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At least 613 records · Page 34Linked to original sources
PubMed1991

The cholinergic REM induction test with RS 86 after scopolamine pretreatment in healthy subjects.

A shortened latency of rapid eye movement (REM) sleep is one of the most stable biological abnormalities described in depressive patients. According to the reciprocal interaction model of non-REM and REM sleep regulation, REM sleep disinhibition at the beginning of the night in depression is a consequence of heightened central nervous system cholinergic transmitter activity in relation to aminergic transmitter activity. A recent study has indicated that muscarinic supersensitivity, rather than quantitatively enhanced cholinergic activity, may be the primary cause of REM sleep abnormalities in depression. The present study tested this hypothesis by treating healthy volunteers for 3 days with a cholinergic antagonist (scopolamine) in the morning, in an effort to induce muscarinic receptor supersensitivity. On the last day of scopolamine administration, RS 86, an orally active cholinergic agonist, was administered before bedtime to test whether this procedure would induce sleep onset REM periods. Whereas scopolamine treatment tended to advance REM sleep and to heighten REM density in healthy controls in comparison to NaCl administration, the additional cholinergic stimulation did not provoke further REM sleep disinhibition. This result underlines the need to take a hypofunction of aminergic transmitter systems into account in attempts to explain the pronounced advance of REM sleep typically seen in depressives.

Adult↗
PubMed1986

Pretreatment of young mice with nerve growth factor enhances scopolamine-induced hyperactivity.

Twenty-one-day-old mice show a characteristic enhancement of locomotor activity upon injection of the cholinergic (muscarinic) blocking drug scopolamine. Intracerebral (third ventricle) injection of nerve growth factor (NGF) 24 h prior to scopolamine injection significantly enhances the drug-induced hyperactivity without modifying baseline activity. Such potentiation of the scopolamine effect was not obtained in 10-week-old mice treated and tested similarly.

Age Factors↗
PubMed1993

Scopolamine impairs recall of one-trial stimulus-reward association in monkeys.

Performance of three rhesus monkeys on a test of one-trial stimulus-reward association, in which recall intervals ranged from 0.5 to 6.5 min, was evaluated during nondrug-control conditions and following administration of the muscarinic-receptor blocker scopolamine. During control sessions, performance averaged 78% correct responses. Following administration of 10.0 and 17.8 micrograms/kg of scopolamine, performance fell significantly, to 69% and 63% correct responses, respectively. This dose-dependent impairment in recall was similar to the impairment we reported previously in recognition. Although the results thus failed to support a suggestion derived from behavioral electrophysiological findings that stimulus-reward association might be more vulnerable to scopolamine than stimulus recognition, they provide additional evidence for a cholinergic contribution to cognitive memory.

Animals↗
PubMed1996

The effects of different types of pre-training on the rat's retention performance in a swim-to-platform task following administration of scopolamine.

Previous research has found that centrally acting antimuscarinic drugs strongly impair the acquisition of a variety of learned behaviors in rats but have little effect on these same behaviors if training is given prior to drug treatment. We gave groups of rats different types of pre-training followed by treatment with scopolamine hydrobromide and subsequent testing on a simple swim-to-platform test. Factors such as practice in swimming without a platform to escape to, or learning to swim to a platform in a different apparatus or even to the test platform located in a different place did not protect the rats from the behavioral disruption produced by scopolamine. However, five training trials on the specific swim-to-platform task used in the retention test afforded almost complete protection against the effect of scopolamine. It appears that the protective effect of pre-training is highly specific and does not involve acquisition of some type of general rule which might survive antimuscarinic blockade.

Animals↗
PubMedDate not supplied

Effects of scopolamine on visual evoked potentials in aging and dementia.

The unusual combination of a normal pattern reversal VEP and a delayed flash VEP has been reported in patients with dementia of Alzheimer's type (DAT). Hyoscine hydrobromide has been reported to produce a similar VEP abnormality in young, healthy subjects. In the present study, we assessed the relative sensitivity of DAT patients and healthy young, middle-aged and elderly subjects to temporary cholinergic blockade. We report VEP latency values following 3 doses of scopolamine and after a peripheral anticholinergic agent. Flash P2 latency was not significantly slower in DAT patients than in the healthy elderly. Scopolamine increased P2 latency in the young controls but did not affect any other group. The pattern reversal P100 was normal in DAT, and a significant increase in latency occurred following scopolamine administration in both the control and patient groups.

