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PubMed1988

Scopolamine in rats impairs acquisition but not retention in a 14-unit T-maze.

To follow up a previous report noting that scopolamine impaired acquisition performance of young rats in a shock-motivated 14-unit T-maze, the present study assessed the effects of muscarinic antagonism on retention aspects of the same task. The broader objective was to further the investigation of possible defects in cholinergic neurotransmission that might underlie the age-related impairments previously observed in this task. Young (3-month) male F-344 rats were given preliminary training to criterion in one-way active avoidance in a straight runway. Then on the first day of complex maze training, each rat received 5 acquisition (AQ) trials followed by a second 10-trial retention (RET) session conducted the following day. Subjects were assigned to one of eight groups receiving an intraperitoneal injection of either scopolamine hydrochloride (1.0 mg/kg) or saline as follows: (a) 30 min prior to training on the first day (PRE-AQ); (b) 30 min prior to training on both the first and second day (PRE-AQ-RET); (c) immediately after completing the trial on the first day (POST-AQ); (d) 30 min prior to testing on the second day (PRE-RET). Dependent measures included errors, alternation errors, run time, number of shocks, and total shock received. On the first day of maze training, all performance measures except for alternation errors were significantly higher for the two acquisition groups (PRE-AQ and PRE-AQ-RET) compared to all other groups which did not differ significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Scopolamine-induced suppression of paradoxical sleep is reversed by the somatostatin analogue SMS 201-995 in rats.

The intraperitoneal administration of the octapeptide somatostatin analogue SMS 201-995 produced a significant increase in paradoxical sleep (PS) in rats. The suppression of PS by the muscarinic receptor blocker scopolamine was reversed by SMS 201-995. These findings confirm previous results demonstrating a role of somatostatin in the generation of PS. In addition they suggest that the suppression of PS by scopolamine may be due to an inhibitory effect on somatostatin release, rather than to an alteration of cholinergic function alone.

Animals↗
PubMed1989

Effects of scopolamine, d-amphetamine, and apomorphine on alternation and position biases.

The sequencing of arm entries in a symmetrical Y-maze was examined in mice treated with either scopolamine, d-amphetamine or apomorphine. These treatments could potentially alter both alternation tendencies and rotational tendencies. Therefore, a measure of spontaneous alternation was evaluated which was computed by taking an average of the right going percent alternation and the left going percent alternation. The number of arm entries was increased by amphetamine, unchanged following scopolamine and reduced by apomorphine. All three drugs reduced spontaneous alternation tendencies and increased the magnitude of a bias to turn consistently in the same direction (rotational tendency). All three drugs thus altered the sequencing of arm entries from patterns consistent with spatial alteration to patterns consistent with egocentrically defined responses. These results indicate that the measure of spontaneous alternation which was an average of the right going percent alternation and the left going percent alternation is a better index of alternation tendencies. Thus, when an animal is not able to navigate on the basis of an extrapersonal (allocentric) system as a result of drug treatment, it will revert to an egocentric system.

Amphetamines↗
PubMed1990

Relationship of the behavioral effects of aprophen, atropine and scopolamine to antagonism of the behavioral effects of physostigmine.

Behavioral effects of aprophen, atropine and scopolamine, in rats, were examined under a multiple schedule of food presentation and at different injection-test times. The effects of the varied treatments were compared to the ability of the drugs, under identical conditions, to prevent the behavioral effects of the anticholinesterase, physostigmine. Potencies of the antagonists to decrease response rates varied across three log units. All three antagonists produced dose-related attenuation of the response suppressant effects of physostigmine. In general, aprophen was a better antagonist than scopolamine or atropine. It blocked behavioral effects of physostigmine across a wider range of doses than the other compounds, and did so with less behavioral disruption. Although substantial differences between the three antagonists were observed, the behavioral effects of all three antagonists (when administered alone) were positively correlated with their efficacy as antagonists of the response suppressant effects of physostigmine.

Animals↗
PubMed1990

A comparison of the effects of diazepam and scopolamine in two positively reinforced learning tasks.

In a helical maze scopolamine (0.5 and 1 mg/kg) significantly impaired the ability of rats to acquire a spatial learning task using reference memory. In contrast, diazepam (0.5-2 mg/kg) did not impair acquisition of this task and the only effect of diazepam (4 mg/kg) was likely to be secondary to sedative effects. Diazepam (0.5-4 mg/kg) did not impair 8-day retention of the helical maze. In a test of working and reference memory in which spatial processing was minimised, scopolamine (0.5 and 1 mg/kg) significantly impaired acquisition and increased the number of reference memory errors. Diazepam (1 and 4 mg/kg) did not impair acquisition of this task, but when a delay was interposed in the middle of a trial the diazepam-treated rats were slower to complete the task than the controls and made more errors of both working and reference memory. In contrast, when the rats were tested with a change of context, the diazepam-treated rats completed the task more quickly than the controls and made fewer errors of both working and reference memory.

Animals↗
PubMed1992

Effect of scopolamine on the electrical resistance of the paw pads of mice.

We examined the electrical resistance of the paw pads of mice under the same conditions as used previously in studies of the passive avoidance response. Administration of scopolamine (0.05-1 mg/kg, SC) 10 or 30 min prior to placement of animals in an experimental box resulted in a profound increase in electrical resistance. In contrast, subcutaneous injection of butylscopolamine (1-20 mg/kg), diazepam (1 or 2 mg/kg), or pentobarbital (10 or 20 mg/kg) did not substantially alter subject resistance. Scopolamine may act on the CNS to induce increased paw skin resistance.

Animals↗
PubMed1994

Effect of DAU 6215, a novel 5-HT3 receptor antagonist, on scopolamine-induced amnesia in the rat in a spatial learning task.

