Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SCOPOLAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed1986

Scopolamine effects on Hamilton search task performance in monkeys.

The Hamilton search task, a test of spatial memory, was given to adult monkeys after administration of scopolamine. Three monkeys had been exposed to lead during development and two were controls. The task consisted of opening eight boxes, one per trial, for food reinforcement, with a 20 second delay between trials. The monkey had to remember which boxes it had already opened and avoid them to obtain the remaining reinforcements. Percent correct response, openings-to-repeat, trials per session, repetitive index and response latency were measured. There were no significant lead-related effects. Significant scopolamine-induced deficits were detected with four of the measures. The low doses of scopolamine (1-3 micrograms/kg) did not affect response accuracy, but 15 and 30 micrograms/kg caused impairments. Only 30 micrograms/kg substantially increased latency. This is like other memory tests in monkeys and rats in that it is sensitive to anticholinergic challenge. Cognitive performance deficits were detected at a dose (15 micrograms/kg) which did not cause increased response latency. The Hamilton search task is a flexible and sensitive memory task for monkeys, analogous to the radial arm maze in the rat.

Animals↗
PubMed1986

Vinpocetine: nootropic effects on scopolamine-induced and hypoxia-induced retrieval deficits of a step-through passive avoidance response in rats.

Vinpocetine, vincamine, aniracetam, and Hydergine, compounds with purported cognition activating activity, were evaluated for their ability to prevent scopolamine-induced and hypoxia-induced impairment of passive avoidance retention (24 hr) in rats. Vinpocetine (peak effect dose [PED]= 200 mg/kg PO), aniracetam (PED = 100 mg/kg PO), vincamine (PED = 30 mg/kg PO), and Hydergine (PED = 1 mg/kg PO) prevented memory disruption by scopolamine. Vinpocetine (PED = 3 mg/kg PO) and aniracetam (PED = 30 mg/kg PO) were also effective in preventing disruption of passive avoidance retention impaired by 7% oxygen hypoxia. In contrast, Hydergine (0.05 to 3 mg/kg PO) and vincamine (0.3 to 100 mg/kg PO) were not effective against hypoxia-induced impairment. Hydergine at doses greater than 10 mg/kg PO markedly impaired motor function. In both tests the protection was dose-related for all test substances in an inverted U-shaped manner. Mecamylamine (1, 3, 10 mg/kg SC), (-)-nicotine (0.1 to 0.4 mg/kg SC), apovincaminic acid (1-400 mg/kg PO) and pemoline (1-100 mg/kg PO) did not protect against memory impairment induced by either procedure. These data support the view that vinpocetine, a compound chemically distinct from the pyrrolidinones, has a cognitive activating ability as defined in models of both scopolamine-induced and hypoxia-induced memory impairment in rats.

Animals↗
PubMed1987

Effects of scopolamine on locomotor activity and metabolic rate in mice.

Reduction of metabolic rate occurs in rodents in response to intoxication with several chemicals, including amphetamine. In the present study, cholinergic mediation of locomotor activity and metabolic rate was investigated by measuring the effects of scopolamine on the frequency of photobeam breaks, the rate of CO2 production, and rectal temperature in unrestrained mice. Increasing doses of scopolamine (0, 0.3, 1.0, 3.0, and 10.0 mg/kg IP) increased locomotor activity over a 72-min observation period. CO2 production (as minute volume exhaled CO2, VECO2), measured simultaneously with locomotor activity, was suppressed equally at all doses of the drug. Rectal temperatures taken 72 min after scopolamine declined slightly in a dose-related manner. These results parallel earlier findings with d-amphetamine and suggest that divergent effects on metabolic rate and locomotor activity may be induced by centrally-acting compounds acting on more than one neurochemical system.

Animals↗
PubMed1989

Effects of scopolamine on extracellular acetylcholine and choline levels and on spontaneous motor activity in freely moving rats measured by brain dialysis.