Adult↗
PubMed1991

Scopolamine intoxication as a model of transient global amnesia.

In Colombia (South America) during recent decades the administration of scopolamine, extracted from plants belonging to the Datura or Brugmansia genus, has become an important neurologic and toxicologic phenomenon. These extracts have been popularly known as "Burundanga." Chemical characteristics and clinical features of scopolamine intoxication are described. Anterograde amnesia and submissive behavior found in patients intoxicated with scopolamine are analyzed. Burundanga intoxication is related to other toxic phenomena found in different countries and similitudes with transient global amnesia are emphasized.

Adult↗
PubMed1988

Scopolamine induces up-regulation of nicotinic receptors in intact brain but not in nucleus basalis lesioned rats.

The effect of chronic scopolamine treatment on muscarinic and nicotinic receptors in frontoparietal cortex in rats was investigated. Administration of the muscarinic antagonist, scopolamine (10 mg/kg i.p./day) for 21 days, produced a significant increase in the density of both muscarinic and nicotinic receptors by 27.7% and 12.1% respectively as measured by the specific binding of (-)-[3H]quinuclidinylbenzilate and (-)-[3H]-nicotine. There was no modification in the affinities for these ligands. Rats, bilaterally lesioned with ibotenic acid at the level of nucleus basalis of Meynert, which innervates the frontoparietal cortex, showed no up-regulation of cortical nicotinic receptors after chronic scopolamine treatment, suggesting the importance of the synaptic integrity in the regulation mechanism.

Animals↗
PubMed1989

Plasticity of brain muscarinic receptors in aging rats: the adaptative response to scopolamine and ethanol treatment.

Young and aged rats were treated chronically with ethanol or scopolamine. Muscarinic receptors were measured in cerebral cortex, hippocampus and striatum. Following scopolamine treatment muscarinic receptor density in cerebral cortex, hippocampus and striatum of young rats increased by 34, 57 and 27%, respectively; in brains of aged rats the increase was 41% in cerebral cortex, 43% in hippocampus and nil in striatum. Affinity of muscarinic receptors was not changed by scopolamine treatment. Following chronic ethanol administration there was a 48% increase in cortical muscarinic receptor density in young, but not aged rats. The density of muscarinic receptors in hippocampus and striatum of both young and aged rats was not affected by ethanol treatment. Affinity of receptors in hippocampus of aged, ethanol-treated rats was increased compared to age-matched controls. Adaptative responses of the muscarinic receptor/transducer system to neurotransmitter availability are present in both young and aged rats, both the ethanol-induced response is present only in young animals. This suggests differences in the mechanism of action of ethanol and receptor agonists and antagonists in modulating receptor plasticity.

Aging↗
PubMed1992

The long-acting cholinesterase inhibitor heptyl-physostigmine attenuates the scopolamine-induced learning impairment of rats in a 14-unit T-maze.

Heptyl-physostigmine (heptyl-Phy), a new carbamate derivative of physostigmine (Phy), has been assessed for potential clinical value by evaluating its in vitro activity against human erythrocyte acetylcholinesterase (AChE) and plasma butyrylcholinesterase (BChE), its duration of in vivo activity against rat plasma AChE, and its effects on attenuating a scopolamine-induced impairment in learning performance of young rats in a 14-unit T-maze. Heptyl-Phy demonstrated potent cholinesterase inhibition, with activity similar to that of Phy against AChE, IC50 values 21.7 +/- 2.0 nM and 27.9 +/- 2.4 nM, respectively, and significantly greater than that of Phy against BChE, IC50 values 5.0 +/- 0.1 nM and 16.0 +/- 2.9 nM, respectively. Heptyl-Phy achieved maximum AChE inhibition of 92.5% at 60 min and maintained a high and relatively constant inhibition for more than 8 h. For analysis of effects on learning performance, heptyl-Phy at 1.0, 1.5, 2.0 or 3.0 mg/kg, or vehicle was administered i.p. to 52 3-month-old male Fischer-344 rats 60 min prior to maze training. Thirty minutes prior to training, each animal received either 0.9% NaCl or scopolamine hydrochloride (0.75 mg/kg). Only a 2.0 mg/kg dose of heptyl-Phy significantly reduced the number of errors in scopolamine-treated rats. The other doses did not improve any aspect of maze performance. Although the therapeutic window of heptyl-Phy did not appear wide enough for clinical use, the longer duration of action of heptyl-Phy would appear beneficial.

