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PubMed2005

BGC20-761, a novel tryptamine analog, enhances memory consolidation and reverses scopolamine-induced memory deficit in social and visuospatial memory tasks through a 5-HT6 receptor-mediated mechanism.

Inhibition of 5-HT(6) receptors has been shown to improve memory consolidation, thus we tested whether a novel tryptamine analog with high affinity for 5-HT(6) receptors, BGC20-761 (5-methoxy-2-phenyl-N,N-dimethyltryptamine, PMDT), can enhance long-term memory. BGC20-761 (10 mg/kg i.p.) alone had no effect on social recognition in young rats, however, at doses of 5 mg/kg and 10 mg/kg i.p, BGC20-761 dose-dependently reversed a deficit of social recognition induced by scopolamine (0.4 mg/kg i.p.), an anticholinergic drug that impairs memory. BGC20-761 (10 mg/kg i.p.), scopolamine (0.2 mg/kg i.p.) or BGC20-761 + scopolamine had no effects on novel object discrimination in young rats (2 months). In mature rats (6 months), recognition of the novel object was improved following administration of BGC20-761. Scopolamine had no effect in object recognition. However, the addition of scopolamine disrupted the memory-enhancing effect of BGC20-761. Based on the high affinity of BGC20-761 for 5-HT(6) receptors, these cognitive enhancing effects are most likely mediated by 5-HT(6) receptor inhibition. The difference in effects of BGC20-761 in young vs. mature rats may reflect the status of memory consolidation in these different age ranges.

Animals↗
PubMed2006

Effect of endogenous histamine in the ventral hippocampus on fear memory deficits induced by scopolamine as evaluated by step-through avoidance response in rats.

In the present study, the effects of endogenous histamine in the ventral hippocampus on fear memory deficits induced by scopolamine were investigated as evaluated by step-through avoidance response in adult male rats. Bilateral ventral hippocampal injection of scopolamine (i.h., 2, 5 microg/site) significantly produced depressant effects on the active avoidance response in a dose-dependent manner. Histamine H(3)-antagonist clobenpropit (5, 10 microg/site) significantly ameliorated the fear memory deficits induced by scopolamine in a dose-dependent manner. Its procognitive effect was completely antagonized by immepip (10 microg/site), a selective histamine H(3)-agonist. Both histamine H(1)-antagonist pyrilamine and H(2)-antagonist cimetidine, also inhibited the procognitive effects of clobenpropit. Additionally, the procognitive effects of clobenpropit on the fear memory deficits induced by scopolamine were significantly potentiated by intraperitoneal (i.p.) injection of histidine, a precursor of histamine, but markedly reversed by i.h. injection of alpha-fluoromethylhistidine (FMH, 10 microg/site), a selective and potent histidine decarboxylase inhibitor. It is concluded that the increased endogenous histamine release in the ventral hippocampus ameliorates the scopolamine-induced fear memory deficits, and its action is mainly mediated by histamine presynaptic H(3)-receptors and postsynaptic H(1)- and H(2)-receptors.

Animals↗
PubMed1998

Micellar electrokinetic chromatography of scopolamine-related anticholinergics.

A simple micellar electrokinetic chromatography (MEKC) method is described for the separation of scopolamine N-oxide hydrobromide (SO), scopolamine hydrobromide (SH), scopolamine N-methylbromide (SM) and scopolamine N-butylbromide (SB), and for the quantitation of SH, SM and SB (using SO as an internal standard). The analysis of these drugs was performed in a phosphate buffer (30 mM; pH 7.00) with sodium dodecyl sulfate (SDS) (30 mM) as an anionic surfactant. Several parameters affecting the separation of the drugs were studied, including the concentrations of the buffer and SDS. The stability of the drugs in the phosphate buffer (pH 7.00) was also examined. Partial application of the method to the determination of scopolamine N-butylbromide in tablets proved to be feasible.

Antiemetics↗
PubMed2001

Effects of MDL 73005 on water-maze performances and locomotor activity in scopolamine-treated rats.

