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PubMed1991

N-methyl-D-aspartate antagonists and working memory performance: comparison with the effects of scopolamine, propranolol, diazepam, and phenylisopropyladenosine.

The effects of the competitive N-methyl-D-aspartate (NMDA) antagonists CPP (5 & 10 mg/kg) and NPC 12626 (25 & 40 mg/kg) and the noncompetitive NMDA antagonists phencyclidine (1, 3, & 6.25 mg/kg) and MK 801 (0.1 & 0.2 mg/kg) on performance of rats on a nonspatial delayed matching-to-sample working memory task were evaluated. At the highest dose, each NMDA antagonist reduced choice accuracy at all retention intervals. In contrast, the reference anticholinergic agent scopolamine selectively reduced accuracy at long retention intervals, suggesting that scopolamine but not the NMDA antagonists directly interfered with time-dependent working memory retention. Propranolol, diazepam, and phenylisopropyladenosine had little or no effect on choice accuracy, suggesting that noradrenergic, gamma-aminobutyric acid-diazepam, and adenosine receptors may be relatively unimportant for working memory performance as assessed in this task. The NMDA antagonists also differed from scopolamine in that doses of NMDA antagonists that reduced response accuracy also reduced response probability, altered bias (competitive antagonists only), and increased intertrial interval responding (noncompetitive antagonists only). It was concluded that NMDA antagonists disrupt cognitive functions including, but not limited to, those required for accurate working memory performance.

Amino Acids↗
PubMed1998

Reactivation treatment prevents the memory-impairing effects of scopolamine in preweanling rats.

The authors report that the expression of a conditioned odor aversion is impaired in preweanling rats when they are conditioned on Postnatal Day 12 and tested under the influence of scopolamine hydrobromide (0.2 or 0.5 mg/kg, intraperitoneal) after a 48-hr, but not after a 2-hr, retention interval (Experiment 1). This effect of scopolamine is not dependent on maturation of the cholinergic system between Days 12 and 14 (Experiment 2), nor is it due to peripheral mechanisms (Experiment 3). When pups are reexposed to the unconditioned stimulus (footshock) before drug administration, performance on the 48-hr retention test is not impaired by scopolamine (Experiment 4). These findings demonstrate that the cholinergic system may be critical for the retrieval and expression of long-term or weak memories in young rats. However, the expression of active memories (recent or recently reactivated) may not be dependent on the cholinergic system to the same extent as is the expression of inactive memories.

Age Factors↗
PubMed1985

Intraseptal scopolamine has differential effects on Pavlovian eye blink and heart rate conditioning.

The effects of intraseptal scopolamine hydrobromide injections on Pavlovian (classical) conditioning were evaluated, with tones used as the conditioned stimulus (CS) and a periorbital electric shock train as the unconditioned stimulus (UCS). Eye blink (EB) and heart rate (HR) conditioned responses were concomitantly recorded. Although injections of scopolamine into the medial septum impaired the acquisition of the Pavlovian conditioned eyelid reflex, these injections enhanced the magnitude of accompanying Pavlovian conditioned HR decelerations. However, scopolamine applied to the lateral septal area had no effect on EB conditioning, relative to the vehicle, but, like medial injections, enhanced the magnitude of the accompanying HR decelerations. These results are compatible with those of previous investigations: Medial septal dysfunction impairs somatomotor conditioning but leaves autonomic conditioning intact, and septal dysfunction produces a parasympathetic bias of the cardiovascular system.

Animals↗
PubMed1975

Effects of hippocampal microinjections of D-amphetamine and scopolamine on active avoidance behavior in rats.