Acetylcholinesterase↗
PubMed1996

Scopolamine augments c-fos and zip/268 messenger RNA expression induced by the full D(1) dopamine receptor agonist SKF-82958 in the intact rat striatum.

It is generally accepted that the widely used, partial dopamine D(1) receptor agonist, SKF-38393, does not induce immediate early gene expression in striatal projection neurons unless D(1) receptors are sensitized and uncoupled from D(2) receptors by 6-hydroxydopamine lesions or reserpine treatment. In contrast, this study demonstrates, using quantitative in situ hybridization, that the full D(1) receptor agonist, SKF-82958, induced robust expression of c-fos and zif/268 messenger RNAs in the intact rat striatum, especially in the entire shell and medial and ventral core areas of the nucleus accumbens and olfactory tubercle, and in the cerebral cortex, 45 min after one injection. The induction of the striatal immediate early genes is characterized by (i) induction in only medium-sized spiny neurons, (ii) dose-dependent induction, which correlates well with dose-dependent increases in motor activity, and (iii) blockade by the D(1) receptor antagonist, SCH-23390. The muscarinic cholinergic receptor antagonist, scopolamine, which itself did not alter striatal gene expression, profoundly augmented the behaviors and expression of the two immediate early genes in the ventral and dorsal striatum induced by 0.1, 0.5 and 2.0 mg/kg SKF-82958. However, scopolamine attenuated basal, and SKF-82958-stimulated, expression of c-fos and zif/268 messenger RNAs in the cortex. Scopolamine also enabled SKF-38393 to induce locomotor stimulation and c-fos and zif/268 messenger RNA expression in the normosensitive striatum of the rat when SKF-38393 alone caused no such changes. These data demonstrate an ability of SKF-82958 to induce immediate early gene messenger RNA expression in normosensitive dorsal and ventral striatum. Furthermore, intrinsic muscarinic receptor-mediated cholinergic transmission in the striatum may provide an activity-dependent inhibitory control on striatal D(1) receptor stimulation.

Animals↗
PubMed1995

Effects of ginsenosides on impaired performance induced in the rat by scopolamine in a radial-arm maze.

The effects of ginsenosides Rg1, Rd and Rb1 on impaired performance induced in the rat by scopolamine were examined in a radial-arm maze. Scopolamine caused a reduction in the number of initial correct responses in the maze. A single IP injection of Rg1, but not Rd or Rb1, prevented the reduction. The inhibition of the reduction in initial correct responses was associated with a bell-shaped dose-response curve for Rg1. A lesion in the medial septum caused spatial learning deficits. Rg1 did not overcome these deficits. It is suggested that cholinergic neurons in the medial septum are involved in the ameliorative effect of Rg1 on impaired performance induced by scopolamine.

Animals↗
PubMed1991

The effects of THA on scopolamine and nucleus basalis lesion-induced EEG slowing.

The effectiveness of THA (an anticholinesterae) on scopolamine (0.4 mg/kg) and nucleus basalis (NB) lesion-induced change in neocortical spectral electroencephalography (EEG) were investigated. Scopolamine increased the amplitudes of all the spectral components in waking-immobility. In the movement-related EEG spectral values, only the alpha power was increased. THA 7.5 mg/kg, but not THA 3 mg/kg, could reverse scopolamine-induced amplitude change. NB lesioning increased delta and theta amplitudes, but decreased beta amplitude. Delta amplitude was increased during movement recordings in NB-lesioned rats. THA 7.5 mg/kg and pilocarpine 10 mg/kg, but not THA 3 mg/kg, could partially reverse the increase of delta and theta amplitudes induced by NB lesions. However, the beta power decrease could not be restored with cholinomimetics. This study demonstrates that quantitative EEG activity analysis may reflect the THA-induced restoration of the function of the cholinergic nucleus basalis.

