ライフサイエンスコーパス: cholinergic antagonist

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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 camylamine and kappa-bungarotoxin, which are cholinergic antagonists able to block the ganglionic alp

4 icrog) or nicotinic (mecamylamine, 1 microg) cholinergic antagonists administered into the rostral ve

5 tivity was only achieved by a combination of cholinergic antagonists and bicuculline, a GABAA antagon

6 hmic spontaneous activity in the presence of cholinergic antagonists and the eventual emergence of wa

7 use bursting was only transiently blocked by cholinergic antagonists, and following recovery, was now

8 Because only cholinergic antagonists are known to abolish early spont

9 xperiments were performed using scopolamine (cholinergic antagonist) as this drug blocks PCP-induced

10 Infusions of the muscarinic cholinergic antagonist atropine (0.5 microgram in 0.2 mi

11 hable from the response of controls, and the cholinergic antagonist atropine effectively blocked thes

12 lus cholinergic blockade with the muscarinic cholinergic antagonist atropine in random sequence.

13 e dopamine antagonist cis-flupentixol or the cholinergic antagonist atropine into the nucleus accumbe

14 18 and partially inhibited by the muscarinic cholinergic antagonist atropine.

15 ve exposed the retina to curare, a nicotinic cholinergic antagonist, because spontaneous bursting by

16 Exposure to cholinergic antagonists, curare and hexamethonium bromid

17 onists, acetylcholine and carbachol, and the cholinergic antagonists, D-tubocurarine and atropine.

18 e independent of cholinergic stimulation, as cholinergic antagonists did not block CPF-induced inhibi

19 Importantly, atropine, a muscarinic cholinergic antagonist, did not induce translocation of

20 the other hand, mecamylamine, the nicotinic cholinergic antagonist, failed to affect either the acut

21 , corticosteroids, dopamine antagonists, and cholinergic antagonists, have yielded valuable efficacy

22 The nicotinic cholinergic antagonist mecamylamine blocks the haltere-t

23 In the presence of cholinergic antagonists, motor axon stimulation triggere

24 er the influence of scopolamine (an amnestic cholinergic antagonist) or vehicle (saline).

25 catecholamine release-inhibitory, nicotinic cholinergic antagonist peptide catestatin.

26 issect this requirement using the muscarinic cholinergic antagonist pirenzepine.

27 Phencynonate hydrochloride, a muscarinic cholinergic antagonist, prevented seizure-like behaviors

28 f human catestatin, a CHGA-derived nicotinic cholinergic antagonist, restored normal blood pressure i

29 extual processing during extinction with the cholinergic antagonist Scop blocked subsequent fear rene

30 duced in subjects who receive the muscarinic cholinergic antagonist scopolamine before fMRI scanning.

31 on of a subeffective dose (0.1 mg/kg) of the cholinergic antagonist scopolamine.

32 Neither the cholinergic antagonists scopolamine, atropine or mecamyl

33 The cholinergic antagonist, scopolamine, significantly reduc

34 fact that AS in P11 rats is not affected by cholinergic antagonists supports the hypothesis that AS

35 most commonly available fish anesthetic, the cholinergic antagonist tricaine methanosulfate (MS222),

36 Cholinergic antagonists were used to investigate the rol

37 Reverse microdialysis of cholinergic antagonists within BF prevents the wake-prom

38 Although previous studies suggest that cholinergic antagonists would worsen pathophysiology, th

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