ライフサイエンスコーパス: scopolamine

1 tion or intravenous drugs (e.g., ketamine or scopolamine).

2 og/kg for atropine and 5.7-10.4microg/kg for scopolamine).

3 depression treated with parenteral doses of scopolamine.

4 fying patients who will respond favorably to scopolamine.

5 ion between the elements was not affected by scopolamine.

6 ntrolled environment chamber and to systemic scopolamine.

7 modified with subcutaneous administration of scopolamine.

8 ed to placebo, 0.5 mg scopolamine, or 0.6 mg scopolamine.

9 specifically the antidepressant efficacy of scopolamine.

10 d recognition memory after administration of scopolamine.

11 antidepressant and antianxiety responses to scopolamine.

12 s activity was reduced in subjects receiving scopolamine.

13 uced if cholinergic receptors are blocked by scopolamine.

14 showed only a minor trend to decrease after scopolamine.

15 n with intracerebroventricular injections of scopolamine.

16 visual images after administration of 0.4 mg scopolamine.

17 uption seen after systemic administration 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 es were blocked by the muscarinic antagonist scopolamine.

22 the cholinergic-muscarinic receptor blocker, scopolamine.

23 n by AMPH was blocked by 62, but not 6.2, mM scopolamine.

24 lease in the rapid antidepressant effects of scopolamine.

25 nd it ameliorated memory deficits induced by scopolamine.

26 necessary for the antidepressant actions of scopolamine.

27 he antidepressant-like behavioral effects of scopolamine.

28 ith the Met allele may be less responsive to scopolamine.

29 system to test anxiety-like compounds using scopolamine.

30 pendent mechanisms underlying the effects of scopolamine.

31 for the rapid antidepressant-like effects of scopolamine.

32 ttenuated the antidepressant-like effects of scopolamine.

33 Before each test, rats were injected with scopolamine (0, 0.03, or 0.1 mg/kg, intraperitoneally),

34 the effects of microinfusion of 0.15 mug of scopolamine (0.075 mug of in 0.5 mul/side) in infralimbi

35 ocedures were used to examine the effects of scopolamine (0.1 and 0.5 mg/kg, i.p.) in male rats.

36 nately administered i.v. lorazepam (1 mg) or scopolamine (0.4 mg) in a double-blind, randomized, cros

37 either placebo, lorazepam (2 mg orally), or scopolamine (0.4 mg, i.v.).

38 s predicted by the model, rats that received scopolamine (0.50 and 0.25 mg/kg) were more impaired at

39 nic mice to desiccating stress (subcutaneous scopolamine [0.5 mg/0.2 mL] 3 times a day, humidity < 40

40 aining days animals were administered either scopolamine (1.0 mg/Kg) or saline (1.0 ml/Kg).

41 Muscarinic blockade with scopolamine (1.0 microg/side or 10.0 microg/side), but n

42 IPSCs by muscarine was completely blocked by scopolamine (10 microM), a muscarinic receptor antagonis

43 The muscarinic antagonist scopolamine (10(-6) M) had no significant effect on the

44 eived intrabasolateral amygdala infusions of scopolamine (2.5 microg or 5.0 microg/0.5 microl) or sal

45 sample containing atropine (11.5 ug kg(-1)), scopolamine (2.8 ug kg(-1)) and apoatropine (7.5 ug kg(-

46 umbens infusion of the muscarinic antagonist scopolamine 3 hr before the testing session significantl

47 mpounds and some analogs with [(3)H]N-methyl scopolamine ([(3)H]NMS) and unlabeled acetylcholine (ACh

48 on the equilibrium binding of l-[3H]N-methyl scopolamine ([3H]NMS) to the five human muscarinic recep

49 drate (MLA) (20 mM) or muscarinic antagonist scopolamine (40 mM) together with neostigmine (20 mM) at

50 kg(-1)), Ro 25-6981 (1, 3 and 10 mg kg(-1)), scopolamine (5, 25 and 100 mug kg(-1)) or vehicle (contr

51 mmediate posttraining (but not delayed 2 hr) scopolamine (5.0 microg) blocked acquisition of food- an

52 -10 microg) NMDA antagonists, or muscarinic (scopolamine, 5 microg) or nicotinic (mecamylamine, 1 mic

53 administration of the muscarinic antagonist scopolamine (50 mg/kg) partially attenuates reserpine-me