The stimulation of 5-HT1A receptors in the raphe or their blockade in the hippocampus can reduce cognitive deficits induced by blockade of muscarinic receptors in the hippocampus. We investigated the effects of MDL 73005 (8-[2-(2,3-dihydro-1,4-benzodioxin-2-ylmethylamino) ethyl]-8-azaspiro[4,5] decane-7,9-dione methyl sulphonate), an agonist at 5-HT1A somatodendritic autoreceptors and an antagonist at postsynaptic 5-HT1A receptors in rats treated systemically with scopolamine. Spatial memory was assessed in a water maze using protocols testing reference and working memory. Home cage locomotor activity was also determined. Working memory and locomotor activity were evaluated before and after para-chlorophenylalanine (pCPA) treatment. Scopolamine produced a weak impairment of reference memory at 0.5 mg/kg, and a more pronounced impairment of working memory at 0.25 and 0.5 mg/kg. MDL 73005 alone (2 mg/kg, i.p.) had no effect, but prevented the memory impairments induced by 0.25 mg/kg of scopolamine. Scopolamine induced hyperlocomotion. MDL 73005 alone did not affect locomotor activity, but exacerbated the hyperlocomotion induced by 0.5 mg/kg of scopolamine. pCPA did not abolish the effects of MDL 73005, suggesting that these effects were not due to an action at presynaptic receptors, or even that they involved receptors other than serotonergic ones (e.g., D2). In conclusion, MDL 73005 is able to antagonise moderate spatial memory dysfunctions induced by systemic muscarinic blockade.

Animals↗
PubMed1997

Reversal of scopolamine-induced deficits in navigational memory performance by the seed oil of Celastrus paniculatus.

Celastrus paniculatus (CP), a medicinal plant from India has been reputed to be useful as a pharmaceutical aid for learning and memory. We investigated the effects of the seed oil of CP on the 6 day performance of young adult rats in a navigational memory task-the Morris water maze. Chronic oral (gavage) daily treatment with CP. (50, 200, or 400 mg/kg) for 14 days completely reversed the scopolamine (0.5 mg/kg)-induced task performance deficit. On the other hand, acute treatment (single injection prior to scopolamine treatment) with CP (200 mg/kg) did not significantly reverse the scopolamine-induced impairment in maze performance. Alone, CP produced a slight, but significant improvement in maze performance on the first day of testing. Acute treatment or chronic 14 day treatment with CP resulted in no significant alteration in normal locomotor activity in an open field. Moreover, CP did not alter the scopolamine-induced increases in locomotor activity. Chronic treatment with CP did not alter brain acetylcholinesterase levels and no signs of cholinergic overstimulation were ever noted during or after treatment. Thus, the seed oil of CP, when administered chronically, selectively reversed the impairment in spatial memory produced by acute central muscarinic receptor blockade, supporting the possibility that one or more constituents of the oil may offer cognitive enhancing properties. The neural mechanism underlying the reversal of scopolamine's mnemonic effects by CP is not yet known, but it is not related to an anticholinesterase-like action.

Acetylcholinesterase↗
PubMed1998

Locomotor stereotypy produced by dexbenzetimide and scopolamine is reduced by SKF 83566, not sulpiride.

Like amphetamine, scopolamine produces locomotor stereotypy (repetitive routes of locomotion) in an open field. To determine whether locomotor stereotypy is a common behavioral effect of anticholingeric agents, several doses of the anticholinergic dexbenzetimide were tested for the ability to produce locomotor stereotypy; like scopolamine, dexbenzetimide produced locomotor stereotypy. To investigate a possible role of dopamine in anticholinergic-induced locomotor stereotypy, we tested the ability of the dopamine D1 antagonist SKF 83566 and the D2 antagonist sulpiride to block the locomotor stereotypy induced by scopolamine as well as dexbenzetimide. SKF 83566 blocked scopolamine- and dexbenzetimide-induced locomotor stereotypy; sulpiride did not reduce dexbenzetimide-induced locomotor stereotypy, but enhanced scopolamine-induced locomotor stereotypy. Hyperlocomotion was reduced by both dopamine antagonists. Results are interpreted in support of the notion that dopamine is the likely candidate mediating locomotor stereotypy.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1999

Scopolamine inhibition of female sexual behavior in rhesus monkeys (Macaca mulatta).