Rats received bilateral injections of 20 or 40 mug. of d-amphetamine or scopolamine into the dorsal or ventral hippocampus prior to each of 8 daily training sessions in a discriminated Y-maze active avoidance task. Scopolamine, but not d-amphetamine, facilitated avoidance responding in both sites, with the effect being greatest following administration of 20 mug. into the dorsal hippocampus. On Days 9 and 10, all animals received saline injections and were tested for transfer of responding to the nondrug state. A decrement of performance occurred irrespective of whether the drug had facilitated avoidance responding. The performance changes were greater following termination of scopolamine than d-amphetamine injections, and in no case were so great as those previously reported following peripheral injections of the drugs.

Animals↗
PubMed1975

Attenuation of "acute" habituation by scopolamine in the black-tailed prairie dog (Cynomys ludovicianus).

The hypothesis after scopolamine attenuates habituation occurring within a training session as well as that occurring between training sessions was tested and confirmed. Scopolamine injections (.5 mg/kg) reduced spontaneous wheel running in the prairie dog. The same dosage did not affect the threshold for wheen running induced by electrical brain stimulation (EBS). Another experiment demonstrated that EBS-induced running declined during a 10-min. stimulation period and indicated that the decline was habituative since the response was repeatedly dishabituated. In a final experiment .5 mg/kg of scopolamine reduced habituation of EBS-induced wheel running during 10-min. sessions.

Animals↗
PubMed1984

Transdermal scopolamine, oral meclizine, and placebo in motion sickness.

The efficacy of transdermal scopolamine, oral meclizine, and placebo in protection against motion sickness was compared in a double-blind crossover study. Thirty-six healthy subjects were exposed to motion three times for 90 min in a ship-motion simulator. Transdermal applications were made and tablets were taken at least 12 and 2 hr before exposure to motion. Transdermal scopolamine provided better protection than placebo or meclizine. Dryness of mouth was the only side effect reported more frequently for one regimen, transdermal scopolamine.

Administration, Oral↗
PubMed1994

A double FDG/PET study of the effects of scopolamine in older adults.

Two consecutive positron emission scans were done in one session using a double injection method of [18F]2-fluoro-2-deoxyglucose administration to examine the effects of the antimuscarinic drug scopolamine on cerebral glucose metabolism in ten older adults. Scopolamine causes temporary memory impairment, and its effects have been used to model aspects of the cognitive impairment that occur in Alzheimer's disease (AD). Cortical metabolic rates of patients with AD have been reported to be depressed, especially in parietal, temporal, and frontal association areas. After scopolamine administration to the elderly volunteers, absolute and normalized glucose metabolic rates were depressed in prefrontal and occipital regions and increased in parietal-occipital cortical regions and a left middle temporal region. These changes in the older volunteers are generally not consistent with changes seen in AD. We conclude that deficits in muscarinic system function may contribute to some but not all of the hypometabolic changes seen in AD patients.

Brain↗
PubMed1999

Nociceptin/orphanin FQ and nocistatin on learning and memory impairment induced by scopolamine in mice.

1. Nociceptin, also known as orphanin FQ, is an endogenous ligand for the orphan opioid receptor-like receptor 1 (ORL1) and involves in various functions in the central nervous system (CNS). On the other hand, nocistatin is recently isolated from the same precursor as nociceptin and blocks nociceptin-induced allodynia and hyperalgesia. 2. Although ORL1 receptors which display a high degree of sequence homology with classical opioid receptors are abundant in the hippocampus, little is known regarding their role in learning and memory. 3. The present study was designed to investigate whether nociceptin/orphanin FQ and nocistatin could modulate impairment of learning and memory induced by scopolamine, a muscarinic cholinergic receptor antagonist, using spontaneous alternation of Y-maze and step-down type passive avoidance tasks in mice. 4. While nocistatin (0.5-5.0 nmol mouse-1, i.c.v.) administered 30 min before spontaneous alternation performance or the training session of the passive avoidance task, had no effect on spontaneous alternation or passive avoidance behaviours, a lower per cent alternation and shorter median step-down latency in the retention test were obtained in nociceptin (1.5 and/or 5.0 nmol mouse-1, i.c.v.)-treated normal mice. 5. Administration of nocistatin (1.5 and/or 5.0 nmol mouse-1, i.c.v.) 30 min before spontaneous alternation performance or the training session of the passive avoidance task, attenuated the scopolamine-induced impairment of spontaneous alternation and passive avoidance behaviours. 6. These results indicated that nocistatin, a new biologically active peptide, ameliorates impairments of spontaneous alternation and passive avoidance induced by scopolamine, and suggested that these peptides play opposite roles in learning and memory.