54 Blocking scans with scopolamine (50 mug/kg) and the M(1)-selective agent AZD

55 ts who were not injected, those who received scopolamine (8 microg/kg) showed (a) overall impairment

56 Scopolamine (800 microM) also had an anxiolytic effect i

57 On the other hand, the microinjection of scopolamine (a muscarinic receptor antagonist) did not b

58 Effects of pilocarpine were blocked by scopolamine, a muscarinic antagonist.

59 nction, including systemic administration of scopolamine, a muscarinic-cholinergic receptor antagonis

60 apid and sustained antidepressant effects of scopolamine, a nonselective acetylcholine muscarinic rec

61 Recent clinical studies demonstrate that scopolamine, a nonselective muscarinic acetylcholine rec

62 Clinical reports have revealed that scopolamine, a nonselective muscarinic acetylcholine rec

63 ral intra-PR infusions with either saline or scopolamine, a nonselective muscarinic receptor antagoni

64 pair (A+B-) and then, under the influence of scopolamine, a novel odor pair (A-C+) with an overlappin

65 Similar to humans, scopolamine acted as an anxiolytic in individual behavio

66 dies to elucidate the specific mechanisms of scopolamine action.

67 Neither scopolamine administered into the dorsal or ventral hipp

68 as significant at the first evaluation after scopolamine administration (P< or =.002).

69 Scopolamine administration also produces an antidepressa

70 Change in BOLD response following scopolamine administration in overlapping areas in the m

71 tum nor did co-administration of SCH23390 or scopolamine affect the levels of PCP-induced striatal ce

72 The model analysis suggests that scopolamine affected both familiarity and recollection.

73 Results showed that scopolamine affected responses to studied items, but not

74 he potential of this methodology to quantify scopolamine alongside sister tropane alkaloid atropine,

75 pine recapitulated the place-cell effects of scopolamine, although neither the mixture nor its separa

76 hronic pretreatment with DU-14 could reverse scopolamine amnesia and/or enhance spacial memory in the

77 en field environments under the influence of scopolamine (an amnestic cholinergic antagonist) or vehi

78 ntagonist of the 5-HT receptor, 5-HT(2A)) or scopolamine (an antagonist of the muscarinic receptor).

79 Clinical studies report that scopolamine, an acetylcholine muscarinic receptor antago

80 gether with established medications, notably scopolamine and antihistamines.

81 ped and validated for the rapid detection of scopolamine and atropine in buckwheat foods.

82 C-MS) results found hallucinogenic alkaloids scopolamine and atropine in the quids, while scanning el

83 Pretreatment with the antimuscarinic drugs scopolamine and atropine was able to greatly suppress no

84 Pretreatment with scopolamine and AZD6088 significantly reduced the brain

85 were inhibited by systemic administration of scopolamine and exposure to an air draft for 12 days in

86 aged 6 to 8 weeks were treated with systemic scopolamine and exposure to an air draft for different l

87 he reproducibility varied from 11 to 38% for scopolamine and from 17 to 44% for atropine at levels ra

88 ntraluminal pressure that were eliminated by scopolamine and intrathecal lidocaine, suggesting an imp

89 Similar to the AT(4) antagonist, scopolamine and mecamylamine prevented acquisition of th

90 The enhanced effects of scopolamine and muscimol produced by SAP are consistent

91 was applied to compute receptor occupancy by scopolamine and nondisplaceable distribution volume.

92 of action of these effects by administering scopolamine and oxotremorine directly into the striatum

93 ALB/c mice were subcutaneously injected with scopolamine and placed in a daytime air-drying device fo

94 nterneurons in mPFC abolished the effects of scopolamine and prevented scopolamine induction of synap

95 nces and similarities between the effects of scopolamine and quinpirole on D(1) agonist-induced Fos e

96 NF Met/Met mice have attenuated responses to scopolamine and that anti-BDNF antibody infusions into t

97 However, scopolamine and tropicamide also produced increases in n

98 the MWM, when compared to respective vehicle-scopolamine and vehicle-saline groups.

99 ecording electrodes, we infused nonspecific (scopolamine) and specific (methoctramine, pirenzepine) a

100 nightshade-specific tropane (l-hyoscyamine, scopolamine) and steroidal alkaloids (alpha-solanine, al

101 intaining low humidity (<40%), injections of scopolamine, and air flow produced by a fan.

