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 1,027 records · Page 57Linked to original sources
PubMed1994

The effects of physostigmine and scopolamine on memory for food caches in the black-capped chickadee.

The possible effects of anticholinesterases on the central nervous system and, in particular, on learning and memory, have generated considerable interest. Food caching in the black-capped chickadee is an excellent natural paradigm of spatial working memory. Its susceptibility to cholinergically active drugs was explored in the present study. Our ultimate objective was to use food caching as a natural paradigm for the study of the consequences in birds of sublethal exposure to anticholinesterase insecticides. Biochemical analyses showed that administration of the anticholinesterase physostigmine (eserine) led to a short-lived effect, with recovery of brain cholinesterase levels already underway 5 min after an intramuscular injection. Birds administered the anticholinergic scopolamine before caching demonstrated significantly impaired recall compared to birds given physostigmine. Birds given saline only had an intermediate performance. Giving the drugs between caching and recovery had no measurable effect. These findings suggest that effects of cholinergic agents on cache recovery in chickadees are comparable to their effects in tests of working memory in mammals.

Animals↗
PubMed1992

A threshold for the protective effect of over-reinforced passive avoidance against scopolamine-induced amnesia.

Acetylcholine-receptor blockers produce amnesia of aversively motivated behaviors. However, when animals are submitted to relatively high intensities of footshock (over-reinforcement), anticholinergic treatment does not induce memory impairments. The aim of this work was to determine whether the antiamnesic effect produced by increasing the magnitude of the negative reinforcer is gradually established or if a threshold should be reached to obtain such an effect. Wistar rats were trained in passive avoidance using 2.5, 2.6, 2.7, 2.8, 2.9 or 3.0 mA; 5 min after training they were given one systemic injection of scopolamine (8 mg/kg). An amnesic state was produced in the groups that were trained with the lower intensities (2.5-2.7 mA); with the three higher intensities near-perfect retention was evident. These results suggest that acetylcholine is critically involved in memory consolidation, and that by increasing the magnitude of the negative reinforcer, a threshold is reached where cholinergic activity of the nervous system is not necessary for the development of the consolidation process.

Animals↗
PubMed1993

D-cycloserine attenuates scopolamine-induced learning and memory deficits in rats.

The muscarinic antagonist scopolamine (SCOP; 1.0 mg/kg, ip) impaired both the acquisition of a learning task in the Morris water maze (MWM) and choice accuracy in the T-maze reinforced alternation procedure in rats. Acetylcholinesterase inhibitors (AChEIs) have been shown to attenuate these deficits. D-Cycloserine (DCS), a partial agonist at the strychnine-insensitive glycine site on the N-methyl-D-aspartate (NMDA) receptor complex, was investigated for its effects on SCOP-induced dementia in the MWM and T-maze paradigms. Combined administration of SCOP and DCS (3.0, 10.0, or 30.0 mg/kg, ip; 30 min pretreat) significantly reversed SCOP-induced deficits in the T-maze as measured by percentage correct choices. In addition, DCS (3.0 or 10.0 mg/kg, ip) significantly attenuated SCOP-induced deficits in the MWM as measured by latency to find the submerged platform. For comparison, the long-acting acetylcholinesterase inhibitor galanthamine (GAL) was tested in the T-maze (1.25, 2.5, or 5.0 mg/kg, ip) and the MWM (2.5 or 5.0 mg/kg, ip). GAL attenuated SCOP-induced deficits in both learning and memory models similar to DCS. These data suggest that the strychnine-insensitive partial glycine agonist, D-cycloserine, may be efficacious in disease states of central cholinergic hypofunction such as Alzheimer's disease.

Animals↗
PubMed1982

Long-term effects on motor activity induced by apomorphine or scopolamine after intracerebral injections of cycloheximide or glutamate shortly after hatching in chickens.

Compared to controls, bilateral forebrain injections of cycloheximide or glutamate in 2-day-old chicks resulted in significantly less activity in response to intraperitoneal injections of the dopaminergic agonist, apomorphine, or the cholinergic antagonist, scopolamine, when tested on stabilimeters four weeks later. These preliminary results are consistent with the idea that amongst other effects neonatal injections of cycloheximide or glutamate may alter dopaminergic and cholinergic neurotransmitter mechanisms involved in motor behavior in birds.