The present study demonstrates the feasibility of measuring acetylcholine (ACh) and choline in perfusate samples collected by in vivo brain dialysis in the frontal cortex and hippocampus of freely moving rats in which spontaneous motor activity could be measured simultaneously. Systemically administered scopolamine increased the output of ACh about 10-fold and 20-fold in the frontal cortex and hippocampus, respectively. By contrast, scopolamine decreased the choline level in the extracellular fluid about 2-fold in both brain regions, possibly owing to enhanced choline uptake into the presynaptic nerve terminals. Scopolamine also increased spontaneous motor activity over the same time course as the changes in ACh and choline. These results indicate that the in vivo brain dialysis technique applied to freely moving rats may be useful in investigating ACh turnover and in studying the relation between cholinergic transmission and behavioral functions.

Acetylcholine↗
PubMed1990

Scopolamine produces locomotor stereotypy in an open field but apomorphine does not.

Both dopaminergic and nondopaminergic drugs produce hyperlocomotion in rats. Dopaminergic drugs also produce focused stereotypy (absence of locomotion and intense sniffing or licking/biting of a restricted area of the environment). Some drugs produce repetitive routes of locomotion; this phenomenon might represent a combination of hyperlocomotion and stereotypy. Scopolamine (an acetylcholine antagonist) and apomorphine (a dopamine agonist) both produce hyperlocomotion in rats; apomorphine also produces focused stereotypy but scopolamine does not. This research determines whether these drugs also produce locomotor stereotypy as measured by gamma. Scopolamine (0.5 and 2.0 mg/kg) produced locomotor stereotypy at both doses. Apomorphine (1.0, 2.0, and 3.0 mg/kg) failed to reliably produce locomotor stereotypy. Thus, there is not necessarily a relationship between the ability of a drug to produce focused stereotypy and the ability of the drug to produce locomotor stereotypy.

Animals↗
PubMed1991

Effect of a new cognition enhancer, alpha-glycerylphosphorylcholine, on scopolamine-induced amnesia and brain acetylcholine.

The present study investigates the effect of the administration of alpha-glycerylphosphorylcholine (alpha-GPC) on scopolamine-induced amnesia and on brain acetylcholine (ACh) levels and release in rats. The results indicate that alpha-GPC, when administered orally, reverses the amnesia caused by scopolamine in passive avoidance. The peak effect is observed using 600 mg/kg IG, 5 h before training. The effect of the drug is long lasting (up 30 h) in accordance with its pharmacokinetic characteristics. Since, alpha-GPC administered IG is cleaved within the gut mucosal cells to glycerophosphate and free choline, it is tempting to speculate that this drug acts by increasing the ACh precursor pool. This view is supported also by the observation that alpha-GPC partially counteracts the decrease of brain ACh levels elicited by scopolamine administration. The effect is observed in the hippocampus and cortex, but not in the striatum. Moreover, in ex vivo experiments, alpha-GPC is able to increase the amount of ACh released by rat hippocampus slices following potassium stimulation.

Acetylcholine↗
PubMed1991

The effects of scopolamine and cues to forget on pigeons' memory for time.

Pigeons were trained with a 0-s delayed symbolic matching-to-sample procedure to indicate whether a houselight sample stimulus was short (2 s) or long (8 s) by pecking a red or a green comparison stimulus. In Experiment 1, the pigeons received injections of scopolamine hydrobromide (0.015 mg/kg), or saline, and the delay interval was manipulated (0, 1, 3, and 9 s). Memory for time was significantly poorer following scopolamine injections than following saline injections. A significant choose-short bias was observed under scopolamine at delays as brief as 3 s, but not under saline. In Experiment 2, a brief postsample cue (a vertical or horizontal line) signaled whether the comparison stimuli would be presented or omitted on each trial. During training, comparison stimuli were always presented following the remember (R) cue, but never following the forget (F) cue. During testing, memory for time was significantly poorer on F-cue trials than on R-cue trials. A significant choose-short bias was observed on F-cue trials at the 5- and 10-s delays, but not on R-cue trials. The results suggest that anticholinergic blockade accelerates the rate at which memory for temporal events is foreshortened in working memory. This effect is similar to that produced by an explicit cue to forget the temporal sample.