Previous research supports the activational role of central cholinergic mechanisms in rodent female sexual behavior. This experiment examined if similar central cholinergic mechanisms facilitate female rhesus monkey (Macaca mulatta) sexual behavior. Eight ovariectomized female rhesus monkeys received daily estradiol benzoate priming (5 microg/kg, SC). After 13-16 days of estrogen priming, animals were injected intravenously with either the cholinergic antagonist, scopolamine (0.70 mg/kg), or saline vehicle (1 ml/kg). Results indicate that the female proceptive behaviors of noncontact presentations significantly decreased 1545 min after scopolamine injection. Scopolamine inhibition was sustained up to 75 min only after 15 days of estrogen priming. Scopolamine did not significantly reduce other female sexual behaviors. Additionally, significant decreases in the number of mounts and intromissions, but not hip touches, were displayed by males exposed to scopolamine-treated females. This research suggests the possibility of a central cholinergic mechanism regulating female sexual behavior in rhesus monkeys. However, the general nature and duration of the cholinergic regulation of primate female sexual behavior differs substantially when compared to rodent behavior.

Animals↗
PubMed2001

Dose- and time-dependent scopolamine-induced recovery of an inhibitory avoidance response after its extinction in rats.

The present investigation was aimed at elucidating the dose and time dependency of scopolamine-induced recovery of inhibitory avoidance after its extinction. Two experiments were conducted: in the first, we analyzed the effects of four doses (1, 2, 4, and 8 mg/kg) of the musacrinic receptor antagonist scopolamine, on the expression of this conditioned response once it had been extinguished. Independent groups of rats were trained in a one-trial, step-through inhibitory avoidance task and submitted to daily retention (extinction) tests. After extinction had occurred, animals were injected intraperitoneally 10 min before retention testing, either with saline or scopolamine. Results show that scopolamine produced a dose-dependent recovery of the avoidance response. The second experiment was carried out in the same animals, which were now tested for retention of inhibitory avoidance at 1, 2, 3, 6, and 9 months after completion of the first experiment. All rats received counterbalanced injections of saline or scopolamine 10 min before testing at each time interval. Reliable recovery of the avoidance response was observed at the 1-month interval with a clear dose dependency while, after the second month, only the groups treated with the two higher doses continued responding. The results indicate that recovery of the extinguished response produced by muscarinic blockade follows dose- and time-dependent curves, and can be achieved long after a single training session. These data suggest that the inhibitory avoidance memory trace is retained in the brain after behavioural extinction of this response, thus supporting the view of extinction as new learning that affects the retrieval of the original memory, but does not modify its storage.

Animals↗
PubMed1992

Raised glucose levels enhance scopolamine-induced acetylcholine overflow from the hippocampus: an in vivo microdialysis study in the rat.

Behavioural studies in both humans and animals have shown that an acute rise in circulating glucose levels at or around the time of training enhances subsequent retention performance and can also afford protection from the amnesia produced by posttraining injections of scopolamine. In an attempt to directly investigate the neurochemical basis for these effects of glucose we have tested the hypothesis that raised glucose levels may enhance acetylcholine (ACh) synthesis and release in the brain during conditions of increased neuronal activity, induced either by training or pharmacological challenge, via a microdialysis study using rats. Microdialysate concentrations of ACh overflow from the hippocampus of fasted rats induced by i.p. injections of scopolamine (1 mg/kg) combined with concurrent s.c. injections of either glucose (2 g/kg) or saline were compared in successive 15-min samples using an on-line HPLC system. Scopolamine injections resulted in an immediate 10-20-fold increase in hippocampal ACh overflow which subsequently progressively declined over a 4-h period to pretreatment baseline levels. The combined injection of glucose with scopolamine resulted in a highly significant enhancement (19.4%; P less than 0.01) in ACh content of the first two samples as compared to saline-injected controls. These results provide the first direct experimental evidence that raised glucose levels, via increased availability of acetyl-coenzyme A (acetyl-coA), transiently facilitates ACh synthesis and release during conditions of increased neuronal activity. This enhancement of ACh availability during states of cholinergic neuronal activation may underlie the previously observed facilitatory effects of glucose on memory performance and its protection from scopolamine-induced amnesia.

Acetylcholine↗
PubMed1998

Concurrent administration of subeffective doses of scopolamine and MK-801 produces a short-term amnesia for the elevated plus-maze in mice.