102 The muscarinic antagonists atropine, scopolamine, and tropicamide (1-2 microM) caused substan

103 long-acting antiemetics such as transdermal scopolamine, aprepitant, and/or palonosetron.

104 rate that the antidepressant-like effects of scopolamine are mediated by GABA interneurons in the med

105 Hyoscyamine and scopolamine are synthesized in the roots of specific gen

106 The tropane alkaloids, hyoscyamine and scopolamine, are medicinal compounds that are the active

107 osteric, extracellular site, and atropine or scopolamine as orthosteric building blocks, both connect

108 nonselective muscarinic receptor antagonist scopolamine as well as the more subtype-selective antago

109 Intrastriatal scopolamine at a concentration of 62 mM, but not 6.2 mM,

110 contrast, microinjections of the antagonist scopolamine at all sites in NAc shell suppressed sucrose

111 holinergic receptor antagonists atropine and scopolamine (atr/scop) produce an amnesic syndrome in hu

112 Neither the cholinergic antagonists scopolamine, atropine or mecamylamine, nor a series of n

113 nt with cholinergic enhancement of encoding, scopolamine attenuated the formation of distinct spatial

114 icrog per side) of the muscarinic antagonist Scopolamine augmented adrenocorticotropin and corticoste

115 Scopolamine augmented extinction across exposure session

116 ation of the muscarinic receptor antagonist, scopolamine, augments, whereas the muscarinic receptor a

117 eceive the muscarinic cholinergic antagonist scopolamine before fMRI scanning.

118 ine is a key intermediate in hyoscyamine and scopolamine biosynthesis that is produced by the condens

119 erence with the sample object trace and that scopolamine blocked the acquisition of this interfering

120 the selective muscarinic receptor antagonist scopolamine blocked the convulsions and prevented increa

121 Conversely, methyl scopolamine, blocked the increased firing activity of no

122 nd 5 healthy subjects completed the baseline-scopolamine blocking protocol.

123 In contrast, systemic scopolamine blocks, whereas oxotremorine augments, AMPH-

124 (atropine, alpha-bungarotoxin (alpha-BTX) or scopolamine) blocks or attenuates ovulating events.

125 nist methiothepin, the muscarinic antagonist scopolamine, both drugs, or saline.

126 body in healthy young individuals without a scopolamine challenge.

127 ric agonists, which do not improve memory in scopolamine-challenged mice in contextual fear condition

128 Equivalent experiments were performed using scopolamine (cholinergic antagonist) as this drug blocks

129 h) were observed after the administration of scopolamine compared with placebo.

130 l-[N-methyl-(3)H]scopolamine competition binding showed a preference of A

131 ial anxiety-reducing (anxiolytic) effects of scopolamine could have great clinical implications for h

132 teral intracerebral injections of 3.5 microg scopolamine did not affect intake stimulated by intrahyp

133 In particular, scopolamine did not affect the frequency with which reco

134 Experiments also showed that scopolamine did not impair operant responding for a food

135 Single drug exposures to methiothepin or scopolamine did not noticeably affect the directional ch

136 y impaired after bilateral microinjection of scopolamine directly into the perirhinal cortex, but not

137 Scopolamine disrupted the learning of negative patternin

138 ther investigation is warranted with varying scopolamine dosages.

139 In contrast, systemic scopolamine dose-relatedly increased LMA.

140 Ketanserin and scopolamine each prevented the ability of SERT knockout

141 The scopolamine effects were dose dependent to an extent tha

142 -injury there was a significant reduction in scopolamine-evoked ACh release.

143 , the finding that the antimuscarinic agent, scopolamine, exerts fast-onset and sustained antidepress

144 the 48-hr retention test is not impaired by scopolamine (Experiment 4).

145 We evaluated the effectiveness of scopolamine for attenuating context renewal of phobic fe

146 iosynthetic pathway of medicinal TAs such as scopolamine, from simple carbon and nitrogen sources in

147 shock therapy, sleep deprivation, ketamine, scopolamine, GLYX-13 and pindolol used in conjunction wi

148 The placebo/scopolamine group showed no significant change during pl

149 n conductance response at context renewal in scopolamine groups relative to the placebo group was con

150 pendent synaptic and behavioral responses to scopolamine have not been determined.

