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1 tion or intravenous drugs (e.g., ketamine or scopolamine).
2 og/kg for atropine and 5.7-10.4microg/kg for scopolamine).
3 nd it ameliorated memory deficits induced by scopolamine.
4 ion between the elements was not affected by scopolamine.
5 ntrolled environment chamber and to systemic scopolamine.
6 modified with subcutaneous administration of scopolamine.
7 specifically the antidepressant efficacy of scopolamine.
8 d recognition memory after administration of scopolamine.
9 necessary for the antidepressant actions of scopolamine.
10 antidepressant and antianxiety responses to scopolamine.
11 s activity was reduced in subjects receiving scopolamine.
12 uced if cholinergic receptors are blocked by scopolamine.
13 showed only a minor trend to decrease after scopolamine.
14 n with intracerebroventricular injections of scopolamine.
15 visual images after administration of 0.4 mg scopolamine.
16 uption seen after systemic administration of scopolamine.
17 he antidepressant-like behavioral effects of scopolamine.
18 ntact controls given a systemic injection of scopolamine.
19 zed rats did not reduce their sensitivity to scopolamine.
20 ects of the cholinergic receptor antagonist, scopolamine.
21 lease in the rapid antidepressant effects of scopolamine.
22 es were blocked by the muscarinic antagonist scopolamine.
23 ith the Met allele may be less responsive to scopolamine.
24 the cholinergic-muscarinic receptor blocker, scopolamine.
25 n by AMPH was blocked by 62, but not 6.2, mM scopolamine.
26 administration of the muscarinic antagonist, scopolamine.
27 se (0.1 mg/kg) of the cholinergic antagonist scopolamine.
28 locarpine, or the muscarinic ACh antagonist, scopolamine.
29 ment or following systemic administration of scopolamine.
30 system to test anxiety-like compounds using scopolamine.
31 pendent mechanisms underlying the effects of scopolamine.
32 for the rapid antidepressant-like effects of scopolamine.
33 ttenuated the antidepressant-like effects of scopolamine.
34 depression treated with parenteral doses of scopolamine.
35 fying patients who will respond favorably to scopolamine.
36 Before each test, rats were injected with scopolamine (0, 0.03, or 0.1 mg/kg, intraperitoneally),
38 the effects of microinfusion of 0.15 mug of scopolamine (0.075 mug of in 0.5 mul/side) in infralimbi
42 nately administered i.v. lorazepam (1 mg) or scopolamine (0.4 mg) in a double-blind, randomized, cros
44 s predicted by the model, rats that received scopolamine (0.50 and 0.25 mg/kg) were more impaired at
45 nic mice to desiccating stress (subcutaneous scopolamine [0.5 mg/0.2 mL] 3 times a day, humidity < 40
48 IPSCs by muscarine was completely blocked by scopolamine (10 microM), a muscarinic receptor antagonis
50 eived intrabasolateral amygdala infusions of scopolamine (2.5 microg or 5.0 microg/0.5 microl) or sal
51 umbens infusion of the muscarinic antagonist scopolamine 3 hr before the testing session significantl
52 mpounds and some analogs with [(3)H]N-methyl scopolamine ([(3)H]NMS) and unlabeled acetylcholine (ACh
53 on the equilibrium binding of l-[3H]N-methyl scopolamine ([3H]NMS) to the five human muscarinic recep
54 drate (MLA) (20 mM) or muscarinic antagonist scopolamine (40 mM) together with neostigmine (20 mM) at
55 kg(-1)), Ro 25-6981 (1, 3 and 10 mg kg(-1)), scopolamine (5, 25 and 100 mug kg(-1)) or vehicle (contr
56 mmediate posttraining (but not delayed 2 hr) scopolamine (5.0 microg) blocked acquisition of food- an
57 -10 microg) NMDA antagonists, or muscarinic (scopolamine, 5 microg) or nicotinic (mecamylamine, 1 mic
58 administration of the muscarinic antagonist scopolamine (50 mg/kg) partially attenuates reserpine-me
59 ts who were not injected, those who received scopolamine (8 microg/kg) showed (a) overall impairment
61 On the other hand, the microinjection of scopolamine (a muscarinic receptor antagonist) did not b
63 Recent clinical studies demonstrate that scopolamine, a nonselective muscarinic acetylcholine rec
65 ral intra-PR infusions with either saline or scopolamine, a nonselective muscarinic receptor antagoni
66 pair (A+B-) and then, under the influence of scopolamine, a novel odor pair (A-C+) with an overlappin
73 tum nor did co-administration of SCH23390 or scopolamine affect the levels of PCP-induced striatal ce
76 pine recapitulated the place-cell effects of scopolamine, although neither the mixture nor its separa
77 hronic pretreatment with DU-14 could reverse scopolamine amnesia and/or enhance spacial memory in the
78 en field environments under the influence of scopolamine (an amnestic cholinergic antagonist) or vehi
79 ntagonist of the 5-HT receptor, 5-HT(2A)) or scopolamine (an antagonist of the muscarinic receptor).