Animals↗
PubMed1991

Clonidine and scopolamine: differences and similarities in how they change human information processing.

1. Humans have been tested on a choice reaction time task designed to disclose interactions between stimulus complexity and drug effect. 2. Tests were carried out using oral scopolamine (1.2 mg) and clonidine (0.2 mg). 3. Reaction times and event related potentials were measured. 4. Both drugs slowed reaction time and the N1 component of the ERP. 5. SCOP slows RTs to easy-to-discriminate stimuli more than RTs to harder stimuli. Its effect on P3 is the same for both types of stimuli. 6. CLON tends to slow P3 latencies to easy stimuli more than P3 latencies to harder stimuli, while the RT slowing is almost identical for both types of stimuli.

Adult↗
PubMed1991

Pertussis toxin-sensitive G-protein mediates galanin's inhibition of scopolamine-evoked acetylcholine release in vivo and carbachol-stimulated phosphoinositide turnover in rat ventral hippocampus.

The effects of intracerebroventricular (i.c.v.) injections of pertussis toxin were investigated on the inhibitory action of galanin on acetylcholine release and phosphoinositide breakdown stimulated by muscarinic agents in rat ventral hippocampus. Pertussis toxin (0.6 micrograms, i.c.v., 96 h) counteracted the in vitro inhibitory effect of galanin (3.1 nmol) on phosphoinositide breakdown stimulated by carbachol without altering the stimulatory action of the cholinergic agonist on signal transduction, in miniprisms from rat ventral hippocampus. Pertussis toxin also abolished the in vivo effect of galanin on scopolamine-stimulated acetylcholine release in vivo but did not affect basal acetylcholine release. The results indicate that pertussis toxin-sensitive G-protein(s) mediates the galanin receptor regulation of pre- and postsynaptic cholinergic functions in the ventral hippocampus.

Acetylcholine↗
PubMed1996

Acute treatment with the N-methyl-D-aspartate receptor antagonist MK-801: effect of concurrent administration of haloperidol or scopolamine on preproenkephalin mRNA levels of the striatum and nucleus accumbens of the rat brain.

We injected rats three times at 3 h intervals (from 0900 h to 1500 h) with the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 at 0.1 or 0.5 mg/kg of body weight. Three hours after the last injection, animals were sacrificed and the brains were processed for in situ hybridization histochemistry. Preproenkephalin (PPE) mRNA levels were significantly decreased throughout the caudate-putamen (CPu) and nucleus accumbens (NAc) at the lower dose. The higher dose produced significant decreases only in anterior CPu (aCPu) and NAc. Concurrent administration of the muscarinic cholinergic receptor antagonist scopolamine at 2 or 5 mg/kg neither potentiated nor prevented the effect of MK-801 on PPE mRNA levels in the neostriatum. In contrast, co-administration of haloperidol (dopamine receptor antagonist) with MK-801 blocked the effect of the latter in the NAc, and elevated PPE mRNA levels throughout the CPu. The data demonstrate that the acute effects of glutamate receptor activity on striatal and accumbal PPE mRNA expression via the NMDA receptor can be modulated by the dopaminergic system in the brain of the rat.

Animals↗
PubMed1993

Protective effect of under-reinforcement of passive avoidance against scopolamine-induced amnesia.

Administration of antimuscarinic drugs induces amnesia of aversively motivated behaviors. However, when relatively high intensities of footshock are used during training (over-reinforcement), animals become protected against such amnesic state. Moreover, the protective effect is established in a none-or-all fashion, i.e., within a series of increasing intensities a minute augmentation of footshock intensity is sufficient to reach the protective threshold. In the present experiment it was found that very low intensities of aversive stimulation (under-reinforcement), sufficient to produce learning, also protected animals from scopolamine-induced amnesia. These results suggest that acetylcholine is critically involved in memory consolidation of passive avoidance, but only within a limited range of training intensities.

