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At least 757 records · Page 42Linked to original sources
PubMed1965

DEVELOPMENT OF BEHAVIORAL COMPENSATION TO THE EFFECTS OF SCOPOLAMINE DURING FIXED-INTERVAL REINFORCEMENT.

Rats were injected with scopolamine before every daily session of water reinforcement on a fixed-interval (FI) schedule. Initially the drug decreased the rate of responding. Control injections of scopolamine following each session did not. Over 119 sessions, the typical FI performance developed more slowly in the animals drugged before the sessions. Their rates of responding increased from session to session, to a level slightly greater than that of the animals drugged after the sessions. Their rates did not increase. The effects of injections before the session were not duplicated by increasing the deprivation of animals drugged after the session.

Animals↗
PubMed2001

Determination of scopolamine, atropine and anisodamine in Flos daturae by capillary electrophoresis.

A capillary electrophoresis method was developed for the separation and determination of tropane alkaloids in Flos daturae plants. Separation was performed on a fused silica capillary(42.1 cm x 50 microm i.d.) at an applied voltage of 20 kV. Scopolamine, atropine and anisodamine were well separated in the buffer of 50 mmol/L phosphate buffer (pH 5.0) containing 20% (v/v) tetrahydrofuran (THF). Beer's law was obeyed in the range of concentration of 2.4-21.8 microg/mL for scopolamine, 4.0-36.0 microg/mL for atropine and 2.6-23.7 microg/mL for anisodamine, respectively, and the correlation coefficients were over 0.999 (n = 6). The developed method was applied for the analysis of herb samples.

Atropine↗
PubMed1976

Scopolamine's effect on passive avoidance behavior in immature rats.

Male albion rats ranging in age from 15-30 days were injected with either scopolamine hydorbromide or saline, prior to training and retention testing on a black-white passive avoidance (PA) task. Pretraining administration of a 1.0-mg/kg dose of scopolamine significantly increased the median number of trails to criterion for 18-, 21-, and 30-day-old rat pups when compared with their saline controls. Fifteen-day-olds showed drug-related PA deficits when a 2.0-mg/kg dose was given. Retention data reflect characteristic age-dependent memory loss over the 1-week acquistionretention period with no apparent state-dependent effects. The data suggest the presence of cholinergic inhibitory mediation of PA responding in preweanling and postweanling pups.

Age Factors↗
PubMed1976

Genetic and ontogenetic variations in locomotor activity following treatment with scopolamine or d-amphetamine.

Highly inbred mice of 3 strains (A/J, DBA/2J, and C57BL/6J) were tested in an open field at 14, 21, or 28 days of age. Ten minutes prior to testing, mice received treatment of saline, scopolamine (.5 or 1.0 mg/kg of body weight), or d-amphetamine (.5, 1.0, or 5.0 mg/kg). The d-amphetamine (5.0 mg/kg) increased activity in all strains at 14 days and 28 days of age, and at 21 days significantly increased activity in all except the C5BL/6. In contrast, increased activity with the scopolamine treatment was seen in DBA/2 at 21 days, but not in A and C57BL/6 until 28 days postnatally. The data support a caudal-rostral gradient of brain development with the inhibitory cholinergic system developing more slowly than the excitatory catecholamine system. In addition, strain-specific differences in activity levels are discussed in relation to the differential rates of chloinergic maturation.

Age Factors↗
PubMed2002

Verbal fluency facilitated by the cholinergic blocker, scopolamine.

This study was designed to explore putative facilitatory effects of low doses of scopolamine (SP) on phonemic (letter) and semantic (category) verbal fluency. A double-blind, parallel-group design was used with 36 subjects who completed a test battery before and 2 h after 0.6 mg or 1.2 mg of SP or placebo. Fluency measures included total number of words generated, clustering (the production of words within semantic or phonemic subcategories) and switching (the ability to shift efficiently to new subcategories). Low doses of scopolamine increased phonemic fluency, as has been shown previously. Semantic fluency was not increased by SP, although subjects treated with 1.2 mg of SP generated higher-frequency words. SP did not affect clustering or switching. It is suggested that phonemic and semantic fluency reflect distinct cognitive processes.

Adolescent↗
PubMed1993

Facilitation of adaptation and acute tolerance to stressful sensory input by doxepin and scopolamine plus amphetamine.

This work characterizes a new methodologic and pharmacologic approach to control terrestrial and space motion sickness (SMS). The experimental design allowed separate evaluation of drug action on susceptibility and adaptability, and used repeated measures to approximate the chronic stressful motion of microgravity. Daily exposure to cross-coupled angular acceleration for 5 consecutive days demonstrated that the efficacy of doxepin and scopolamine plus amphetamine in the prevention of autonomic system dysfunction was not only apparent on the first test day (P < .01), but was also evident in the substantially enhanced resistance developed over the 5-day test period (P < .01) as compared with placebo. This indicates that daily use of these medications does not diminish therapeutic efficacy (tolerance). The efficacy of doxepin was anticipated because it possesses pharmacologic properties similar to those of established anti-motion sickness drugs. Comparable efficacy after doxepin loading for 4 hours, 3 days, or 21 days suggests a mechanism distinct from its antidepressant effects, possibly related to its potent antihistaminergic actions. Use of doxepin has operational significance to the National Aeronautics and Space Administration, in comparison with current preparations of scopolamine plus amphetamine, because of doxepin's minimal impact on cognitive performance, and most importantly, its favorable pharmacokinetic profile, particularly its long half-life.