83 Pretreatment with the antimuscarinic drugs scopolamine and atropine was able to greatly suppress no
84 were inhibited by systemic administration of scopolamine and exposure to an air draft for 12 days in
85 aged 6 to 8 weeks were treated with systemic scopolamine and exposure to an air draft for different l
86 ntraluminal pressure that were eliminated by scopolamine and intrathecal lidocaine, suggesting an imp
89 of action of these effects by administering scopolamine and oxotremorine directly into the striatum
90 ALB/c mice were subcutaneously injected with scopolamine and placed in a daytime air-drying device fo
91 nces and similarities between the effects of scopolamine and quinpirole on D(1) agonist-induced Fos e
92 NF Met/Met mice have attenuated responses to scopolamine and that anti-BDNF antibody infusions into t
94 ecording electrodes, we infused nonspecific (scopolamine) and specific (methoctramine, pirenzepine) a
95 nightshade-specific tropane (l-hyoscyamine, scopolamine) and steroidal alkaloids (alpha-solanine, al
99 rate that the antidepressant-like effects of scopolamine are mediated by GABA interneurons in the med
102 osteric, extracellular site, and atropine or scopolamine as orthosteric building blocks, both connect
104 contrast, microinjections of the antagonist scopolamine at all sites in NAc shell suppressed sucrose
105 holinergic receptor antagonists atropine and scopolamine (atr/scop) produce an amnesic syndrome in hu
107 nt with cholinergic enhancement of encoding, scopolamine attenuated the formation of distinct spatial
108 icrog per side) of the muscarinic antagonist Scopolamine augmented adrenocorticotropin and corticoste
109 ation of the muscarinic receptor antagonist, scopolamine, augments, whereas the muscarinic receptor a
111 muscarinic antagonist displaced [N-methyl-3H]scopolamine binding with high-affinity binding constant
112 ine is a key intermediate in hyoscyamine and scopolamine biosynthesis that is produced by the condens
113 erence with the sample object trace and that scopolamine blocked the acquisition of this interfering
114 the selective muscarinic receptor antagonist scopolamine blocked the convulsions and prevented increa
117 (atropine, alpha-bungarotoxin (alpha-BTX) or scopolamine) blocks or attenuates ovulating events.
120 ric agonists, which do not improve memory in scopolamine-challenged mice in contextual fear condition
121 Equivalent experiments were performed using scopolamine (cholinergic antagonist) as this drug blocks
125 ial anxiety-reducing (anxiolytic) effects of scopolamine could have great clinical implications for h
126 teral intracerebral injections of 3.5 microg scopolamine did not affect intake stimulated by intrahyp
129 Single drug exposures to methiothepin or scopolamine did not noticeably affect the directional ch
130 y impaired after bilateral microinjection of scopolamine directly into the perirhinal cortex, but not
137 shock therapy, sleep deprivation, ketamine, scopolamine, GLYX-13 and pindolol used in conjunction wi
140 tal Day 12 and tested under the influence of scopolamine hydrobromide (0.2 or 0.5 mg/kg, intraperiton
141 Pretreatment with the muscarinic antagonist scopolamine hydrobromide (1.5-6 mg/kg) potentiated the r
142 he administration of the antimuscarinic drug scopolamine hydrobromide (4 microg/kg intravenously) com
144 r received subcutaneous injections of either scopolamine hydrobromide (SCOP; 0.5 mg/0.2 mL) or saline
147 und 7z was active in reversing the effect of scopolamine in the novel object recognition (NOR) paradi
151 tetradecanoyl tyramine (DU-14) could reverse scopolamine induced amnesia in rats in a passive avoidan
153 fold, and produced a significant blockade of scopolamine-induced amnesia as measured by a passive avo
154 dinyl benzilate binding, in vivo reversal of scopolamine-induced behavioral deficits, and subsequentl
155 antly, pretreatment with verapamil prevented scopolamine-induced behavioral responses and BDNF-tropom
157 These temporal relationships suggest that scopolamine-induced changes in gene expression and synap
159 ther assessed for their ability to attenuate scopolamine-induced contextual memory impairment in mice
160 benzilate binding) and in vivo (reversal of scopolamine-induced dementia) as potential agents for th
171 investigated the effects of microinfusion of scopolamine into the medial septum (MS Scp) on hippocamp
172 by direct infusion of neostigmine, MLA, and scopolamine into the OB during olfactory behavioral task
173 e cholinergic muscarinic receptor antagonist scopolamine into the rat perirhinal cortex during differ
174 al hippocampus increased errors of omission, scopolamine into the ventral hippocampus decreased sampl
175 ssed and bipolar populations have found that scopolamine is also effective at reducing depression and
177 anism for studying the anxiolytic effects of scopolamine, its mechanisms of action and side effects.