Acetylcholinesterase↗
PubMed1991

Modulation of EEG rhythmicity and spike activity in the rat hippocampus by systemically administered tetrahydroaminoacridine, scopolamine and atipamezole.

The hippocampal EEG recording electrodes were implanted bilaterally in the hilus of the dentate gyrus (DG) and the stratum radiatum layer of the CA1 area in young (2-3-month-old) and aged (17-20-month-old) rats. In the subgroups of rats, brain noradrenaline (NA) was depleted by DSP-4 neurotoxin (50 mg/kg, IP). The aged animals were included in DSP-4-lesioned group in order to diminish the plastic regeneration of the noradrenergic system which may be more effective in young subjects. All the EEG recordings, after the administration of different agents or vehicle, were made while rats were awake and immobile. Approximately 40% decrease of brain NA had no noticeable effects on the nonrhythmical hippocampal EEG in either age group. In all the rats, compared to the baseline recordings, scopolamine hydrobromide (2 mg/kg, IP, a muscarinic antagonist) increased the incidence of spontaneous EEG spikes, while tetrahydroaminoacridine (THA, 12.5 mg/kg, IP, an acetylcholine esterase inhibitor) decreased the spike activity and induced theta rhythm. Atipamezole (3 mg/kg, SC), a noradrenergic alpha 2-antagonist, increased the baseline amplitude of the nonrhythmical EEG in the DG and increased slightly the spike activity in the CA1 area. The combined blockade of muscarinic receptors by scopolamine (2 mg/kg) and noradrenergic alpha 2-receptors by atipamezole (3 mg/kg) resulted in irregular EEG pattern and corresponding power spectra differed from the scopolamine spectra. The last combination treatment suggests that the effect of atipamezole was not mediated by the secondary cholinergic activation. In the DG, the spectral power increase caused by atipamezole may be related to the increased excitability/bursting liability of granular cells because NA turnover is increased by this agent and NA increases the excitability of granular cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1993

Scopolamine injected into the rat amygdala impairs working memory in the double Y-maze.

Recent neurochemical results suggest the hypothesis that the nucleus basalis magnocellularis (nbm) cholinergic projection to the amygdala may play a role in memory. The present study investigated the effects of intra-amygdaloid injections of the cholinergic antagonist scopolamine on working and reference memory in the double Y-maze. Rats were pretrained until working and reference memory choice accuracy stabilized to a criterion of > or = 86% correct. Bilateral cannulae were then surgically implanted in the basolateral amygdaloid complex. Rats (n = 9) received scopolamine in doses of 8.0, 24.0, and 72.0 micrograms/0.5 microliter and saline (0.5 microliter) in a counterbalanced order with retraining to criterion between injections. Intra-amygdaloid scopolamine produced a dose-dependent and differential impairment of working and reference memory. A dose of 24.0 micrograms impaired working memory without significantly affecting reference memory; doses of 8.0 micrograms and 72.0 micrograms affected neither and both types of memory, respectively. Results implicate amygdaloid acetylcholine in memory.

Amygdala↗
PubMedDate not supplied

Scopolamine does not differentially affect Morris maze performance in adult rats exposed prenatally to alcohol.