Animals↗
PubMed2002

Ultrasonographic evaluation of reticular motility in cows after administration of atropine, scopolamine and xylazine.

The goal of this study was to evaluate the effect of various dosages and routes of administration of atropine, scopolamine and xylazine on reticular motility in cows. Groups of five cows received atropine, scopolamine or xylazine at dosages varying from 0.01 to 0.20 mg/kg. The drugs were administered intramuscularly and intravenously; atropine was also given subcutaneously. A total of 17 trials, each using five cows, were carried out. Reticular motility was assessed for 3 min immediately prior to the administration of a drug and for 21 min after administration, and the latter period was divided into seven 3-min intervals. The motility was further assessed during 3-min periods every 10 min starting 28 min and ending 141 min after administration of a drug. During each 3-min interval, the number of reticular contractions or the occurrence of reticular atony was determined. Onset and duration of reticular atony were assessed. All three drugs inhibited reticular motility but onset varied with route of administration and dosage. As expected, the onset of reticular atony occurred most rapidly after intravenous administration of each drug, followed by intramuscular and subcutaneous administration. Reticular atony occurred 0-3.0 min after the intravenous administration of each drug and at all dosages except the lowest dosage of atropine. Atony lasted for 3-111 min. Reticular atony occurred 3-18 min and 9-15 min after intramuscular and subcutaneous administration, respectively. It lasted 32-108 min and 39-122 min for the intramuscular and subcutaneous routes, respectively. For each drug, higher dosages resulted in a more rapid onset and longer duration of reticular atony than did lower dosages. This study demonstrated that administration of atropine, scopolamine and xylazine results in reticular atony. Whether this has clinical relevance requires further investigation.

Adrenergic alpha-Agonists↗
PubMed2000

Effects of scopolamine on a novel choice serial reaction time task.

Rats were trained on a novel attentional task adapted from the five-choice serial reaction time test first developed by Carli et al. [1983; Behav. Brain. Res., 9, 361-80]. The novel task required rats to detect the occurrence of brief light flashes in one of two spatial locations following trial initiation by a lever press. Blank trials were interleaved with stimulus trials and the rat had to make a different response to indicate the absence of a light. Occasional light-alone trials were also presented in which the visual stimulus appeared without forewarning. Pre-exposure to food for 60 min prior to test increased response omissions for all trials and slowed correct response latency, but failed to significantly alter accuracy. A decrease in light-stimulus duration (1-0.4 s) decreased accuracy, increased the reporting of blank trials and the number of light-alone trial omissions. Scopolamine (0.03-0.1 mg/kg) and scopolamine methylbromide (0.1 mg/kg) failed to affect accuracy, but increased light-alone trial omissions and lengthened correct response latency. The results confirm that the novel task is able to distinguish between motivational and attentional manipulations, and imply that scopolamine affected performance via nonattentional mechanisms.

Animals↗
PubMed1996

Effects of Gastrodia elata and its active constituents on scopolamine-induced amnesia in rats.

The effects of the rhizome of Gastrodia elata Blume (Orchidaceae) (abbreviated as GE) and its active constituents on learning and memory by using the one-trial passive avoidance task were studied in rats. At the 1.0 g/kg dose administered for one week, the methanol extract of GE significantly prolonged the shortened step-through latency induced by scopolamine in the passive avoidance task. Furthermore, at the 50.0 mg/kg dose administered for one week, the ethyl acetate and n-butanol fractions of the methanol extract prolonged the shortened step-through latency induced by scopolamine in rats. Gastrodin, isolated from the n-butanol fraction of the methanol extract, and p-hydroxybenzyl alcohol, isolated from the ethyl acetate fraction of the methanol extract, also significantly prolonged the shortened step-through latency induced by scopolamine on the passive avoidance task. These results suggested that gastrodin and p-hydroxybenzyl alcohol may be the active constituents of GE.