151 tal Day 12 and tested under the influence of scopolamine hydrobromide (0.2 or 0.5 mg/kg, intraperiton

152 Pretreatment with the muscarinic antagonist scopolamine hydrobromide (1.5-6 mg/kg) potentiated the r

153 he administration of the antimuscarinic drug scopolamine hydrobromide (4 microg/kg intravenously) com

154 ncluding intravenous infusions of placebo or scopolamine hydrobromide (4 microg/kg).

155 r received subcutaneous injections of either scopolamine hydrobromide (SCOP; 0.5 mg/0.2 mL) or saline

156 Scopolamine (hyoscine) is a muscarinic acetylcholine rec

157 Noninvasive and well-tolerated scopolamine impaired hippocampal processes and augmented

158 Scopolamine impaired performance on a cognitive task of

159 Pre- and postoperative injections of scopolamine in a subset of monkeys revealed only subtle

160 und 7z was active in reversing the effect of scopolamine in the novel object recognition (NOR) paradi

161 Conversely, scopolamine increased aversive 'disgust' reactions elici

162 Scopolamine increased the time rats were stationary, but

163 Rodent studies demonstrate that scopolamine increases glutamate transmission and synapto

164 tetradecanoyl tyramine (DU-14) could reverse scopolamine induced amnesia in rats in a passive avoidan

165 t, Radial Arm Maze Test and AChE activity in scopolamine induced amnetic rats.

166 Both CP-101,606 and scopolamine induced similar positive biases in decision-

167 fold, and produced a significant blockade of scopolamine-induced amnesia as measured by a passive avo

168 isodic/working memory in both time-delay and scopolamine-induced amnesia paradigms in the novel objec

169 antly, pretreatment with verapamil prevented scopolamine-induced behavioral responses and BDNF-tropom

170 est the necessity of BDNF release in driving scopolamine-induced behavioral responses.

171 These temporal relationships suggest that scopolamine-induced changes in gene expression and synap

172 In a scopolamine-induced cognitive impairment model using Wis

173 ther assessed for their ability to attenuate scopolamine-induced contextual memory impairment in mice

174 BQCA reverses scopolamine-induced memory deficits in contextual fear c

175 hed the effects of scopolamine and prevented scopolamine induction of synaptic plasticity.

176 Scopolamine infused at 4.0 mug/kg intravenously produced

177 Scopolamine infusion profoundly reduced freezing in the

178 Scopolamine infusions directly before the retrieval stag

179 Scopolamine infusions profoundly impaired trace conditio

180 Furthermore, scopolamine injected before associative conditioning can

181 To describe the scopolamine-injected subjects' data, the authors constru

182 t received infusion of saline into the MS or scopolamine into the cortex.

183 Scopolamine into the dorsal and ventral hippocampus incr

184 Unilateral injection of scopolamine into the dorsal striatum augmented, and oxot

185 investigated the effects of microinfusion of scopolamine into the medial septum (MS Scp) on hippocamp

186 by direct infusion of neostigmine, MLA, and scopolamine into the OB during olfactory behavioral task

187 e cholinergic muscarinic receptor antagonist scopolamine into the rat perirhinal cortex during differ

188 al hippocampus increased errors of omission, scopolamine into the ventral hippocampus decreased sampl

189 ssed and bipolar populations have found that scopolamine is also effective at reducing depression and

190 This effect of scopolamine is not dependent on maturation of the cholin

191 anism for studying the anxiolytic effects of scopolamine, its mechanisms of action and side effects.

192 Scopolamine led to lower skin conductance response at lo

193 Within the retrosplenial cortex, scopolamine lowered PCP-induced apoptotic-like cell deat

194 symptoms, the muscarinic receptor antagonist scopolamine manifested antidepressant effects that were

195 Scopolamine-mediated reduction was significantly reverse

196 hese experiments, rats received infusions of scopolamine methyl bromide (10 microg/0.5 microl) into t

197 ction of muscarinic cholinergic antagonists, scopolamine methyl bromide or quinuclidinyl benzilate, o

198 the orthosteric radioligands, [N-methyl-(3)H]scopolamine methyl chloride (M(2) pEC(50,diss) = 6.73 +/

199 s were determined using a l-[N-methyl]-[(3)H]scopolamine methyl chloride competition binding assay in

200 lly active muscarinic antagonist) but not by scopolamine methylbromide (a peripherally restricted mus

201 Similar effects were not produced by scopolamine methylbromide, which fails to cross the bloo

202 Injections of scopolamine, methylscopolamine, or saline were started a

203 ile mecamylamine and prazosin had no effect, scopolamine, methysergide and MDL 72222 partially antago

204 Finally, scopolamine microinjections localized to the caudal half

205 However, REM sleep was not reduced by scopolamine microperfusion in this same region, at a con

206 nctions, and learning abilities of mice in a scopolamine model of dementia.

