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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),
37                                              Scopolamine (0.001-1.0 mg/kg) administered subsequent to
38  the effects of microinfusion of 0.15 mug of scopolamine (0.075 mug of in 0.5 mul/side) in infralimbi
39 ocedures were used to examine the effects of scopolamine (0.1 and 0.5 mg/kg, i.p.) in male rats.
40                            Pretreatment with scopolamine (0.3 and 0.5 mg/kg, i.p.) produced a dose-re
41                                              Scopolamine (0.3 mg/kg) impaired both place and reversal
42 nately administered i.v. lorazepam (1 mg) or scopolamine (0.4 mg) in a double-blind, randomized, cros
43  either placebo, lorazepam (2 mg orally), or scopolamine (0.4 mg, i.v.).
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
46 aining days animals were administered either scopolamine (1.0 mg/Kg) or saline (1.0 ml/Kg).
47                     Muscarinic blockade with scopolamine (1.0 microg/side or 10.0 microg/side), but n
48 IPSCs by muscarine was completely blocked by scopolamine (10 microM), a muscarinic receptor antagonis
49                    The muscarinic antagonist scopolamine (10(-6) M) had no significant effect on the
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
60                                              Scopolamine (800 microM) also had an anxiolytic effect i
61     On the other hand, the microinjection of scopolamine (a muscarinic receptor antagonist) did not b
62       Effects of pilocarpine were blocked by scopolamine, a muscarinic antagonist.
63     Recent clinical studies demonstrate that scopolamine, a nonselective muscarinic acetylcholine rec
64          Clinical reports have revealed 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
67                           Similar to humans, scopolamine acted as an anxiolytic in individual behavio
68 dies to elucidate the specific mechanisms of scopolamine action.
69                                      Neither scopolamine administered into the dorsal or ventral hipp
70 as significant at the first evaluation after scopolamine administration (P< or =.002).
71                                              Scopolamine administration also produces an antidepressa
72            Change in BOLD response following scopolamine administration in overlapping areas in the m
73 tum nor did co-administration of SCH23390 or scopolamine affect the levels of PCP-induced striatal ce
74             The model analysis suggests that scopolamine affected both familiarity and recollection.
75                          Results showed that scopolamine affected responses to studied items, but not
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).
80                 Clinical studies report that scopolamine, an acetylcholine muscarinic receptor antago
81 gether with established medications, notably scopolamine and antihistamines.
82 ped and validated for the rapid detection of scopolamine and atropine in buckwheat foods.
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
87             Similar to the AT(4) antagonist, scopolamine and mecamylamine prevented acquisition of th
88                      The enhanced effects of scopolamine and muscimol produced by SAP are consistent
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
93 the MWM, when compared to respective vehicle-scopolamine and vehicle-saline groups.
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
96 intaining low humidity (<40%), injections of scopolamine, and air flow produced by a fan.
97         The muscarinic antagonists atropine, scopolamine, and tropicamide (1-2 microM) caused substan
98  long-acting antiemetics such as transdermal scopolamine, aprepitant, and/or palonosetron.
99 rate that the antidepressant-like effects of scopolamine are mediated by GABA interneurons in the med
100                              Hyoscyamine and scopolamine are synthesized in the roots of specific gen
101       The tropane alkaloids, hyoscyamine and scopolamine, are medicinal compounds that are the active
102 osteric, extracellular site, and atropine or scopolamine as orthosteric building blocks, both connect
103                                Intrastriatal scopolamine at a concentration of 62 mM, but not 6.2 mM,
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
106          Neither the cholinergic antagonists scopolamine, atropine or mecamylamine, nor a series of n
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
110 eceive the muscarinic cholinergic antagonist scopolamine before fMRI scanning.
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
115                           Conversely, methyl scopolamine, blocked the increased firing activity of no
116                        In contrast, systemic scopolamine blocks, whereas oxotremorine augments, AMPH-
117 (atropine, alpha-bungarotoxin (alpha-BTX) or scopolamine) blocks or attenuates ovulating events.
118 nist methiothepin, the muscarinic antagonist scopolamine, both drugs, or saline.