Amnesia↗
PubMed1998

[Toxic psychoses from atropine and scopolamine].

Psychoses caused by an intoxication with atropine or scopolamine are rarely published. Nevertheless atropine and scopolamine were being used in the ancient civilisations and are still in use today. The intoxication is characterised by dose-dependent and substance-dependent syndrome with specific central and peripheral symptoms. Atropine and scopolamine cause a central and peripheral anticholinergic blockade of the muscarine receptor. Psychiatric symptoms include restlessness, excitement, hallucinations, euphoria, disorientation but also stupor, coma and respiratory depression. History, pathophysiology and clinical symptoms of the intoxication due to the alkaloids of the solanaceae are presented. A review of literature is given and four own cases observed in one year are introduced.

Atropine↗
PubMed1982

Effects of scopolamine hydrobromide on the development of the chick and rabbit embryo.

When 100 or 200 microgram of scopolamine hydrobromide were injected into hen eggs after they had been incubated for 96 h the major malformations of the embryo found were gastroschisis, exencephaly, reduction deformities of the limbs, microphthalmia and buphthalmia when the eggs were opened on the 12th day of incubation. Eight foetuses of one of eight New Zealand white rabbit does given scopolamine hydrobromide at the rate of 473 microgram/kg in their drinking water from the 10th to the 14th day of gestation showed malformations consisting of microphthalmia, buphthalmia, exencephaly and hydrocephaly. A second doe which similarly received 520 microgram/kg of the hydrobromide had four malformed foetuses showing microphthalmia and had two foetuses which were resorbed. However, there were no malformations in foetuses of eight does given bolus doses of scopolamine hydrobromide ranging from 37 to 184 microgram/kg by intramuscular injection every 12 h from the 10th to the 14th day of gestation. Results indicate interference by the drug with the function of the cholinergic nerves on the development of the chick and rabbit embryo.

Animals↗
PubMed2004

Repeated exposure to low-level extremely low frequency-modulated microwaves affects baseline and scopolamine-modified electroencephalograms in freely moving rats.

PURPOSE: To compare in the electroencephalogram of rats the effects of scopolamine (an acetylcholine receptor antagonist) alone and after repeated exposure to low-level microwaves modulated at extremely low frequency. MATERIALS AND METHODS: Averaged frequency spectra (0.5-30 Hz) of the electroencephalogram were studied in freely moving rats with carbon electrodes implanted into the somatosensory cortex. The rats were repeatedly (3 days, 30 min day(-1)) exposed to low-intensity (approximately = 0.3 mW cm(-2)) microwaves (915 MHz, 20-ms pulse duration), amplitude modulated (square-wave) at extremely low frequency (4 Hz). RESULTS: The exposure to extremely low frequency microwaves alone significantly enhanced the fast electroencephalographic rhythms (18-30 Hz). This effect was observed neither in subsequent sham-exposure experiment nor in radiation-naïve animals. In the microwave-exposed rats, scopolamine (0.1 mg kg(-1), subcutaneously) did not cause a slowing in the electroencephalogram that was shown in non-exposed rats. A similarity between the scopolamine-induced electroencephalogram effect in the microwave-exposed rats and that of physostigmine (enhancing the acetylcholine level in the brain) in radiation-naïve animals was noted. This paradoxical phenomenon stimulates new experimentation for understanding its mechanism(s). CONCLUSIONS: The data obtained provide additional evidence that repeated low-level exposure to extremely low frequency microwaves can modify an activity of cholinergic system in the brain.