Animals↗
PubMed1991

Naftidrofuryl oxalate, nootropic effects on the scopolamine- and the basal forebrain lesion-induced amnesia in rats.

We studied the effects of naftidrofuryl oxalate on scopolamine- and basal forebrain (BF) lesion-induced amnesia using passive avoidance and multiple T-maze tasks, in comparison with Ca-hopantenate and physostigmine in rats. In the passive avoidance task, one-week treatment with naftidrofuryl oxalate (12.5 and 25 mg/kg, IP) ameliorated BF lesion-induced amnesia. The multiple T-maze task was done with two training sessions per day for five continuous days. We measured the number of errors made from start box to goal box. Naftidrofuryl oxalate (12.5 mg/kg, IP, b.i.d.) and physostigmine (0.1 mg/kg, IP, b.i.d.) attenuated scopolamine- and BF lesion-induced amnesia. However, treatment with naftidrofuryl oxalate for one week failed to inhibit the decrease of the choline acetyltransferase induced by the BF lesion. Ca-hopantenate did not show attenuation of amnesia induced by the scopolamine or BF lesion. These results suggest that naftidrofuryl oxalate enhances the storage of spatial information, and that the nootropic effects of naftidrofuryl oxalate may be produced by an indirect activation of the cholinergic system through serotonergic neuronal systems.

Amnesia↗
PubMed1992

Minaprine cancels scopolamine effects on the rat's acquisition of passive avoidance responses in two multitrial paradigms.

The antiamnesic activity of minaprine has been studied in male Wistar rats. Two multitrial paradigms were employed: the light-dark box test (aversive stimulus: 0.6-mA foot-shocks) and the tail-handling test (aversive stimulus: manual tail-handling). In both paradigms, intraperitoneal scopolamine administration 30 min before testing significantly impaired the acquisition of the passive avoidance conditioned response. There were no significant differences in either paradigm between control rats and those to whom scopolamine and minaprine were simultaneously administered. These results show that minaprine fully protects the acquisition process of conditioned responses against scopolamine impairment not only in one-trial tests but also in multitrial paradigms. The effects of minaprine in reversing memory deficits are discussed in relation to its stimulating activity on central cholinergic systems.

Amnesia↗
PubMed1992

Scopolamine suppresses both locomotion and object contact in a free-exploration situation.

It was recently reported by Buhot et al. that presession cholinergic disruption with scopolamine decreases time spent in proximity to novel objects while increasing locomotor behavior. Male Long-Evans rats (Rattus norvegicus, 80 days old) were given low-light access to an arena containing objects but were not forced to remain in the arena. On day 1, each subject was injected with saline (SAL). This session was used for familiarization with the apparatus and procedure. On days 2 and 3, four groups were given saline (SAL) or scopolamine (SCO, 1 mg/kg or 0.25 mg/kg), resulting in SAL-SAL, SAL-SCO, SCO-SAL, and SCO-SCO groups. Videotapes of these sessions were scored according to a standard protocol that allows separate quantification of locomotion, general activity, and object interaction behaviors. Scopolamine suppressed object investigation (both gross contact measures and indices of interaction character) whenever present. In contrast to Buhot et al. (using a forced-exploration situation), in this free-exploration context SCO also suppressed locomotor behavior. This study supports the conclusion that anticholinergics impair information gathering instead of affecting memory directly, which calls into question memory-related explanations of cholinergic treatments.

Acetylcholine↗
PubMed1992

Effect of oxiracetam on scopolamine-induced amnesia in the rat in a spatial learning task.

The effects of the nootropic agent 4-hydroxy-2-oxopyrrolidinoacetamide (oxiracetam) on memory and performance impairments induced by scopolamine were evaluated in the Morris water maze task. No effect was seen on the performance of rats when treated with oxiracetam (30 mg/kg, IP) alone. Task performance of scopolamine (0.2 mg/kg, SC)-treated rats was impaired as compared to that of control animals. The behavioral deficits expressed in the task by scopolamine treatment were attenuated by the same dose of oxiracetam.

