Slow Synaptic Responses in Neuronal Tumor Cells: Dual Regulation of ADP-Ribosyl Cyclase and Inhibition of M-Current by Muscarinic Receptor Stimulation

2000 ◽  
pp. 35-41
Author(s):  
H. Higashida ◽  
S. Yokoyama ◽  
M. Hashii ◽  
M. Taketo
Keyword(s):  
Tumor Cells ◽  
Muscarinic Receptor ◽  
Receptor Stimulation ◽  
M Current ◽  
Adp Ribosyl Cyclase ◽  
Neuronal Tumor ◽  
Synaptic Responses

Effect of acetylcholine infusion on adrenal vasculature and catecholamine secretion

1993 ◽  
Vol 265 (3) ◽  
pp. H966-H972 ◽  
Author(s):  
J. R. Tobin ◽  
M. J. Breslow ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Muscarinic Receptor ◽  
Cholinergic Receptor ◽  
Catecholamine Secretion ◽  
Receptor Stimulation ◽  
Similar Dose ◽  
Adrenal Vasculature ◽  
Higher Doses

To evaluate effects of cholinergic receptor stimulation on regional adrenal blood flow (Q, radiolabeled microspheres) and catecholamine secretion, acetylcholine (ACh) was infused into pentobarbital-anesthetized, ventilated dogs. Unilateral adrenal denervation and placement of lumboadrenal catheters preceded intra-aortic infusion of 1) ACh alone (n = 6), 2) ACh plus hexamethonium (Hex) 20 mg/kg (n = 6), or 3) ACh plus atropine (Atr) (0.5 mg/kg) and Hex. ACh alone and in combination with Hex elicited similar dose-related (2, 20, and 100 mumol/min) increases in catecholamine secretion (181 +/- 61 to 1,055 +/- 229, 31,644 +/- 9,411, and 179,181 +/- 69,659 ng.min-1 x g medulla-1), whereas Hex and Atr together inhibited ACh-induced secretion by 95%. ACh caused marked medullary vasodilation (0.71 +/- 0.05 to 0.14 +/- 0.03 mmHg.ml-1 x min.100 g) in all three groups. To determine whether medullary vasodilation was due to incomplete muscarinic blockade, Hex-pretreated animals (n = 4) received ACh (100 mumol/min) and three increasing doses of Atr (0.5, 5, and 25 mg/kg). Catecholamine secretion was inhibited by all doses of Atr; however, vasodilation was blocked only by the two higher doses of Atr. These data suggest possible different mechanisms of muscarinic receptor-mediated catecholamine secretion and vasodilation.

Antilaminin IgG triggers the murine atria phosphoinositide hydrolysis through muscarinic receptor stimulation

1992 ◽  
Vol 14 (8) ◽  
pp. 1321-1328 ◽  
Author(s):  
S. Bacman ◽  
L. Sterin-Borda ◽  
G. Gorelik ◽  
L. Lustig ◽  
B. Denduchis ◽  
...  
Keyword(s):  
Muscarinic Receptor ◽  
Phosphoinositide Hydrolysis ◽  
Receptor Stimulation

Evidence that noradrenaline modulates the increase in striatal dopamine metabolism induced by muscarinic receptor stimulation

1980 ◽  
Vol 68 (4) ◽  
pp. 427-435 ◽  
Author(s):  
Marta Weinstock ◽  
Anthony P. Azvadil ◽  
Eric A. Muth ◽  
William R. Crowley ◽  
Thomas L. O'Donohue ◽  
...  
Keyword(s):  
Muscarinic Receptor ◽  
Dopamine Metabolism ◽  
Striatal Dopamine ◽  
Receptor Stimulation

scholarly journals Rapid accumulation and sustained turnover of inositol phosphates in cerebral-cortex slices after muscarinic-receptor stimulation

1989 ◽  
Vol 260 (1) ◽  
pp. 237-241 ◽  
Author(s):  
I H Batty ◽  
S R Nahorski
Keyword(s):  
Cerebral Cortex ◽  
Muscarinic Receptor ◽  
Metabolic Flux ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Receptor Activation ◽  
Inositol Polyphosphate ◽  
Receptor Stimulation ◽  
Cortex Slices ◽  
Rapid Kinetics

The rapid kinetics of [3H]inositol phosphate accumulation and turnover were examined in rat cerebral-cortex slices after muscarinic-receptor stimulation. Markedly increased [3H]inositol polyphosphate concentrations were observed to precede significant stimulated accumulation of [3H]inositol monophosphate. New steady-state accumulations of several 3H-labelled products were achieved after 5-10 min of continued agonist stimulation, but were rapidly and effectively reversed by subsequent receptor blockade. The results show that muscarinic-receptor activation involves phosphoinositidase C-catalysed hydrolysis initially of polyphosphoinositides rather than of phosphatidylinositol. Furthermore, prolonged carbachol stimulation is shown not to cause receptor desensitization, but to allow persistent hydrolysis of [3H]phosphatidylinositol bisphosphate and permit sustained metabolic flux through the inositol tris-/tetrakis-phosphate pathway.

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