Animals↗
PubMed2005

Scopolamine treatment for severe extra-pyramidal signs following organophosphate (chlorpyrifos) ingestion.

BACKGROUND: The use of competitive inhibitors of acetylcholine other than atropine, for patients with organophosphate poisoning is controversial. Because scopolamine ability to cross the blood-brain barrier is better than that of atropine, it has been suggested that it should be used in patients with organophosphate poisoning who have central nervous system manifestations. CASE DESCRIPTION: A 17-year-old girl was admitted to the pediatric ward after ingesting chlorpyrifos as a suicidal attempt. She reported vomiting three times. She had no other symptoms for 12 hours and then over the course of 36 hours gradually developed extrapyramidal signs and became comatose. She was treated with intravenous scopolamine. Within 3 minutes the patient started to respond to verbal commands and answered simple questions rigidity subsided, and she was able to sit in bed. She was discharged after 4 days with no neurological sequelae. CONCLUSIONS: We suggest, that in patients with organophosphate poisoning who have mainly central nervous system toxicity scopolamine administration might be considered.

Adolescent↗
PubMedDate not supplied

Scopolamine poisoning from homemade 'moon flower' wine.

LH, a 76-year-old Caucasian male, ingested 3 teaspoons (15 mL) of a homemade wine over a 1-h period and became ill. Approximately 1.5 h later, he was taken to the emergency room of a local hospital with symptoms of respiratory distress and weakness. The plant used in making the wine was Angel's trumpet (Datura suaveolens), which reportedly contains varying amounts of scopolamine and atropine. A sample of the wine was collected and analyzed for these two compounds by reversed-phase HPLC chromatography using 97% methanol-3% deionized water. The filtered wine contained an estimated 29 mg scopolamine/mL, which produced a total ingested dose of 435 mg. No atropine was detected. The scopolamine was confirmed by TLC. An oral dose of 50 mg of atropine sulfate in humans has been reported fatal, but there is no reported fatal dose for scopolamine. The alcohol content and 3.8 pH of the homemade wine may have increased the extraction of this compound from the plant material, and the wine fermentation process may have concentrated the original extract.

Aged↗
PubMed1991

Scopolamine enhances expression of an amphetamine-conditioned place preference.

Animals in the present investigation were trained for conditioned place preference by pairing the non-preferred compartment of a two chamber apparatus with either 1.5 mg kg-1 D-amphetamine or 0.05 mg kg-1 scopolamine. Some of the amphetamine-conditioned rats were injected with 0.05 mg kg-1 scopolamine as an acute treatment on the test day which followed conditioning. Although the scopolamine by itself did not induce either a preference or an aversion to the drug-paired side, it enhanced the expression of place preference in animals conditioned with amphetamine. Potentiation of this conditioned response (CR) was observed in the absence of changes in locomotor activation which would implicate general arousal as a potential mechanism. Hypotheses regarding anticholinergic mediation of CR expression via central reward mechanisms, memory retrieval, cue function and stimulus saliency are discussed, and possible neurosubstrates considered.

Animals↗
PubMed2002

Scopolamine impairs eyeblink conditioning in cerebellar LTD-deficient mice.

We investigated the effect of the muscarinic acetylcholine receptor (mAChR) antagonist scopolamine on eyeblink conditioning in glutamate receptor subunit 62 null mice, which have severe impairments in cerebellar long-term depression (LTD). Mice were injected intraperitoneally with scopolamine (0.5 mg/kg) or saline, and conditioned using a delay paradigm with tone and periorbital shock but with no overlap between them. The saline-injected mutant mice learned this paradigm normally, as predicted from our previous study. When scopolamine was injected, learning was impaired more severely in the mutant mice than in the wild type mice. Basic sensory and motor performances were not affected. These results suggest that eyeblink conditioning in cerebellar LTD deficient mice depends largely on neural functions susceptible to blocking of mAChRs.

Animals↗