Amnesic properties of scopolamine, a muscarinic receptor antagonist, and MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, were evaluated in mice by means of the elevated plus-maze test. In this test, transfer latency, the time mice took to move from the open arm to the enclosed arm, was used as an index of learning and memory. The 3-day pretreatment training dramatically decreased transfer latencies. On the 4th day, the retention trial was performed 30 min after the intraperitoneal injection of scopolamine (Experiment 1) or MK-801 (Experiment 2). The doses of 0.25 and 0.5 mg/kg of scopolamine as well as the doses of 0.1, 0.15, 0.2 and 0.4 mg/kg of MK-801 significantly prolonged the transfer latency as compared with both that in the saline-treated group and that measured on the 3rd day. In Experiment 3, subthreshold doses of these two drugs given in combination (which were ineffective when given alone: scopolamine 0.25 mg/kg, MK-801 0.075 mg/kg) significantly prolonged the transfer latency on the fourth day. However, an amnesic effect of scopolamine plus MK-801 was transient. On the 5th day, no differences in the transfer latency were found. This finding clearly indicates that there is a close relationship between cholinergic and glutamatergic systems and that both systems play an important role in a spatial orientation of mice on the elevated plus-maze.

Amnesia↗
PubMed1997

Dose-related impairment of spatial learning by intrahippocampal scopolamine: antagonism by ondansetron, a 5-HT3 receptor antagonist.

To study the role of hippocampal muscarinic receptors in spatial learning, various doses of scopolamine were injected bilaterally into the CA1 region of the dorsal hippocampus of rats trained in a two-platform spatial discrimination task. Scopolamine administered 10 min before each training session at doses ranging from 3.75 to 15 micrograms/microliter impaired choice accuracy, had no effect on choice latency and increased the errors of omission only with 7.5 micrograms on day 1 and with 15 micrograms on days 1 and 2 of training. No dose affected choice accuracy or latency of a non-spatial visual discrimination task. A subcutaneous dose of 1 microgram/kg ondansetron, a 5-HT3 receptor antagonist, 30 min before each training session prevented the impairment of choice accuracy by intrahippocampal 3.75 micrograms scopolamine but 0.1 microgram/kg ondansetron had no such effect. No dose of ondansetron by itself modified the acquisition of spatial learning. The results suggest that relatively low doses of scopolamine in the dorsal hippocampus selectively impair the acquisition of a spatial discrimination task, and that blockade of 5-HT3 receptors prevents the deficit caused by the muscarinic antagonist. The utility of the deficit of spatial learning induced by intrahippocampal scopolamine for modelling some aspects of memory disturbances in Alzheimer's disease is discussed.

Animals↗
PubMed2001

A role for the angiotensin AT4 receptor subtype in overcoming scopolamine-induced spatial memory deficits.

There is increasing interest in the role of the brain angiotensin AT4 receptor subtype in cognitive processing. This receptor subtype is activated by angiotensin IV (AngIV), is heavily distributed in the mammalian hippocampus, neocortex, and cerebellum, and has been linked with a learning and memory function. The present investigation utilized intracerebroventricular (i.c.v.)-infused scopolamine hydrobromide (scop), a muscarinic receptor antagonist, to disrupt acquisition of the circular water maze task of spatial memory. All animals received 2 days of training trials (five trials/day) using a visible platform in an effort to preclude subsequent confounding by scopolamine-induced sensory and/or motor impairments. In the first experiment, i.c.v.-infused scopolamine (70 nmol) was followed by 0, 10, 100, or 1000 pmol i.c.v. doses of Nle(1)-AngIV in separate groups of rats. Results indicated that each dose of Nle(1)-AngIV improved the poor acquisition of this task induced by scopolamine treatment. However, the 100- and 1000-pmol doses were most effective with respect to latency and distance to find the submerged pedestal. A second experiment demonstrated that treatment with a specific AT4 receptor antagonist, Nle(1), Leual(3)-AngIV (1000 pmol), blocked the ability of Nle(1)-AngIV (100 pmol) to improve the performance of scopolamine-compromised rats. These results support the notion that hippocampal AT4 receptors are involved in spatial memory processing, and that activation of these binding sites can overcome the disruption of spatial memory accompanying treatment with a muscarinic receptor antagonist.