207 trometorphan (NMDA receptor antagonist), and scopolamine (muscarinic receptor antagonist) blocked rap

208 ognition sites of nAChR (e.g., mecamylamine, scopolamine, N-methylspiperone and ketanserin) had no ef

209 160209 retarded dissociation of [3H]N-methyl scopolamine (NMS).

210 tidepressant responses to the antimuscarinic scopolamine occurred in currently depressed patients who

211 (fMRI) to study the effects of lorazepam and scopolamine on a face-name associative encoding paradigm

212 The effects of scopolamine on attention, but not memory, in a delayed r

213 Further, we also found an effect of scopolamine on both cycling and behavior.

214 zed the effects of systemically administered scopolamine on movement-induced theta and gamma rhythms

215 The influence of scopolamine on mTORC1 signaling was determined by analys

216 We conclude that the effects of scopolamine on place cells likely result from a combinat

217 ures, demonstrating an unambiguous effect of scopolamine on recognition memory.

218 uscarinic receptor antagonists (atropine and scopolamine) on clonidine-elicited nitrite release was m

219 Scopolamine only gave this effect when it was administer

220 n reward value--we found no effect of either scopolamine or mecamylamine.

221 Following retraining, scopolamine or MK-801 were administered prior to session

222 Intraseptal scopolamine or muscimol impaired the choice accuracy of

223 Pretreatment with either scopolamine or quinpirole increased staining in the late

224 Individuals were randomized to a placebo/scopolamine or scopolamine/placebo sequence (series of 3

225 e muscarinic cholinergic receptor antagonist scopolamine or the nicotinic cholinergic receptor antago

226 onditioning, with either a mAChR antagonist (scopolamine) or saline.

227 speaking were randomized to placebo, 0.5 mg scopolamine, or 0.6 mg scopolamine.

228 ontrolled-environment chamber or to systemic scopolamine, or by performing extraorbital lacrimal glan

229 ing 1 week later, the effects of intraseptal scopolamine, oxotremorine, and muscimol were tested in a

230 The magnitude of treatment response to scopolamine (percentage of change in the Montgomery-Asbe

231 The scopolamine/placebo group also showed reductions in depr

232 were randomized to a placebo/scopolamine or scopolamine/placebo sequence (series of 3 placebo sessio

233 ine potentiation of CR responding altered by scopolamine pretreatment.

234 beta-endorphin analgesia on either measure, scopolamine produced small (23%) and transient (30 min)

235 Scopolamine produces rapid antidepressant effects and th

236 c acetylcholine receptor (mAChR) blockade by scopolamine produces similar anti-parkinsonian effects.

237 n which subjects were pretreated with either scopolamine, quinpirole, or a combination of the two dru

238 sults demonstrate that a single, low dose of scopolamine rapidly increases mTORC1 signaling and the n

239 In vitro experiments show that scopolamine rapidly stimulates BDNF release and tropomyo

240 thermore, applying the muscarinic antagonist scopolamine reduced attentional modulation, whereas the

241 Scopolamine reduced both the rate of place cell discharg

242 hen saline was administered, suggesting that scopolamine reduced encoding of the testing enclosure.

243 Unexpectedly, dialysis of scopolamine reduced locomotor activity, again duplicatin

244 We found that scopolamine reduced overall neuronal firing rate and imp

245 P<.001 for both) after the administration of scopolamine, relative to baseline, and these effects per

246 monstrate that the antidepressant actions of scopolamine require mTORC1 signaling and are associated

247 Pretreatment with quinpirole, but not scopolamine, resulted in a markedly "patchy" pattern of

248 A challenge with scopolamine revealed that ovariectomy-induced cognitive

249 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

250 nd an emerging literature that characterizes scopolamine's effects on neurobiological systems beyond

251 pressant response are considered in light of scopolamine's pharmacokinetic properties and an emerging

252 (Withania somnifera) restores memory loss in scopolamine (SC)-induced mice.

