scholarly journals Preface: Cholinergic Mechanisms

2017 ◽  
Vol 142 ◽  
pp. 3-6 ◽  
Author(s):  
Marco A.M. Prado ◽  
Pascale Marchot ◽  
Israel Silman
2021 ◽  
Author(s):  
Noah A. Omeiza ◽  
Halimat A. Abdulrahim ◽  
Abdullateef I. Alagbonsi ◽  
Precious U. Ezurike ◽  
Talha K. Soluoku ◽  
...  

1988 ◽  
Vol 43 (4) ◽  
pp. 507-514 ◽  
Author(s):  
L.S. Kaufman ◽  
B.S. McEwen ◽  
D.W. Pfaff

1996 ◽  
Vol 9 (12) ◽  
pp. 2468-2473 ◽  
Author(s):  
K. Matsumoto ◽  
H. A Izawa ◽  
H. Inoue ◽  
S. Takata ◽  
M. Shigyo ◽  
...  

2011 ◽  
Vol 31 (6) ◽  
pp. 606-616 ◽  
Author(s):  
Madhu Lata Sankhwar ◽  
Rajesh S Yadav ◽  
Rajendra K Shukla ◽  
Aditya B Pant ◽  
Dhirendra Singh ◽  
...  

Studies on the neurobehavioral toxicity of monocrotophos, an organophosphate, have been carried out on rats following their exposure from postnatal day (PD) 22 to PD 49 to investigate whether neurobehavioral changes are transient or persistent. Exposure of rats to monocrotophos (0.50 or 1.0 mg/kg body weight, p.o.) decreased body weight (10% and 30%) and impaired grip strength (28% and 32%) and learning ability (65% and 68%) at both the doses, respectively in comparison to controls. A trend of recovery was observed in body weight and learning, while decrease in grip strength persisted in rats 15 days after withdrawal. Activity of acetylcholinesterase was decreased in frontal cortex (36% and 67%), hippocampus (21% and 49%) and cerebellum (29% and 51%) in monocrotophos-treated rats at both the doses. The decrease in the activity of acetylcholinesterase persisted in frontal cortex and hippocampus; however, a trend of recovery was observed in cerebellum 15 days after withdrawal. Binding of 3 H-quinuclidinyl benzilate ( 3 H-QNB) to frontocortical (19% and 35%), hippocampal (32% and 39%) and cerebellar (19% and 28%) membranes was decreased in monocrotophos-treated rats compared to controls. The decrease in the binding of 3 H-QNB persisted in frontocortical, hippocampal and cerebellar membranes 15 days after withdrawal. The results suggest that repeated exposure to monocrotophos in rats may cause behavioral and neurochemical modifications which may persist even after withdrawal. The findings are of concern in view of the high consumption of monocrotophos in many countries.


2000 ◽  
Vol 118 (4) ◽  
pp. A618
Author(s):  
Brent Harris ◽  
Satish SC Rao ◽  
Bruce Brown ◽  
Vani Vernuri ◽  
Konrad Schulze

1996 ◽  
Vol 270 (2) ◽  
pp. H442-H446 ◽  
Author(s):  
C. M. Martin ◽  
A. Beltran-Del-Rio ◽  
A. Albrecht ◽  
R. R. Lorenz ◽  
M. J. Joyner

To determine whether local cholinergic mechanisms evoke nitric oxide (NO)-mediated flow-induced vasorelaxation, canine coronary artery rings without endothelium were suspended beneath an organ chamber that contained a stainless steel tube and a femoral artery segment with endothelium. The rings were superfused at a basal rate of 1 ml/min with physiological salt solution that was bubbled with 95% O2-5% CO2 and maintained at 37 degrees C. They were stretched to optimal length and contracted with prostaglandin F 2 alpha (2 x 10(-6) M). When flow through the stainless steel tube (direct superfusion) was increased from the basal rate of 1 to 4 ml/min, coronary force did not change. Superfusion of the rings (n = 8) with effluent from the femoral segment (endothelial superfusion) at 4 ml/min to study flow-induced vasodilation caused a 67.3 +/- 10.8% relaxation. Treatment of the segment with the NO synthase blocker NG-monomethyl-L-arginine (10(-4) M) eliminated the relaxation seen during endothelial superfusion (P < 0.05 vs. control). Application of atropine (10(-6) M) to additional femoral segments (n = 8) abolished the coronary relaxation observed during endothelial superfusion at 1 ml/ min, and the flow-induced relaxation observed at 4 ml/min was reduced from 64 +/- 8.3 to 27 +/- 5.6% (P < 0.05 vs. control). In studies on additional segments and rings (n = 6), the flow-induced relaxations at 4 ml/min of endothelial superfusion were blunted from 86 +/- 10 to 28 +/- 13% after the segments were treated with acetylcholinesterase (0.00028 U/min for 20 min). These data indicate that basal- and flow-induced release of NO from the vascular endothelium can be mediated by local cholinergic mechanisms. It is possible that flow causes acetylcholine release from certain endothelial cells, which stimulates NO release from these cells or from neighboring endothelial cells.


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