Effects of methyllycaconitine (MLA), an α 7 nicotinic receptor antagonist, on nicotine- and cocaine-induced potentiation of brain stimulation reward

2000 ◽  
Vol 149 (4) ◽  
pp. 388-396 ◽  
Author(s):  
G. Panagis ◽  
A. Kastellakis ◽  
C. Spyraki ◽  
G. Nomikos
Keyword(s):  
Receptor Antagonist ◽  
Brain Stimulation ◽  
Nicotinic Receptor ◽  
Brain Stimulation Reward ◽  
Nicotinic Receptor Antagonist

Nicotinic and M1-, M2-muscarinic cholinergic control of ACTH response to insulin-induced hypoglycaemia in man

1987 ◽  
Vol 116 (4) ◽  
pp. 531-536 ◽  
Author(s):  
V. Coiro ◽  
M. Passeri ◽  
G. Gelmini ◽  
C. Davoli ◽  
G. Bianconcini ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Nicotinic Receptor ◽  
Insulin Injection ◽  
Tolerance Test ◽  
Injection Time ◽  
Nicotinic Cholinergic Receptors ◽  
Muscarinic Cholinergic ◽  
Normal Men ◽  
Nicotinic Receptor Antagonist ◽  
Acth Release

Abstract. The possible mediation of muscarinic and/or nicotinic-cholinergic receptors in the response of ACTH to insulin-induced hypoglycaemia was evaluated in 18 normal men. Subjects were tested with the insulin (0.15 U/kg) tolerance test (ITT) in basal conditions and in the presence of the M1- and M2-muscarinic antagonist atropine (600 μg iv just before insulin injection (time 0) plus 600 μg 20 min later in 6 subjects) or the M1-muscarinic receptor blocker pirenzepine (40 mg iv 10 min before ITT or 20 mg at time 0 plus 30 mg at time 20 in 6 subjects). The remaining 6 men were treated with the nicotinic receptor antagonist trimethaphan (0.3 mg/min × 30 min before ITT). ACTH rose 4.7 times in response to hypoglycaemia. The ACTH response to hypoglycaemia did not change after pirenzepine administration, whereas it was significantly increased by atropine and decreased by trimethaphan treatment. These data indicate that nicotinic and muscarinic (M2 but not M1) receptors participate in a different manner in the regulation of the hypoglycaemia-induced ACTH release.

scholarly journals r-bPiDI, an α6β2* Nicotinic Receptor Antagonist, Decreases Nicotine-Evoked Dopamine Release and Nicotine Reinforcement

2015 ◽  
Vol 40 (10) ◽  
pp. 2121-2130 ◽  
Author(s):  
Joshua S. Beckmann ◽  
Andrew C. Meyer ◽  
M. Pivavarchyk ◽  
David B. Horton ◽  
Guangrong Zheng ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Nicotinic Receptor ◽  
Dopamine Release ◽  
Nicotinic Receptor Antagonist

Spinal Muscarinic and Nicotinic Subtypes Activated by Clonidine in Postincisional Pain

2005 ◽  
Vol 103 (6) ◽  
pp. 1253-1258 ◽  
Author(s):  
Frédéric Duflo ◽  
Emmanuel Boselli ◽  
Philippe Ryvlin ◽  
Dominique Chassard
Keyword(s):  
Postoperative Pain ◽  
Receptor Antagonist ◽  
Muscarinic Receptor ◽  
Nicotinic Receptor ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Muscarinic Antagonist ◽  
Alpha7 Nicotinic Receptor ◽  
Intrathecal Clonidine ◽  
Nicotinic Receptor Antagonist

Background A recent model of acute incisional pain has been characterized that strongly parallels the postoperative period in patients experiencing evoked pain. In that setting, abundant literature has revealed antihypersensitive effects produced by intrathecally administered alpha2-adrenergic receptor agonists, such as clonidine, in both animals and humans. Recent reports have suggested an obligatory role of spinal acetylcholine receptors in the analgesic action of intrathecal clonidine. The authors sought to determine the involvement of spinal muscarinic and nicotinic receptor subpopulations in the antihypersensitivity effect of intrathecal clonidine in a rodent model for human postoperative pain. Methods After intrathecal catheterization, rats underwent superficial plantar incision. Clonidine or a combination of clonidine and muscarinic receptor subtype antagonists (M1, M2, M3, and M4) or nicotinic receptor subtype antagonists (alpha4beta2 and alpha7) were intrathecally administered, and withdrawal thresholds to mechanical stimuli were examined. Results Spinal clonidine maximally reduced hypersensitivity adjacent to the wound 30 min after its injection. When animals were intrathecally pretreated with the M1 muscarinic antagonist toxin MT-7, the M3 muscarinic antagonist 4-diphenylacetoxy-N-methylpiperidine, and the M4 muscarinic antagonist toxin MT-3, clonidine lost its antihypersensitive action. When animals were intrathecally pretreated with the alpha4beta2 nicotinic receptor antagonist dihydro-beta-erythroidine, but not with the alpha7 nicotinic receptor antagonist methyllycaconitine, the antihypersensitivity action of clonidine was abolished. Conclusions These data indicate for the first time that the clonidine-induced increase in punctuate mechanical threshold is mediated via the activation of all but M2 muscarinic receptor subtypes, and via the activation of alpha4beta2 but not alpha7 nicotinic receptor subtypes in a rodent model for human postoperative pain.

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