Amnesia↗
PubMed1996

Death rattle: an audit of hyoscine (scopolamine) use and review of management.

This study investigated the pattern and determinants of hyoscine (scopolamine) use for death rattle by a retrospective analysis of 100 consecutive deaths in a 22-bed hospice. Patient diagnoses, duration of stay, and doses and route of administration of hyoscine used in the final 48 hr before death were recorded. One-half of the patients received hyoscine in some form during the final 24 hr before death. Patients who were in the hospice for longer than 9 days and those with cerebral malignancy were given the highest doses of hyoscine in the final 24 hr (z = -2.558, P = 0.011, and z = -1.968, P = 0.048, respectively). Response to hyoscine appears to be variable, and a distinction is proposed between death while due to salivary secretions (type 1) and that due to bronchial secretions (type 2) to explain the observed patterns of use. It is likely that hyoscine is more efficacious in treating type 1 death rattle than it is in treating type 2 death rattle.

Aged↗
PubMed1995

Reversal of scopolamine induced amnesia in rats by the steroid sulfatase inhibitor estrone-3-O-sulfamate.

The intent of the study was to determine whether altering the metabolism of neurosteroids via blockade of the enzyme, steroid sulfatase, could enhance retention test performance in rats. The steroid sulfatase inhibitor estrone-3-O-sulfamate (EMATE) was administered alone and in combination with the neurosteroid dehydroepiandrosterone sulfate (DHEAS) to rats which were then tested for the reversal of scopolamine induced amnesia. EMATE enhanced the reversal of amnesia by DHEAS as measured by a passive avoidance test. When administered without DHEAS, as a single acute dose, EMATE had no effect. When administered without DHEAS over 10 consecutive days, however, EMATE significantly improved retention. These results suggest that steroid sulfatase inhibition can potentiate the memory enhancing properties of DHEAS. The study also suggests that increasing the levels of endogenous sulfated neurosteroids via the inhibition of steroid sulfatase activity may enhance learning and/or memory function.

Amnesia↗
PubMed2006

Improvement of cationic albumin conjugated pegylated nanoparticles holding NC-1900, a vasopressin fragment analog, in memory deficits induced by scopolamine in mice.

NC-1900, an active fragment analog of arginine vasopressin [arginine vasopressin-(4-9)], has proved to be capable of improving the spatial memory deficits and the impairments in passive avoidance test. In this study, a novel drug carrier for brain delivery, cationic bovine serum albumin conjugated pegylated nanoparticles (CBSA-NPs) holding NC-1900, was developed and its improvement on scopolamine-induced memory deficits was investigated in mice using the platform-jumping avoidance test. CBSA-NPs loaded with NC-1900 in spherical shape and uniform size below 100 nm were prepared by the double emulsion/solvent evaporation procedure, and the zeta potential of CBSA-NPs was about -8mV with the loading capacity of NC-1900 around 0.46%. The in vitro study showed that approximately 10% NC-1900 was released from CBSA-NPs in pH 7.4 phosphate buffer saline (PBS) during 56 h incubation with about 15% NC-1900 released in pH 4.0 PBS during 7 days, indicating the sustained release of this carrier. Furthermore, the half-life of NC-1900 loaded in CBSA-NPs in plasma was about 78 h, which was 4-fold longer than that of free NC-1900 (19 h). The active avoidance behavioral results showed that the s.c. administration of NC-1900 tended to improve memory deficits, but the difference did not present any statistical significance, whereas this peptide failed to produce any positive effects by i.v. administration. However, the i.v. injection of CBSA-NPs loaded with NC-1900 greatly improved memory impairments to a normal level, but the efficacy was slight if the loaded nanoparticles (NPs) were exclusive of the conjugation of CBSA, indicating that CBSA-NP was a promising brain delivery carrier for NC-1900 with CBSA as a potent brain targetor. It was concluded that CBSA-NP loaded with NC-1900 was potentially efficacious in the treatment of memory deficits via i.v. administration.

Animals↗
PubMed2005

The cholinesterase inhibitor, phenserine, improves Morris water maze performance of scopolamine-treated rats.