Rats exposed prenatally to alcohol have shown deficits in spatial learning in radial-arm and Morris mazes. Prenatal exposure to alcohol in rats has also been shown to alter central nervous system (CNS) cholinergic function. Since cholinergic dysfunction disrupts spatial learning in normal rats, the present experiment assessed the role of putative prenatal alcohol-induced cholinergic dysfunction in spatial learning in rats. Pregnant rats were fed alcohol via liquid diet from gestation day 6 to 20. Control dams were pair-fed liquid diet without alcohol or fed ad lib lab chow and water. Group housed adult male and female offspring (postnatal days 110 to 135) were given scopolamine-HCl (0, 0.5, or 1.0 mg/kg/day) and tested in a Morris maze, with four trials per day for four days. A 15-s probe trial preceded testing on days 2-4. On day 5, the rats were given four trials to learn a new platform location. Scopolamine produced dose-dependent increases in latency to find the platform for all groups. There were no significant differences among prenatal treatment groups in scopolamine-induced shifts in performance. The results did not support the hypothesis that prenatal alcohol-induced CNS cholinergic dysfunction is related to spatial learning performance in these rats.

Animals↗
PubMed1993

Cognitive impairment following traumatic brain injury: the effect of pre- and post-injury administration of scopolamine and MK-801.

In order to examine the effectiveness of pre- and post-injury administration of muscarinic cholinergic and NMDA antagonists in reducing cognitive deficits following traumatic brain injury (TBI), rats were injected with either scopolamine (1 mg/kg) or MK-801 (0.3 mg/kg) 15 min prior to or 15 min after fluid percussion TBI. Cognitive performance was assessed with the Morris water maze procedure on days 11-15 after TBI or sham injury. When scopolamine and MK-801 were injected 15 min before injury, Morris water maze deficits were significantly reduced (P < 0.01 and P < 0.05, respectively). When scopolamine and MK-801 were injected 15 min after TBI, neither drug was effective in attenuating Morris water maze deficits. Consistent with other research, these results suggest that the cognitive deficits produced by TBI are the consequence of a brief period of excessive excitation of cholinergic and NMDA receptor systems. The results of this experiment also suggest that the temporal therapeutic window for the treatment of cognitive dysfunction with receptor antagonist intervention appears to be quite brief (< 15 min) in the rat.

Animals↗
PubMed2006

Post-training intra-striatal scopolamine or flupenthixol impairs radial maze learning in rats.

Systemic treatments with acetylcholine (ACh) or dopamine (DA) receptor antagonists during hours 0-4 but not during hours 5-8 following training on a radial arm maze (RAM) or lesions of the dorsal striata impair learning. This suggested that intra-striatal infusions of ACh or DA receptor antagonists during hours 0-4 following training may impair learning. Rats were randomly assigned to groups (ns=5-11) receiving dorsal striatal infusions of the ACh receptor antagonist scopolamine (0-18 microg/microL at 0 and 2h or at 4 and 6h after training), the DA receptor antagonist cis-flupenthixol (0-25 microg/microL at 0, 4 or 12h after training) or the inactive isomer trans-flupenthixol (6 microg/microL at 0 h after training). Scopolamine and cis-flupenthixol impaired the habit-learning version of the task. Given after hours 0-4 following training, the effects of scopolamine were diminished but those of cis-flupenthixol were not. Trans-flupenthixol produced less impairment than cis-flupenthixol. Results suggest that ACh and DA receptors in the dorsal striatum during hours 0-4 following training play a role in habit learning.

Acetylcholine↗
PubMed2006

Gomisin A improves scopolamine-induced memory impairment in mice.

Gomisin A is a component of the fruits of Schizandra chinesis which are widely used as a tonic in traditional Chinese medicine. In the present study, we assessed the effect of gomisin A on the learning and memory impairments induced by scopolamine. The cognition-enhancing effect of gomisin A was investigated using a passive avoidance test, the Y-maze test, and the Morris water maze test in mice. Drug-induced amnesia was induced by treating animals with scopolamine (1 mg/kg, i.p.). Gomisin A (5 mg/kg, p.o.) administration significantly reversed scopolamine-induced cognitive impairments in mice by the passive avoidance test and the Y-maze test (P<0.05), and also improved escape latency in the Morris water maze test at 5 mg/kg (P<0.05). Moreover, in an in vitro study, gomisin A was found to inhibit acetylcholinesterase activity in a dose-dependent manner (IC50 value; 15.5 microM). These results suggest that gomisin A may be a useful cognitive impairment treatment, and its beneficial effects are mediated, in part, via enhancing the cholinergic nervous system.

Acetylcholinesterase↗