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1 ls that are depressed, but not abolished, by cholinergic antagonists.
2 f solAPPcyt, a process that was inhibited by cholinergic antagonists.
3 rainstem, before and after administration of cholinergic antagonists.
4 camylamine and kappa-bungarotoxin, which are cholinergic antagonists able to block the ganglionic alp
5 icrog) or nicotinic (mecamylamine, 1 microg) cholinergic antagonists administered into the rostral ve
6 tivity was only achieved by a combination of cholinergic antagonists and bicuculline, a GABAA antagon
7 hmic spontaneous activity in the presence of cholinergic antagonists and the eventual emergence of wa
8 use bursting was only transiently blocked by cholinergic antagonists, and following recovery, was now
9                                 Because only cholinergic antagonists are known to abolish early spont
10 xperiments were performed using scopolamine (cholinergic antagonist) as this drug blocks PCP-induced
11                  Infusions of the muscarinic cholinergic antagonist atropine (0.5 microgram in 0.2 mi
12 hable from the response of controls, and the cholinergic antagonist atropine effectively blocked thes
13 lus cholinergic blockade with the muscarinic cholinergic antagonist atropine in random sequence.
14 e dopamine antagonist cis-flupentixol or the cholinergic antagonist atropine into the nucleus accumbe
15 18 and partially inhibited by the muscarinic cholinergic antagonist atropine.
16 ve exposed the retina to curare, a nicotinic cholinergic antagonist, because spontaneous bursting by
17                                  Exposure to cholinergic antagonists, curare and hexamethonium bromid
18 onists, acetylcholine and carbachol, and the cholinergic antagonists, D-tubocurarine and atropine.
19 e independent of cholinergic stimulation, as cholinergic antagonists did not block CPF-induced inhibi
20          Importantly, atropine, a muscarinic cholinergic antagonist, did not induce translocation of
21  the other hand, mecamylamine, the nicotinic cholinergic antagonist, failed to affect either the acut
22 , corticosteroids, dopamine antagonists, and cholinergic antagonists, have yielded valuable efficacy
23                                The nicotinic cholinergic antagonist mecamylamine blocks the haltere-t
24                           In the presence of cholinergic antagonists, motor axon stimulation triggere
25 er the influence of scopolamine (an amnestic cholinergic antagonist) or vehicle (saline).
26  catecholamine release-inhibitory, nicotinic cholinergic antagonist peptide catestatin.
27 issect this requirement using the muscarinic cholinergic antagonist pirenzepine.
28     Phencynonate hydrochloride, a muscarinic cholinergic antagonist, prevented seizure-like behaviors
29 f human catestatin, a CHGA-derived nicotinic cholinergic antagonist, restored normal blood pressure i
30 extual processing during extinction with the cholinergic antagonist Scop blocked subsequent fear rene
31 duced in subjects who receive the muscarinic cholinergic antagonist scopolamine before fMRI scanning.
32 on of a subeffective dose (0.1 mg/kg) of the cholinergic antagonist scopolamine.
33                                  Neither the cholinergic antagonists scopolamine, atropine or mecamyl
34                                          The cholinergic antagonist, scopolamine, significantly reduc
35                      Injection of muscarinic cholinergic antagonists, scopolamine methyl bromide or q
36  fact that AS in P11 rats is not affected by cholinergic antagonists supports the hypothesis that AS
37 most commonly available fish anesthetic, the cholinergic antagonist tricaine methanosulfate (MS222),
38                                              Cholinergic antagonists were used to investigate the rol
39                     Reverse microdialysis of cholinergic antagonists within BF prevents the wake-prom
40       Although previous studies suggest that cholinergic antagonists would worsen pathophysiology, th