119  body in healthy young individuals without a scopolamine challenge.
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
122 h) were observed after the administration of scopolamine compared with placebo.
123                             l-[N-methyl-(3)H]scopolamine competition binding showed a preference of A
124                              Higher doses of scopolamine completely blocked the effects of arecoline.
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
127                               In particular, scopolamine did not affect the frequency with which reco
128                 Experiments also showed that scopolamine did not impair operant responding for a food
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
131                                              Scopolamine disrupted the learning of negative patternin
132                        In contrast, systemic scopolamine dose-relatedly increased LMA.
133                               Ketanserin and scopolamine each prevented the ability of SERT knockout
134                                          The scopolamine effects were dose dependent to an extent tha
135 -injury there was a significant reduction in scopolamine-evoked ACh release.
136  the 48-hr retention test is not impaired by scopolamine (Experiment 4).
137  shock therapy, sleep deprivation, ketamine, scopolamine, GLYX-13 and pindolol used in conjunction wi
138                                  The placebo/scopolamine group showed no significant change during pl
139 pendent synaptic and behavioral responses to scopolamine have not been determined.
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
143 ncluding intravenous infusions of placebo or scopolamine hydrobromide (4 microg/kg).
144 r received subcutaneous injections of either scopolamine hydrobromide (SCOP; 0.5 mg/0.2 mL) or saline
145                                              Scopolamine (hyoscine) is a muscarinic acetylcholine rec
146         Pre- and postoperative injections of scopolamine in a subset of monkeys revealed only subtle
147 und 7z was active in reversing the effect of scopolamine in the novel object recognition (NOR) paradi
148                                  Conversely, scopolamine increased aversive 'disgust' reactions elici
149                                              Scopolamine increased the time rats were stationary, but
150              Rodent studies demonstrate that scopolamine increases glutamate transmission and synapto
151 tetradecanoyl tyramine (DU-14) could reverse scopolamine induced amnesia in rats in a passive avoidan
152 t, Radial Arm Maze Test and AChE activity in scopolamine induced amnetic rats.
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
156 est the necessity of BDNF release in driving scopolamine-induced behavioral responses.
157    These temporal relationships suggest that scopolamine-induced changes in gene expression and synap
158                                         In a scopolamine-induced cognitive impairment model using Wis
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
161                                BQCA reverses scopolamine-induced memory deficits in contextual fear c
162                                              Scopolamine infused at 4.0 mug/kg intravenously produced
163                                              Scopolamine infusion profoundly reduced freezing in the
164                                              Scopolamine infusions directly before the retrieval stag
165                                              Scopolamine infusions profoundly impaired trace conditio
166                                 Furthermore, scopolamine injected before associative conditioning can
167                              To describe the scopolamine-injected subjects' data, the authors constru
168 t received infusion of saline into the MS or scopolamine into the cortex.
169                                              Scopolamine into the dorsal and ventral hippocampus incr
170                      Unilateral injection of scopolamine into the dorsal striatum augmented, and oxot
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
176                               This effect of scopolamine is not dependent on maturation of the cholin
177 anism for studying the anxiolytic effects of scopolamine, its mechanisms of action and side effects.
178             Within the retrosplenial cortex, scopolamine lowered PCP-induced apoptotic-like cell deat
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
184         Similar effects were not produced by scopolamine methylbromide, which fails to cross the bloo
185                                Injections of scopolamine, methylscopolamine, or saline were started a
186 ile mecamylamine and prazosin had no effect, scopolamine, methysergide and MDL 72222 partially antago
187                                     Finally, scopolamine microinjections localized to the caudal half
188        However, REM sleep was not reduced by scopolamine microperfusion in this same region, at a con
189 nctions, and learning abilities of mice in a scopolamine model of dementia.
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
192 160209 retarded dissociation of [3H]N-methyl scopolamine (NMS).