Male Fischer-344 rats (n = 38) at 5 months old were tested in a Morris water maze to determine if treatment with the cholinesterase inhibitor, phenserine (PHEN), would overcome a learning impairment induced by scopolamine (SCOP), a muscarinic cholinergic receptor antagonist. Each rat was randomly assigned to one of five groups to receive two intraperitoneal injections 60 and 30 min, prior to testing, respectively, as follows: (1) saline-saline (SAL); (2) saline-1.0 mg/kg (SCOP); (3) 2 mg/kg PHEN- SCOP (PHEN2); (4) 4 mg/kg PHEN-SCOP (PHEN4); and (5) 1 mg/kg PHEN-SAL (PHEN1). Maze testing occurred across 5 days with 4 days of acquisition trials (4 trials per day) and a fifth day consisting of a single 120 sec probe trial. PHEN1 and SAL were combined into one control (CON) group for purposes of statistical analysis for both acquisition and probe trials as comparison of the two groups revealed that they did not significantly differ on any measure. SCOP-treated rats were significantly impaired compared to CON in learning the location of the submerged platform as measured by latency to locate the platform and the distance traversed to find the platform across days of testing. The PHEN4 group had significantly lower latencies and traveled a shorter distance to reach the submerged platform when compared to SCOP on the fourth day of trials while the PHEN2 group traveled more directly to the submerged platform but did not have shorter latencies than the SCOP group. For probe trials, CON rats swam closer to the target area (a measure of proximity to the removed platform) than did all other groups, and the PHEN4 group swam in an area more proximate to the target area than did the SCOP-treated group. These findings demonstrate the ability of this drug to improve learning when cholinergic function has been impaired in a spatial memory task.

Animals↗
PubMed2006

The ameliorating effect of oroxylin A on scopolamine-induced memory impairment in mice.

Oroxylin A is a flavonoid and was originally isolated from the root of Scutellaria baicalensis Georgi., one of the most important medicinal herbs in traditional Chinese medicine. The aim of this study was to investigate the ameliorating effects of oroxylin A on memory impairment using the passive avoidance test, the Y-maze test, and the Morris water maze test in mice. Drug-induced amnesia was induced by administering scopolamine (1 mg/kg, i.p.) or diazepam (1 mg/kg, i.p.). Oroxylin A (5 mg/kg) significantly reversed cognitive impairments in mice by passive avoidance and the Y-maze testing (P<.05). Oroxylin A also improved escape latencies in training trials and increased swimming times and distances within the target zone of the Morris water maze (P<.05). Moreover, the ameliorating effects of oroxylin A were antagonized by both muscimol and diazepam (0.25 mg/kg, i.p., respectively), which are GABA(A) receptor agonists. Furthermore, oroxylin A (100 microM) was found to inhibit GABA-induced inward Cl(-) current in a single cortical neuron. These results suggest that oroxylin A may be useful for the treatment of cognitive impairments induced by cholinergic dysfunction via the GABAergic nervous system.

Amnesia↗
PubMed2004

Improvement of scopolamine-induced memory impairment by Z-ajoene in the water maze in mice.

Z-ajoene, a major compound containing sulfur in oil-macerated garlic products, exhibited inhibitory effects against scopolamine-induced memory impairment in mice using the Morris water maze test. The effects of Z-ajoene were observed dose-dependently (0.25-25 mg/kg). At the highest dosage, the memory performance of mice was improved compared to normal mice. The acetylcholinesterase (AChE) activity in the brain was reduced by administration of Z-ajoene dose-dependently. However, alliin and diallyl disulfide, organosulfur compounds from garlic, did not improve memory performance nor AChE inhibitory effect. These results suggest that Z-ajoene may act on the cholinergic system and on memory impairment caused by excess activity of AChE.

Acetylcholinesterase↗
PubMed2005

Stress adversely affects efficacy of physostigmine-scopolamine pretreatment against soman in guinea pigs.

