The role of cholinergic transmission in learning

1976 ◽  
pp. 115-119
Author(s):  
H. Matthies ◽  
E. Kammerer ◽  
Christine Rauca
Keyword(s):  
Cholinergic Transmission

The role of efferent cholinergic transmission for the insulinotropic and glucagonostatic effects of GLP-1

2015 ◽  
Vol 309 (5) ◽  
pp. R544-R551 ◽  
Author(s):  
Astrid Plamboeck ◽  
Simon Veedfald ◽  
Carolyn F. Deacon ◽  
Bolette Hartmann ◽  
Tina Vilsbøll ◽  
...  
Keyword(s):  
Area Under The Curve ◽  
Glucagon Secretion ◽  
Glucose Turnover ◽  
High Dose ◽  
Cholinergic Transmission ◽  
Blinded Study ◽  
Muscarinic Cholinergic ◽  
Glucagon Like Peptide 1 ◽  
Insulinotropic Effect

The importance of vagal efferent signaling for the insulinotropic and glucagonostatic effects of glucagon-like peptide-1 (GLP-1) was investigated in a randomized single-blinded study. Healthy male participants ( n = 10) received atropine to block vagal cholinergic transmission or saline infusions on separate occasions. At t = 15 min, plasma glucose was clamped at 6 mmol/l. GLP-1 was infused at a low dose (0.3 pmol·kg−1·min−1) from t = 45–95 min and at a higher dose (1 pmol·kg−1·min−1) from t = 95–145 min. Atropine blocked muscarinic, cholinergic transmission, as evidenced by an increase in heart rate [peak: 70 ± 2 (saline) vs. 90 ± 2 (atropine) beats/min, P < 0.002] and suppression of pancreatic polypeptide levels [area under the curve during the GLP-1 infusions (AUC45–145): 492 ± 85 (saline) vs. 247 ± 59 (atropine) pmol/l × min, P < 0.0001]. More glucose was needed to maintain the clamp during the high-dose GLP-1 infusion steady-state period on the atropine day [6.4 ± 0.9 (saline) vs. 8.7 ± 0.8 (atropine) mg·kg−1·min−1, P < 0.0023]. GLP-1 dose-dependently increased insulin secretion on both days. The insulinotropic effect of GLP-1 was not impaired by atropine [C-peptide AUCs45–145: 99 ± 8 (saline) vs. 113 ± 13 (atropine) nmol/l × min, P = 0.19]. Atropine suppressed glucagon levels additively with GLP-1 [AUC45–145: 469 ± 70 (saline) vs. 265 ± 50 (atropine) pmol/l × min, P = 0.018], resulting in hypoglycemia when infusions were suspended [3.6 ± 0.2 (saline) vs. 2.7 ± 0.2 (atropine) mmol/l, P < 0.0001]. To ascertain whether atropine could independently suppress glucagon levels, control experiments ( n = 5) were carried out without GLP-1 infusions [AUC45–145: 558 ± 103 (saline) vs. 382 ± 76 (atropine) pmol/l × min, P = 0.06]. Our results suggest that efferent muscarinic activity is not required for the insulinotropic effect of exogenous GLP-1 but that blocking efferent muscarinic activity independently suppresses glucagon secretion. In combination, GLP-1 and muscarinic blockade strongly affect glucose turnover.

A modulatory role of central cholinergic transmission in control of the 10-Hz rhythm in sympathetic nerve discharge

1994 ◽  
Vol 661 (1-2) ◽  
pp. 283-288 ◽  
Author(s):  
Hakan S. Orer ◽  
Susan M. Barman ◽  
Sheng Zhong ◽  
Gerard L. Gebber
Keyword(s):  
Sympathetic Nerve ◽  
Cholinergic Transmission ◽  
Nerve Discharge

scholarly journals Effects of simvastatin and fenofibrate on butyrylcholinesterase activity in the brain, plasma, and liver of normolipidemic and hyperlipidemic rats