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
195                               The effects of scopolamine on attention, but not memory, in a delayed r
196          Further, we also found an effect of scopolamine on both cycling and behavior.
197 zed the effects of systemically administered scopolamine on movement-induced theta and gamma rhythms
198                             The influence of scopolamine on mTORC1 signaling was determined by analys
199              We conclude that the effects of scopolamine on place cells likely result from a combinat
200 ures, demonstrating an unambiguous effect of scopolamine on recognition memory.
201 uscarinic receptor antagonists (atropine and scopolamine) on clonidine-elicited nitrite release was m
202                                              Scopolamine only gave this effect when it was administer
203 n reward value--we found no effect of either scopolamine or mecamylamine.
204                        Following retraining, scopolamine or MK-801 were administered prior to session
205                                  Intraseptal scopolamine or muscimol impaired the choice accuracy of
206                     Pretreatment with either scopolamine or quinpirole increased staining in the late
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
209 onditioning, with either a mAChR antagonist (scopolamine) or saline.
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
212       The magnitude of treatment response to scopolamine (percentage of change in the Montgomery-Asbe
213                                          The scopolamine/placebo group also showed reductions in depr
214  were randomized to a placebo/scopolamine or scopolamine/placebo sequence (series of 3 placebo sessio
215 ine potentiation of CR responding altered by scopolamine pretreatment.
216  beta-endorphin analgesia on either measure, scopolamine produced small (23%) and transient (30 min)
217                                              Scopolamine produces rapid antidepressant effects and th
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
221               In vitro experiments show that scopolamine rapidly stimulates BDNF release and tropomyo
222 thermore, applying the muscarinic antagonist scopolamine reduced attentional modulation, whereas the
223                                              Scopolamine reduced both the rate of place cell discharg
224 hen saline was administered, suggesting that scopolamine reduced encoding of the testing enclosure.
225                    Unexpectedly, dialysis of scopolamine reduced locomotor activity, again duplicatin
226                                We found that scopolamine reduced overall neuronal firing rate and imp
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
229        Pretreatment with quinpirole, but not scopolamine, resulted in a markedly "patchy" pattern of
230                             A challenge with scopolamine revealed that ovariectomy-induced cognitive
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
240  muscarinic cholinergic receptor antagonist, scopolamine (SCP).
241 series of 3 placebo sessions and series of 3 scopolamine sessions).
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
245              In addition, both 6.2 and 62 mM scopolamine significantly augmented AMPH-stimulated PPD
246   Both low (0.5 mM) and high (2.0 or 3.0 mM) scopolamine significantly decreased in-field firing rate
247                       Presample infusions of scopolamine significantly impaired object recognition co
248                  The cholinergic antagonist, scopolamine, significantly reduces the delay to onset of
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
254 trolled environment chamber and administered scopolamine to induce experimental DED.
255 on, 0.2 ms) in the presence of capsaicin and scopolamine (to inhibit 'sensory' and cholinergic nerves
256 as non-dopaminergic treatments (diazepam and scopolamine) to examine non-specific effects.
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
259                         Atropine or N-methyl scopolamine treatment reduced the incidence of ictal bra
260 a low-humidity environment supplemented with scopolamine treatment.
261 was correlated with change in BOLD response (scopolamine vs baseline).
262 en the preinjection and recovery trials when scopolamine was administered during the intervening inje
263                     The anxiolytic effect of scopolamine was dose dependent and biphasic, reaching ma
264                               When 0.1 mg/kg scopolamine was given to young rats prior to arecoline,
265                               Accumbens core scopolamine was subsequently shown to reduce the amount
266                                     The drug scopolamine was used to block muscarinic acetylcholine r
267                                     Systemic scopolamine was without effect in an aversive trace cond
268                                     However, scopolamine was without effect in the aversive procedure
269                        Behavioral effects of scopolamine were assessed in BDNF Val/Met knock-in mice,
270 n barrier, demonstrating that the actions of scopolamine were centrally mediated.
271                               The actions of scopolamine were examined in the forced swim test in the
272                               The effects of scopolamine were further compared to those of the D(2)-l
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
276             However, postsample infusions of scopolamine with sample-to-infusion delays of up to 20 h
277 f the general muscarinic receptor antagonist scopolamine with single-cell recordings while monkeys pe

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