Animals↗
PubMed1993

Scopolamine reversal of nicotine enhanced delayed matching-to-sample performance in monkeys.

The basis for the memory enhancing action of nicotine was evaluated in five adult monkeys (Macaca fascicularis) well trained in the performance of a delayed matching-to-sample (DMTS) paradigm. Nicotine (1.25-20 micrograms/kg, IM) produced a dose-dependent improvement in performance of the task. The optimal dose of nicotine for each monkey also improved performance when the animals were tested 24 h later in the no-drug situation. In the same animals, low doses of scopolamine produced a dose-dependent decrement in DMTS performance. A subthreshold dose (defined by DMTS performance decrement) of scopolamine was administered 20 min prior to the optimal dose of nicotine. Scopolamine pretreatment completely blocked the enhanced performance observed earlier with nicotine. The results of this study are consistent with the hypothesis that the enhanced cognitive performance associated with nicotine is due to central acetylcholine release and subsequent muscarinic receptor stimulation.

Acetylcholine↗
PubMed1993

Behavioral effects of neonatal treatment with clomipramine, scopolamine, and idazoxan in male rats.

It has been suggested that REM sleep deprivation due to the administration of clomipramine, during early developmental stages, results in dramatic behavioral changes during adulthood. One of the main alterations is the impairment of masculine sexual behavior (MSB). Clomipramine increase monoaminergic availability at the synaptic level and also suppresses REM sleep. This study was performed to compare the effect on masculine sexual behavior of three different neonatal treatments: clomipramine, which increases monoaminergic availability at the synaptic level and suppresses REM sleep; scopolamine, a cholinergic antagonist that suppresses REM sleep; and idaxozan, a selective adrenergic agonist. Subjects (Ss) were treated neonatally and tested for masculine sexual behavior during adulthood with standard techniques. Results obtained with clomipramine administration showed a marked impairment of MSB, mainly reflected by the decrease in the percentage of active Ss and the decrease in the percentage of Ss reaching ejaculation. In contrast, idaxozan and scopolamine produce a facilitation of MSB. The effect of idaxozan was not significantly different when compared to saline control rats. The effect of scopolamine was greater, and the percentage of Ss reaching ejaculation was significantly larger than saline control. These results suggest that the alterations of sexual behavior induced with neonatally administered clomipramine are not due to early REM sleep deprivation. As idaxozan did not replicate clomipramine results, it is also possible that noradrenergic transmission is not involved in the generation of these effects. It remains possible that the serotonin system could be responsible for the impairment of sexual behavior due to neonatal clomipramine treatment.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed1993

Differential effects of scopolamine and mecamylamine on working and reference memory in the rat.

The effects of the muscarinic antagonist scopolamine (0.1-0.6 mg/kg, IP) and the nicotinic antagonist mecamylamine (1-10 mg/kg) were compared in T-maze alternation and discrimination tasks in the rat. Scopolamine dose dependently disrupted performance on the alternation task and potentiated the increase in errors made in controls when the delay between forced and choice runs was increased from 0 to 30 s. Mecamylamine disrupted performance at the 10-mg/kg dose only and dose dependently inhibited the increase in errors made in controls when the delay between forced and choice runs was increased to 30 s. In simple T-maze discrimination, only the 0.6-mg/kg dose of scopolamine disrupted performance of the task, while mecamylamine at both 5 and 10 mg/kg disrupted task performance. These results confirm that working memory tasks are more sensitive to central muscarinic blockade than reference memory tasks. They also demonstrate that in delay conditions working memory performance is enhanced following central nicotinic blockade while reference memory performance is disrupted. This suggests that centrally active muscarinic and nicotinic antagonists have dissociable effects on memory processes in the rat.

Animals↗
PubMed1994

The effects of scopolamine, diazepam, and lorazepam on working memory in pigeons: an analysis of reinforcement procedures and sample problem type.