2019 ◽  
Vol 70 (1) ◽  
pp. 30-35
Author(s):  
Antonija Vukšić ◽  
Jasna Lovrić ◽  
Paško Konjevoda ◽  
Nina Blažević ◽  
Marinko Bilušić ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Lipid Lowering ◽  
Cholinergic Transmission ◽  
Control Groups ◽  
Study Objective ◽  
Simvastatin Treatment ◽  
Butyrylcholinesterase Activity ◽  
The Brain ◽  
Pharmacological Function

AbstractThe study objective was to test the hypothesis that simvastatin and fenofibrate should cause an increase in butyrylcholinesterase (BuChE) activity not only in the plasma and liver but also in the brain of normolipidemic and hyperlipidemic rats. Catalytic enzyme activity was measured using acetylthiocholine (ATCh) and butyrylthiocholine (BTCh) as substrates. Normolipidemic and hyperlipidemic rats were divided in four groups receiving 50 mg/kg of simvastatin a day or 30 mg/kg of fenofibrate a day for three weeks and three control groups receiving saline. Simvastatin and fenofibrate caused an increase in brain BuChE activity in both normo- and hyperlipidemic rats regardless of the substrate. The increase with BTCh as substrate was significant and practically the same in normolipidemic and hyperlipidemic rats after simvastatin treatment (14–17% vs controls). Simvastatin and fenofibrate also increased liver and plasma BuChE activity in both normolipidemic and hyperlipidemic rats regardless of the substrate. In most cases the increase was significant. Considering the important role of BuChE in cholinergic transmission as well as its pharmacological function, it is necessary to continue investigations of the effects of lipid-lowering drugs on BuChE activity.

Somatostatin inhibits cAMP-mediated cholinergic transmission in the myenteric plexus

1987 ◽  
Vol 253 (5) ◽  
pp. G607-G612 ◽  
Author(s):  
J. Wiley ◽  
C. Owyang
Keyword(s):  
Adenylate Cyclase ◽  
Cholera Toxin ◽  
Myenteric Plexus ◽  
Inhibitory Action ◽  
Inhibitory Effect ◽  
Cholinergic Transmission ◽  
Ach Release ◽  
Maximal Inhibition ◽  
Camp System

The mechanism by which somatostatin acts to modulate cholinergic transmission is not clear. In this study we investigated the role of the adenosine 3',5'-cyclic monophosphate (cAMP) system in mediating cholinergic transmission in the guinea pig myenteric plexus and examined the ability of somatostatin to alter acetylcholine (ACh) release stimulated by various cAMP agonists. Forskolin, 8-bromo-cAMP, vasoactive intestinal peptide (VIP), and cholera toxin each stimulated the release of [3H]ACh in a dose-related manner. Addition of theophylline enhanced the release of [3H]ACh stimulated by these cAMP agonists. In contrast 2',5'-dideoxyadenosine, an inhibitor of adenylate cyclase, antagonized the action of forskolin, VIP, and cholera toxin but had no effect on that evoked by 8-bromo-cAMP. These observations suggest that cAMP may serve as a physiological mediator for ACh release from myenteric neurons. Somatostatin inhibited release of [3H]ACh evoked by various cAMP agonists in a dose-related manner. Maximal inhibition, observed in the presence of 10(-6) M somatostatin was 48 +/- 5, 47 +/- 9, and 43 +/- 12% of control for forskolin-, VIP-, and cholera toxin-evoked release of [3H]ACh. In contrast somatostatin at 10(-6) M inhibited only 20 +/- 5% of the release of [3H]ACh stimulated by 8-bromo-cAMP. Pretreatment with pertussis toxin antagonized the inhibitory effect of somatostatin on the release of [3H]ACh evoked by forskolin, VIP, or cholera toxin but had no effect on the inhibitory action of somatostatin on the release of [3H]ACh evoked by 8-bromo-cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

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