253 mecamylamine (MECA) and antimuscarinic agent scopolamine (SCOP) and were tested on a comprehensive ba

254 lel studies have found that intrahippocampal scopolamine (Scop) blocks contextual fear conditioning.

255 uction was inhibited by applying transdermal scopolamine (scop) patches to the depilated midtail of f

256 M. E. Hasselmo demonstrated that 0.25 mg/kg scopolamine (SCOP) selectively increased proactive inter

257 Nanoinjections of the mAChR antagonist, scopolamine (SCOP), in the rRPa of warm rats increased B

258 ane and other alkaloids, including atropine, scopolamine, scopoline, tropine, tropinone, and tyramine

259 muscarinic cholinergic receptor antagonist, scopolamine (SCP).

260 series of 3 placebo sessions and series of 3 scopolamine sessions).

261 humans; however, rats and mice administered scopolamine showed increased anxiety in standard behavio

262 n mouse brain for 42; however, blocking with scopolamine showed that uptake was not muscarinic cholin

263 th the administration of either lorazepam or scopolamine, significant decreases were observed in both

264 In addition, both 6.2 and 62 mM scopolamine significantly augmented AMPH-stimulated PPD

265 Both low (0.5 mM) and high (2.0 or 3.0 mM) scopolamine significantly decreased in-field firing rate

266 Presample infusions of scopolamine significantly impaired object recognition co

267 The cholinergic antagonist, scopolamine, significantly reduces the delay to onset of

268 duce the medicinal alkaloids hyoscyamine and scopolamine, starting from simple sugars and amino acids

269 ersistence of the antidepressant response to scopolamine suggest a mechanism beyond that of direct mu

270 and FFA alterations in animals treated with scopolamine suggests that activation of muscarinic recep

271 ade of muscarinic acetylcholine receptors by scopolamine suppresses intake and may have anti-reward e

272 which produce compounds such as atropine and scopolamine, this reaction is known to be catalyzed by e

273 ArAT4 disrupted synthesis of hyoscyamine and scopolamine through reduction of phenyllactic acid level

274 trolled environment chamber and administered scopolamine to induce experimental DED.

275 on, 0.2 ms) in the presence of capsaicin and scopolamine (to inhibit 'sensory' and cholinergic nerves

276 as non-dopaminergic treatments (diazepam and scopolamine) to examine non-specific effects.

277 ther experiments showed that acute accumbens scopolamine treatment increased locomotor activity and r

278 Atropine or N-methyl scopolamine treatment reduced the incidence of ictal bra

279 a low-humidity environment supplemented with scopolamine treatment.

280 at catalyzes the oxidation of hyoscyamine to scopolamine via two separate reactions: hydroxylation fo

281 was correlated with change in BOLD response (scopolamine vs baseline).

282 en the preinjection and recovery trials when scopolamine was administered during the intervening inje

283 The anxiolytic effect of scopolamine was dose dependent and biphasic, reaching ma

284 Accumbens core scopolamine was subsequently shown to reduce the amount

285 Scopolamine was used in 34 FVE and 24 CAE, with no assoc

286 The drug scopolamine was used to block muscarinic acetylcholine r

287 Systemic scopolamine was without effect in an aversive trace cond

288 However, scopolamine was without effect in the aversive procedure

289 Both biperiden and scopolamine were also able to reverse a haloperidol-indu

290 The LOQs for atropine and scopolamine were around 0.4 and 1.2 ug/kg in cereal prod

291 Behavioral effects of scopolamine were assessed in BDNF Val/Met knock-in mice,

292 n barrier, demonstrating that the actions of scopolamine were centrally mediated.

293 The actions of scopolamine were examined in the forced swim test in the

294 The effects of scopolamine were further compared to those of the D(2)-l

295 eptal lesions and rabbits receiving systemic scopolamine were significantly slower to condition than

296 hly effective against the amnestic action of scopolamine when tested in young-adult rats, these data

297 gonist, CP-101,606 and muscarinic antagonist scopolamine which have both been shown to have RAAD effe

298 d after an intraperitoneal administration of scopolamine, which evokes ACh release by blocking autore

299 However, postsample infusions of scopolamine with sample-to-infusion delays of up to 20 h

300 f the general muscarinic receptor antagonist scopolamine with single-cell recordings while monkeys pe