Two groups of pigeons were trained on a delayed-matching-to-sample (DMTS) task with both identity and symbolic problems, that had either a) specific outcomes correlated (differential group) or b) outcomes uncorrelated (nondifferential group), for each correct sample-choice sequence. After reaching a criterion of 90% correct at the 0 s delay, subjects were tested under saline, methylscopolamine (0.03 mg/kg), scopolamine (0.007, 0.015, 0.03 mg/kg), diazepam (0.0, 1.0, 1.75, 2.5 mg/kg), and lorazepam (0.0, 0.5, 0.75, 1.0 mg/kg) at delays of 0 to 8 s. Scopolamine, diazepam, and lorazepam at all doses impaired performance in the nondifferential group; however, in the differential group, the medium and high doses of both scopolamine and lorazepam, and only the high dose of diazepam impaired performance. The differential outcomes procedure, relative to the nondifferential procedure, enhanced retention in the non-drug state and under these amnestic drugs. Impairments observed in the differential group were a result of decreased performance only on samples correlated with a secondary reinforcer (flashing hopper light); there was no decreased performance on samples correlated with a primary reinforcer (grain). Neither group showed any differences in performance as a function of identity versus symbolic problems in a nondrug or drug state.

Animals↗
PubMed1995

NS-3(CG3703), a TRH analog, ameliorates scopolamine-induced memory disruption in rats.

The effects of a metabolically stable TRH analog, N-[[(3R, 6R)-6-methyl-5-oxo-3-thiomorpholinyl]carbonyl]-L-histidyl-L- prolinamide tetrahydrate (NS-3, CG3703) on the scopolamine-induced memory disruption in maze performance tests were investigated in rats. a) In the delayed nonmatching-to-sample (DNMS) task using a T-maze, NS-3 (0.3 mg/kg) produced a significant reversal of the marginal disruption of choice accuracy induced by scopolamine (0.3 mg/kg) at the short (5 s) and long (120, 480 s) interval delays. Physostigmine (0.5 mg/kg) produced a significant reversal only at a 5-s interval delay. b) In the eight-arm radial maze task, NS-3 (0.3 mg/kg) significantly reversed the deficit of choice accuracy induced by scopolamine (0.3 mg/kg), whereas neither TRH (3-30 mg/kg) nor physostigmine (0.1-1 mg/kg) had any effect. The consistent reversal of these maze-learning performances by NS-3, but not by TRH or physostigmine, may be due to its potent enhancement of cholinergic and noradrenergic neuronal activities.

Animals↗
PubMed1994

Effects of vasoactive intestinal peptide (VIP) on scopolamine-induced amnesia in the rat.

The effects of vasoactive intestinal peptide (VIP) on spatial cognitive deficits induced in the rat by injections of scopolamine were examined in a radial arm maze. A single intraperitoneal (i.p.), subcutaneous (s.c.) or intracerebroventricular (i.c.v.) injection of VIP inhibited the reduction in the number of initial correct responses in rats with scopolamine-induced amnesia. The inhibition was associated with a bell-shaped dose-response curve. Thus, VIP appears to have an ameliorating effect on spatial cognitive deficits induced by scopolamine in the rat.

Amnesia↗
PubMed1993

The action of scopolamine on retrieval and memory storage in rats evaluated in the staircase maze.

Rats were trained to run on staircase stopping on the 3rd, 6th, 9th, and 12th steps (correct responses). Stopping on any other step was considered an error. The acute administration of scopolamine (1.5 mg/kg) 20 min before the trial caused a reduction of the correct responses. An interruption of the daily training for 20 days caused, in the controls, a 24% reduction of correct responses. A chronic administration of scopolamine, at doses over 10 mg/kg in the first 15 days of the no-training period, nullified the behavioral deterioration observed in the controls. The interpretation of these results is that scopolamine damages the retrieval process and blocks the spontaneous decay of memory, as was observed in the controls after 20 days of interruption of the daily training.

Animals↗