Adaptation, Physiological↗
PubMedDate not supplied

Transdermal scopolamine in motion sickness.

Motion sickness is a common clinical malady. Until recently, the use of scopolamine, the drug of choice for the treatment of motion-induced nausea and vomiting, has been sometimes associated with a variety of unacceptable side effects. These side effects could result from the unpredictable blood levels attained with oral dosage (pulse delivery). A new system of drug delivery, the transdermal therapeutic system (TTS)--Transderm-V--has been developed. The TTS delivers scopolamine across the skin at a constant rate. This permits a drug with a very short half life to be administered over prolonged periods, thereby maintaining blood concentrations at the defined therapeutic level. This precludes the necessity for frequent dosing and increases patient acceptability and compliance while minimizing the untoward effects associated with conventional dosage forms of the drug.

Administration, Topical↗
PubMed2002

A signal transduction pharmacodynamic model of the kinetics of the parasympathomimetic activity of low-dose scopolamine and atropine in rats.

We used a novel pharmacokinetic-pharmacodynamic (PK-PD) approach that had been applied for signal transduction kinetics to investigate the kinetics of the parasympathomimetic effect of scopolamine and atropine in rats. The parasympathetic tone was assessed by continuous measurement of the power of the high frequency band (HF) of electrocardiogram (ECG) R-R intervals obtained by power spectral analysis (PSA) of heart rate variability (HRV). To overcome the inherent noise of the HRV-HF data and to quantitatively identify temporal changes in the autonomic tone, a new approach of stepwise regression of the cumulative HF data was applied. The elevation of the parasympathetic tone occurred after a significant lag time (>70 min) following scopolamine administrations [0.25 and 0.5 mg/kg intravenous (iv) bolus or infusion over 100 min], followed by a gradual return to the baseline levels. A similar lag time in parasympathetic stimulation was observed following iv bolus administration of atropine (0.1 mg/kg). The plasma drug concentration versus time data were linked to the response versus time data using a signal transduction pharmacodynamic model that was fitted simultaneously to all four experimental data sets. This PK-PD model resolved the significant discrepancy between the concentration versus time and the response versus time patterns and successfully described the kinetics of the parasympathetic stimulation obtained for different drugs and different rates of administration. This work paves the way for further PK-PD preclinical investigations in this field.

Animals↗
PubMed1975

Submicrogram assay for scopolamine in plasma and urine.

A GLC-mass spectrometric method for scopolamine, sensitive to 50 pg/ml for a 4-ml plasma or urine sample, was developed. The method used a deuterated internal standard to minimize variability in absolute recovery in the extraction procedure. Scopoline and deuterated scopoline were formed from the base-catalyzed hydrolysis of scopolamine and the internal standard and were analyzed as the heptafluorobutyrates, using a GLC-mass spectrometric system by monitoring the m/e 138 and 141 fragments, respectively.

Chromatography, Gas↗
PubMed1995

Scopolamine selectively disrupts the acquisition of contextual fear conditioning in rats.

Muscarinic cholinergic antagonism produces learning and memory deficits in a variety of hippocampal-dependent tasks. Hippocampal lesions produce both acquisition deficits and retrograde amnesia for contextual fear conditioning, but do not impact fear conditioning to discrete cues. In order to examine the effects of muscarinic antagonism in this paradigm, rats were given scopolamine (1 mg/kg) either before or for 3 days after a Pavlovian fear-conditioning session in which tones were paired with aversive footshocks. Fear to the context and the tone was assessed by measuring freezing in separate tests. It ws found that pretraining, but not posttraining, scopolamine severely impaired contextual fear conditioning; tone conditioning was not affected under either condition (cf., Young, Bohenek, & Fanselow, Neurobiology of Learning and Memory, 63, 174-180, 1995).

Animals↗
PubMed1987

Promethazine, scopolamine and cinnarizine: comparative time course of psychological performance effects.

Single oral doses of promethazine (12.5 mg, 25 mg), scopolamine (0.6 mg), and cinnarizine (30 mg), were compared in a double-blind, placebo controlled trial. Twelve normal volunteers undertook a battery of psychological performance tests and a feeling state questionnaire, before drug administration, and at 2-h intervals after. Promethazine and cinnarizine significantly impaired psychomotor performance, information processing and feelings of alertness. With promethazine these reductions were maximal 3-4 h post-drug, with performance returning near to baseline 8-9 h post-drug. With cinnarizine these impairments were maximal 5-6 h post-drug, and performance remained depressed 8-9 h post-drug. Scopolamine significantly reduced feelings of alertness, and memory task performance; the overall performance effects were most evident 1-4 h post-drug.

Adolescent↗
PubMed1987

Antihistaminics enhance morphine-, but not amphetamine- and scopolamine-induced hyperactivity in mice.