During military operations, soldiers may be exposed to mixtures of chemicals and to physical, emotional and psychological stress factors, which all may influence efficacy of any treatment, including the nerve agent pretreatment regimen. The purpose of this study was therefore to investigate the influence of chronic intermittent, variable, unpredictable and uncontrollable stress conditions on the side effects and therapeutic efficacy of the combination of physostigmine (0.025 mg/kg/h) and scopolamine (0.018 mg/kg/h) as a pretreatment against 2 x LD50 soman intoxication in guinea pigs. Stress during pretreatment led to an increase of motor activity and an increase of power in the EEG delta2 frequency band. After chronic stress, exposure of pretreated animals to 2 x LD50 soman resulted in more severe intoxication symptoms, a more persistent effect on the startle response, and considerable more severe and persistent effects on the EEG power-spectrum, indicating irreversible brain damage.

Animals↗
PubMed2006

Bovine brain phosphatidylserine attenuates scopolamine induced amnesia in mice.

This study verifies the effects of bovine brain phosphatidylserine (PS) on passive avoidance (PA) and contextual fear conditioning (CFC) tests in scopolamine-treated mice. Mice received daily i.p. 50 mg/kg PS or 0.2 M Tris pH 7.4 (TRIS) for 5 days. On day 6, mice received saline (TRIS-SAL and PS-SAL) or 1 mg/kg SCO (TRIS-SCO and PS-SCO) i.p. After 20 min, the animals were submitted to PA (experiment 1) or CFC (experiment 2) training sessions, and tests were performed 24 h later. Latency in entering the dark chamber of the PA apparatus presented by TRIS-SCO (but not PS-SCO) group in the test was significantly higher than those presented by controls. Except for TRIS-SCO, all the groups presented higher latencies in the test compared to the training session. In experiment 2, the TRIS-SCO (but not PS-SCO) group presented significantly lower freezing duration than that presented by the TRIS-SAL group in the test. Animals treated with PS alone presented higher freezing duration than that presented by the TRIS-SAL group. The results demonstrate that PS attenuates SCO-induced amnesia in both PA and CFC tests. In addition, PS per se improves retention in the CFC test.

Amnesia↗
PubMed2001

Effects of cyclazocine and scopolamine on swim-to-platform performance in rats.

DL-Cyclazocine (0.5-2.0 mg/kg, i.p.) produced no impairment in rats' acquisition and retention of the behavior of swimming to a large visible platform in a water tank. However, cyclazocine produced a significant enhancement or potentiation of the impairment in swim-to-platform behavior produced by scopolamine. Since cyclazocine has previously been shown to abolish serotonin-dependent electrocortical activation (enabling it, in combination with central muscarinic blockade, to block all cortical activation), the results lend further support to the hypothesis that blockade of electrocortical activation produces dementia rather than sleep or coma as was previously believed.

Acetylcholine↗
PubMed1996

Simultaneous determination of cholecystokinin-like immunoreactivity and dopamine release after treatment with veratrine, NMDA, scopolamine and SCH23390 in rat medial frontal cortex: a brain microdialysis study.

The release of cholecystokinin (CCK) and dopamine (DA) was measured simultaneously in the medial frontal cortex of the rat using an in vivo microdialysis technique coupled to either enzyme immunoassay or high performance liquid chromatography with electrochemical detection method. Basal levels of CCK-like immunoreactivity (CCK-LI) and DA in the dialysates were 0.29 +/- 0.05 pg/50 microliters and 4.98 +/- 0.56 fmol/20 microliters respectively. After perfusion of 100 micrograms/ml veratrine into rat medial frontal cortex through the microdialysis probe, the release of those neurotransmitters was significantly enhanced. Perfusion of 10 mM NMDA induced significant increases of CCK-LI and DA levels. Co-perfusion of 1 mM SCH23390, a D1 receptor antagonist, suppressed NMDA-evoked CCK-LI release and slightly raised NMDA-evoked DA release. Treatment with scopolamine, a muscarinic receptor antagonist, suppressed veratrine-induced CCK-LI and DA release, but did not change NMDA-evoked CCK-LI and DA release. These results suggest that NMDA may regulate CCK-LI release through the activation of D1 receptor existing on the afferent CCK neurons or interneurons in rat medial frontal cortex, and changes of endogenous CCK release may be involved in NMDA receptor-mediated long-term potentiation.

Animals↗