179 symptoms, the muscarinic receptor antagonist scopolamine manifested antidepressant effects that were
180 hese experiments, rats received infusions of scopolamine methyl bromide (10 microg/0.5 microl) into t
181 the orthosteric radioligands, [N-methyl-(3)H]scopolamine methyl chloride (M(2) pEC(50,diss) = 6.73 +/
182 s were determined using a l-[N-methyl]-[(3)H]scopolamine methyl chloride competition binding assay in
183 lly active muscarinic antagonist) but not by scopolamine methylbromide (a peripherally restricted mus
186 ile mecamylamine and prazosin had no effect, scopolamine, methysergide and MDL 72222 partially antago
190 trometorphan (NMDA receptor antagonist), and scopolamine (muscarinic receptor antagonist) blocked rap
191 ognition sites of nAChR (e.g., mecamylamine, scopolamine, N-methylspiperone and ketanserin) had no ef
193 tidepressant responses to the antimuscarinic scopolamine occurred in currently depressed patients who
194 (fMRI) to study the effects of lorazepam and scopolamine on a face-name associative encoding paradigm
197 zed the effects of systemically administered scopolamine on movement-induced theta and gamma rhythms
201 uscarinic receptor antagonists (atropine and scopolamine) on clonidine-elicited nitrite release was m
207 Individuals were randomized to a placebo/scopolamine or scopolamine/placebo sequence (series of 3
208 e muscarinic cholinergic receptor antagonist scopolamine or the nicotinic cholinergic receptor antago
210 ontrolled-environment chamber or to systemic scopolamine, or by performing extraorbital lacrimal glan
211 ing 1 week later, the effects of intraseptal scopolamine, oxotremorine, and muscimol were tested in a
214 were randomized to a placebo/scopolamine or scopolamine/placebo sequence (series of 3 placebo sessio
216 beta-endorphin analgesia on either measure, scopolamine produced small (23%) and transient (30 min)
218 c acetylcholine receptor (mAChR) blockade by scopolamine produces similar anti-parkinsonian effects.
219 n which subjects were pretreated with either scopolamine, quinpirole, or a combination of the two dru
220 sults demonstrate that a single, low dose of scopolamine rapidly increases mTORC1 signaling and the n
222 thermore, applying the muscarinic antagonist scopolamine reduced attentional modulation, whereas the
224 hen saline was administered, suggesting that scopolamine reduced encoding of the testing enclosure.
227 P<.001 for both) after the administration of scopolamine, relative to baseline, and these effects per
228 monstrate that the antidepressant actions of scopolamine require mTORC1 signaling and are associated
231 ere given 0.3 mg/kg MK-801 (M) and 1.0 mg/kg scopolamine (S) alone or combined (M-S) before or 45 min
232 nd an emerging literature that characterizes scopolamine's effects on neurobiological systems beyond
233 pressant response are considered in light of scopolamine's pharmacokinetic properties and an emerging
234 mecamylamine (MECA) and antimuscarinic agent scopolamine (SCOP) and were tested on a comprehensive ba
235 lel studies have found that intrahippocampal scopolamine (Scop) blocks contextual fear conditioning.
236 uction was inhibited by applying transdermal scopolamine (scop) patches to the depilated midtail of f
237 M. E. Hasselmo demonstrated that 0.25 mg/kg scopolamine (SCOP) selectively increased proactive inter
238 Nanoinjections of the mAChR antagonist, scopolamine (SCOP), in the rRPa of warm rats increased B
239 ane and other alkaloids, including atropine, scopolamine, scopoline, tropine, tropinone, and tyramine
242 humans; however, rats and mice administered scopolamine showed increased anxiety in standard behavio
243 n mouse brain for 42; however, blocking with scopolamine showed that uptake was not muscarinic cholin
244 th the administration of either lorazepam or scopolamine, significant decreases were observed in both
246 Both low (0.5 mM) and high (2.0 or 3.0 mM) scopolamine significantly decreased in-field firing rate
249 ersistence of the antidepressant response to scopolamine suggest a mechanism beyond that of direct mu
250 and FFA alterations in animals treated with scopolamine suggests that activation of muscarinic recep
251 ade of muscarinic acetylcholine receptors by scopolamine suppresses intake and may have anti-reward e
252 which produce compounds such as atropine and scopolamine, this reaction is known to be catalyzed by e
253 ArAT4 disrupted synthesis of hyoscyamine and scopolamine through reduction of phenyllactic acid level
255 on, 0.2 ms) in the presence of capsaicin and scopolamine (to inhibit 'sensory' and cholinergic nerves
257 The attenuation of lactate accumulation in scopolamine-treated rats suggests that TBI-induced musca
258 ther experiments showed that acute accumbens scopolamine treatment increased locomotor activity and r
262 en the preinjection and recovery trials when scopolamine was administered during the intervening inje
273 eptal lesions and rabbits receiving systemic scopolamine were significantly slower to condition than
274 hly effective against the amnestic action of scopolamine when tested in young-adult rats, these data
275 d after an intraperitoneal administration of scopolamine, which evokes ACh release by blocking autore
277 f the general muscarinic receptor antagonist scopolamine with single-cell recordings while monkeys pe
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