Analysis of Variance↗
PubMed1998

The role of the central cholinergic projections in cognition: implications of the effects of scopolamine on discrimination learning by monkeys.

In humans, administration of the cholinergic antagonist scopolamine impairs the encoding of information into long-term memory and has effects on other cognitive processes. It has been supposed that it is inhibition of the rising cholinergic projections from the basal forebrain, specifically from the basal nucleus of Meynert (NBM) to the neocortex and from the medial septum/vertical limb of the diagonal band of Broca (MS/VDB) to the hippocampus, that results in these cognitive impairments. In this paper, we describe the effects of scopolamine treatment in monkeys on learning different sorts of visual discrimination and visuospatial conditional tasks and compare these results to the effects of lesions of the rising cholinergic projections. Experiments in rodents in which these projections have been selectively destroyed have failed to produce a consensus view of the functions of these two areas. In particular, highly specific immunotoxic lesions of the NBM have largely failed to produce changes in task performance that can be interpreted as resulting from a cognitive impairment. In monkeys, lesions of the NBM produce modest or short-lasting, impairments in visual discrimination learning, retention, and reversal, whereas lesions of the MS/VDB produce large and permanent impairments of certain types of conditional learning. Similar impairments produced by scopolamine in monkeys and additive effects of lesions of the NBM or MS/VDB with scopolamine suggest that scopolamine has these effects by acting on the rising cholinergic pathways rather than on other cholinergic systems in the brain. It is argued that the rising cholinergic projections sustain the functions of the target areas; in the case of the hippocampus in humans, the function is usually regarded as being the analysis of information in a way that is pertinent to the formation of episodic memories and in the case of the neocortex, is the analysis of information in a manner that is relevant to the cognitive processing of on-going events and the acquisition of semantic knowledge.

Acetylcholine↗
PubMed1999

Age-related effects of scopolamine on REM sleep regulation in normal control subjects: relationship to sleep abnormalities in depression.

In order to assess the influence of development on the regulation of rapid eye movement (REM) sleep by cholinergic systems, the REM sleep responses to scopolamine were assessed in five normal adolescent and seven adult control subjects in this preliminary investigation. Subjects were studied on two separate occasions for three consecutive nights. Subjects received placebo or scopolamine (1.5 ug/kg, i.m.) on night 2; night 3 was considered the "recovery" night. As expected, scopolamine delayed REM latency and suppressed REM sleep on night 2 in both the adolescents and adults. Subtle developmental differences occurred, with scopolamine having a tendency to suppress REM sleep less effectively in younger subjects. On night 3, REM latency was shortened and REM sleep was increased to comparable extent in both the adolescents and adults. The comparable REM sleep responses to scopolamine between normal adolescents and adults, particularly on night 3, are discussed in relation to the age-related expression of REM sleep abnormalities in depression.

Adolescent↗
PubMed1999

Scopolamine and Pavlovian fear conditioning in rats: dose-effect analysis.

Muscarinic-cholinergic antagonism produces learning and memory deficits in a wide variety of hippocampal-dependent tasks. Hippocampal lesions produce both acquisition deficits and retrograde amnesia of contextual fear (fear of the place of conditioning), but do not impact fear conditioning to discrete cues (such as a tone). In order to examine the effects of muscarinic antagonism in this paradigm, rats were given 0.01 to 100 mg/kg of scopolamine (or methylscopolamine) either before or after a fear conditioning session in which tones were paired with aversive footshocks. Fear to the context and the tone were assessed by measuring freezing in separate tests. It was found that pretraining, but not post-training, scopolamine severely impaired fear conditioning; methylscopolamine was ineffective in disrupting conditioning. Although contextual fear conditioning was more sensitive to cholinergic disruption, high doses of scopolamine also disrupted tone conditioning. Scopolamine did not affect footshock reactivity, but did produce high levels of activity. However, hyperactivity was not directly responsible for deficits in conditioning. It was concluded that scopolamine disrupts CS-US association formation or CS processing, perhaps through an attenuation of hippocampal theta rhythm.

Acoustic Stimulation↗
PubMed1997

Scopolamine-induced convulsions in food given fasted mice: effects of physostigmine and MK-801.