Three histamine H1-receptor antagonists, chlorpheniramine, diphenhydramine and tripelennamine, were tested alone or in combination with morphine, amphetamine and scopolamine on locomotor activity in mice. All three antihistaminics, at some dosage levels, enhanced morphine-induced hyperactivity, but did not change or even reduce locomotor stimulation induced by amphetamine and scopolamine. The results suggest that H1-blocking agents may specifically interact, though not necessarily directly, with opiate mechanisms in producing behavioural effects.

Animals↗
PubMed1988

Age-related scopolamine effects on social and individual behaviour in rats.

The modulation of spontaneous (social and individual) behaviour as a function of the age of the rat (1, 3, 6, 12, 18 and 24 months) and of scopolamine dose (0.1, 0.2, 0.3 and 0.5 mg/kg) was studied. Observations were conducted during the dark phase of the reverse light/dark schedule using a reintroduction procedure. Results showed a marked effect of scopolamine on most of the behavioural patterns considered. Environmental interaction was enhanced whilst agonistic and social active interactions (social grooming) and play fighting were reduced by the drug. A slight hyposensitivity in the youngest rats and a marked hyposensitivity to the drug in the oldest ones were observed. The relationship to biochemical data and human sensitivity on the one hand and to learning and memory tasks and cholinergic specificity on the other hand, are discussed.

Aggression↗
PubMed1981

3H-methyl scopolamine binding to dispersed pancreatic acini.

Maximal amylase release occurred with 10(-5) M carbachol and slightly greater than half maximal response occurred with 3 x 10(-7) M carbachol in dispersed pancreatic acini. The preparation released more than 45% of its initial amylase content after 60 min of maximal carbachol stimulation. Electron microscopy revealed depletion of zymogen granules and the presence of secretory material in the ductules after carbachol stimulation. At 37 degrees C, maximal binding of methyl scopolamine occurred in about 45 min with 3 x 10(-10) M 3H-methyl scopolamine. The dissociation constant for 3H-methylscopolamine was 6.8 x 10(-10) M and saturation occurred at 109 pm/g protein. The I.C. 50 for 3H-methylscopolamine inhibition of carbachol-induced amylase secretion was 7 x 10(-10) M.

Amylases↗
PubMed1987

Effects of scopolamine and physostigmine on recognition memory in monkeys with ibotenic-acid lesions of the nucleus basalis of Meynert.

Monkeys with bilateral ibotenic-acid lesions of the nucleus basalis of Meynert, an area rich in cholinergic neurons that innervate the cerebral cortex, were compared with unoperated control monkeys on a recognition memory task. Although animals with large lesions had substantial reductions of cortical choline acetyltransferase activity, none showed impairment in the task. Lesion effects were observed, however, when performance was assessed following administration of a muscarinic receptor blocker (scopolamine) or a cholinesterase inhibitor (physostigmine). Although scopolamine produced dose-related impairments in both groups, this effect was greater in the experimental animals. Conversely, whereas physostigmine produced modest improvement in performance in the control group, no such improvement was observed in the experimental animals. The altered sensitivity to the mnemonic effects of cholinergic agents in the experimental group suggests that the cholinergic neurons of the nucleus basalis of Meynert contribute to recognition memory.

Acetylcholinesterase↗
PubMed1986

Selective potentiations in opioid analgesia following scopolamine pretreatment.

The effects of the muscarinic receptor antagonist scopolamine upon analgesia induced by D-ala-D-leu-enkephalin (DADL), beta-endorphin (BEND) and morphine were examined. While scopolamine (10 mg/kg, IP) significantly potentiated the analgesic responses following DADL (40 micrograms, ICV) and morphine (5 mg/kg, SC) on the jump test, it failed to alter significantly BEND (1 microgram, ICV) analgesia.

Animals↗
PubMed1991

RU 41,656 does not reverse the scopolamine-induced cognitive deficit in healthy volunteers.

The potential antagonism of a single oral dose of RU 41,656 10 mg on the memory and attention disturbances induced by scopolamine 0.6 mg s.c. have been investigated in a 3 period, placebo controlled, double blind, cross over study in 12 healthy, young volunteers. The effects of the compounds were evaluated by objective tests (Buschke selective reminding test, CFF, simple reaction time, tapping, arithmetical calculation) and subjective measurements (visual analogue scale, side effects questionnaire). Measurements were taken before treatment and 2, 4 and 7 h after RU 41,656. Scopolamine caused anterograde amnesia and sedative effects as which were not counteracted by RU 41,656.

Adult↗
PubMed1981

Amphetamine-, scopolamine- and caffeine-induced locomotor activity following 6-hydroxydopamine lesions of the mesolimbic dopamine system.

As previously reported, 6-hydroxydopamine (6-OHDA) lesions to the region of the nucleus accumbens blocked the locomotor activation induced by low doses of d-amphetamine, and produced a supersensitive locomotor response to the dopamine (DA) agonist, apomorphine. This same lesion, however, failed to block the locomotor activation induced by scopolamine or caffeine. These results suggest that scopolamine and caffeine activate locomotion in the rat by acting independently of presynaptic terminals in the mesolimbic DA system.

Animals↗