◽  
T. Florio ◽  
M. Grimaldi ◽  
...  

ABSTRACT The effect of adenosine and its analogue ( − )-N6-R-phenylisopropyladenosine (PIA) on both anterior pituitary adenylate cyclase activity and prolactin secretion was examined in the rat. Adenosine inhibited basal adenylate cyclase activity in a dose-dependent manner and also reduced the stimulation of the enzyme by vasoactive intestinal peptide (VIP). Likewise, in primary cultures of anterior pituitary cells, adenosine decreased prolactin secretion in both basal and VIP-stimulated conditions. In perifusion experiments, adenosine also inhibited prolactin release in both basal and TRH-stimulated conditions. PIA produced a biphasic pattern of response of basal adenylate cyclase activity, being inhibitory at low and stimulatory at high concentrations. In VIP-stimulated conditions, low concentrations of PIA inhibited both adenylate cyclase activity and prolactin release from primary cultures of pituitary cells, while no additive stimulatory effect was seen at high concentrations. Similarly, low concentrations of PIA reduced both basal and TRH-stimulated prolactin release from perifused pituitaries, while increasing PIA concentrations restored prolactin release. These data show that adenosine affects basal and stimulated prolactin secretion from anterior pituitary cells. Adenosine receptors seem to be coupled to the adenylate cyclase system in the anterior pituitary gland, suggesting a possible relationship between the effect of adenosine on adenylate cyclase activity and prolactin secretion.


1988 ◽  
Vol 154 (2) ◽  
pp. 169-178 ◽  
Author(s):  
Anton N.M. Schoffelmeer ◽  
Kenner C. Rice ◽  
Arthur E. Jacobson ◽  
Johannus G. Van Gelderen ◽  
François Hogenboom ◽  
...  

Life Sciences ◽  
1992 ◽  
Vol 51 (10) ◽  
pp. PL89-PL94 ◽  
Author(s):  
Bernard J. Van Vliet ◽  
Corinne H. Dotman ◽  
George Wardeh ◽  
Arie H. Mulder ◽  
Anton N.M. Schoffelmeer

Author(s):  
L.S. Cutler

Many studies previously have shown that the B-adrenergic agonist isoproterenol and the a-adrenergic agonist norepinephrine will stimulate secretion by the adult rat submandibular (SMG) and parotid glands. Recent data from several laboratories indicates that adrenergic agonists bind to specific receptors on the secretory cell surface and stimulate membrane associated adenylate cyclase activity which generates cyclic AMP. The production of cyclic AMP apparently initiates a cascade of events which culminates in exocytosis. During recent studies in our laboratory it was observed that the adenylate cyclase activity in plasma membrane fractions derived from the prenatal and early neonatal rat submandibular gland was retractile to stimulation by isoproterenol but was stimulated by norepinephrine. In addition, in vitro secretion studies indicated that these prenatal and neonatal glands would not secrete peroxidase in response to isoproterenol but would secrete in response to norepinephrine. In contrast to these in vitro observations, it has been shown that the injection of isoproterenol into the living newborn rat results in secretion of peroxidase by the SMG (1).


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