We recently reported that scopolamine pretreated mice fasted for 48 h developed clonic convulsions soon after they were allowed to eat a small amount of food for 30 s. The present experiments were performed to determine whether animals also develop convulsions when they were allowed to eat ad libitum and to find some evidence for the contribution of the cholinergic and/or glutamatergic systems in the underlying mechanism(s) of convulsions. Animals fasted for 48 h were treated with 3 mg/kg scopolamine or saline. Twenty minutes later, they were allowed to eat either ad libitum or a small portion of food for 30 s. Scopolamine pretreated animals after starting to eat ad libitum or a small amount in a restricted time developed convulsions in a few minutes, the incidence being 76 and 54%, respectively. Pretreatment of 0.17 mg/kg MK-801, the noncompetitive NMDA antagonist, decreased the incidence of scopolamine-induced convulsions (22%) without affecting latency to the onset of seizures. Pretreatment of 0.1 mg/kg physostigmine, the cholinesterase inhibitor, changed neither the incidence (90%) nor latency to the onset of scopolamine-induced convulsions.

Animals↗
PubMed1999

Scopolamine-induced convulsions in food given fasted mice: effects of clonidine and tizanidine.

We recently reported that scopolamine pretreated mice fasted for 48 h developed clonic convulsions soon after they were allowed to eat ad libidum. Pretreatment with MK-801, the non-competitive NMDA antagonist, decreased the incidence of these convulsions. We suggested that a possible scopolamine-induced glutamatergic hyperactivity could account for these convulsions. Using alpha2-agonists, clonidine, which has been shown to inhibit glutamate release, and tizanidine, the present study was performed to find some additional data for the role of glutamate in the underlying mechanism of scopolamine-induced convulsions in food given fasted mice. Animals fasted for 48 h and pretreated (i.p.) with saline, clonidine (0.05, 0.10, 1 mg/kg) or tizanidine (0.10, 0.15, 0.30, 0.45 mg/kg) were treated (i.p.) with either saline or scopolamine (3 mg/kg). Then 20 min later, they were allowed to eat ad libidum and were observed for 30 min for the incidence and onset of clonic convulsions. All doses of clonidine pretreatment completely suppressed (0%) scopolamine-induced clonic convulsions (75%). On the other hand, only 0.15 mg/kg tizanidine pretreatment significantly decreased (15%) the incidence of convulsions; however as well as 0.15 mg/kg, both 0.30 and 0.45 mg/kg tizanidine pretreatments significantly increased latency to the onset of convulsions.

Animals↗
PubMed2003

Scopolamine into the anterior cingulate cortex diminishes nociception in a neuropathic pain model in the rat: an interruption of 'nociception-related memory acquisition'?

The cingulate cortex plays a key role in the affective component related to pain perception. This structure receives cholinergic projections and also plays a role in memory processing. Therefore, we propose that the cholinergic system in the anterior cingulate cortex is involved in the nociceptive memory process. We used scopolamine (10 microg in 0.25 mircrol/saline) microinjected into the anterior cingulate cortex, either before thermonociception followed by a sciatic denervation, between thermonociception and denervation or after both procedures (n=10 each). The vehicle group (saline solution 0.9%, n=14) was microinjected before thermonociception. Chronic nociception was measured by the autotomy score, which onset and incidence were also determined. Group scopolamine-thermonociception-denervation (STD) presented the lowest autotomy score as compared to vehicle and group thermonociception-denervation-scopolamine (TDS) (vehicle vs. STD, p=0.002, STD vs. TDS, p=0.001). Group thermonociception-scopolamine-denervation (TSD) showed a diminished autotomy score when compared to TDS (p=0.053). STD group showed a delay in the onset of AB as compared to the rest of the groups. Group TSD presented a significative delay (p=0.048) in AB onset when compared to group TDS. There were no differences in the incidence between groups. The results show that nociception-related memory processed in the anterior cingulate cortex is susceptible of being modified by the cholinergic transmission blockade. When scopolamine is microinjected prior to the nociceptive stimuli, nociception-related memory acquisition is prevented. The evidence obtained in this study shows the role of the anterior cingulate cortex in the acquisition of nociception-related memory.

Acetylcholine↗