The effects of different doses (1, 10, 30, and 100 micrograms/kg, IP) of a new 5-hydroxytryptamine3 (5-HT3) receptor antagonist, 3-alpha-tropanyl)1H-benzimidazolone-3-carboxamide chloride (DAU 6215), on memory and performance deficits induced by SC 0.2 mg/kg scopolamine were assessed in the Morris water maze task. No effect was observed on the performance of rats treated with DAU 6215 alone. The doses of 10 and 30 micrograms/kg DAU 6215 attenuated these scopolamine-induced behavioral deficits.

Amnesia↗
PubMed1996

Aniracetam restores object recognition impaired by age, scopolamine, and nucleus basalis lesions.

Object recognition was investigated in adult and aging male rats in a two-trials, unrewarded, test that assessed a form of working-episodic memory. Exploration time in the first trial, in which two copies of the same object were presented, was recorded. In the second trial, in which one of the familiar objects and a new object were presented, the time spent exploring the two objects was separately recorded and a discrimination index was calculated. Adult rats explored the new object longer than the familiar object when the intertrial time ranged from 1 to 60 min. Rats older than 20 months of age did not discriminate between familiar and new objects. Object discrimination was lost in adult rats after scopolamine (0.2 mg/kg SC) administration and with lesions of the nucleus basalis, resulting in a 40% decrease in cortical ChAT activity. Both aniracetam (25, 50, 100 mg/kg os) and oxiracetam (50 mg/kg os) restored object recognition in aging rats, in rats treated with scopolamine, and with lesions of the nucleus basalis. In the rat, object discrimination appears to depend on the integrity of the cholinergic system, and nootropic drugs can correct its disruption.

Aging↗
PubMed1989

Transdermal scopolamine attenuates methacholine-induced bronchospasm.

Anticholinergic agents have been widely used in the management of asthma. The use of scopolamine has been limited by significant side effects. Transdermal delivery of scopolamine (TS) has, however, been used successfully for the prevention of motion sickness. The purpose of this study was to determine if TS would decrease methacholine-induced bronchospasm in a group of subjects with mild asthma. Bronchoprovocational challenges with inhaled methacholine were performed on three separate occasions in 10 male subjects who each had a past history of asthma. After a baseline challenge, each subject received, in a double-blinded fashion, either a placebo patch or TS patch. The challenge was then repeated after at least 36 hours, and the alternate patch was then dispensed. The provocative dose producing a fall in FEV1 by 20% from baseline was then calculated by linear regression analysis. No significant change in baseline pulmonary function was noted with placebo patch or TS. With the use of TS, there was a small but significant increase in the provocative dose producing a fall in FEV1 by 20% from baseline for the group (p less than 0.05). In conclusion, we were able to demonstrate that a TS patch worn for a short period of time, can significantly decrease airway reactivity to methacholine in some patients with hyperactive airways.

Administration, Cutaneous↗
PubMed1986

Dexamethasone mimicks the antimotion sickness effects of amphetamine and scopolamine.

Based on preliminary suggestions that individual differences in susceptibility to stressful motion might be related to physiological differences in responses of the hypothalamic-pituitary-adrenal axis, we tested the efficacy of dexamethasone and metyrapone in subjects exposed to cross-coupled accelerative semicircular canal stimulation on a rotating chair. Subjects given 0.5 mg of dexamethasone every 6 h for 48 h could endure 80% more stressful motion (P = 0.03) in a within-subjects design study, whereas, no improvement followed treatment with 750 mg of metyrapone[correction of metryapone] every 4 h for 24 h. The efficacy of dexamethasone might be explained in terms of its neurochemical actions on several neurotransmitter systems which are also modulated by such classical antimotion sickness drugs as amphetamine and scopolamine. Because dexamethasone induces adaptive changes within the central nervous system it may prove superior to scopolamine and amphetamine which possess significant side effects, are short acting, and rapidly tolerated.

Adrenocorticotropic Hormone↗
PubMed1994

Effect of physostigmine on relative acetylcholine output induced by systemic treatment with scopolamine in in vivo microdialysis of rat frontal cortex.

By means of an in vivo brain microdialysis, the effect of different concentrations of physostigmine on the acetylcholine level in the dialysate of rat frontal cortex was studied. Perfusion of the various degrees of physostigmine (eserine) concentration (10 nM-10 microM) into the cortex through the dialysis membrane increased the basal acetylcholine level in a dose-dependent manner. In the presence of 10 nM, 0.1 microM and 10 microM physostigmine in the perfusate, systemic treatment with scopolamine (0.5 mg/kg, i.p.) increased 200, 270 and 510%, respectively, the relative acetylcholine level in the dialysates in comparison with the corresponding basal levels, while in the absence of physostigmine the treatment increased it only 40%. From these results, it appears that perfusion of physostigmine at a variety of concentrations, changes not only the basal level of acetylcholine induced by the inhibition of acetylcholinesterase but also the relative acetylcholine output induced by systemic treatment with scopolamine.

Acetylcholine↗
PubMedDate not supplied

Methanesulfonyl fluoride (MSF) blocks scopolamine-induced amnesia in rats.

Cholinesterase inhibitors, such as physostigmine and tetrahydroaminoacridine, have been found to alleviate some of the memory deficits characteristic of senile dementia of the Alzheimer's type (SDAT). Many toxic side effects, however, have been associated with the use of these compounds. Recently, a cholinesterase inhibitor, methanesulfonyl fluoride (MSF), was discovered to have low toxicity, central nervous system (CNS) selectivity, and a long therapeutic duration. The purpose of this research was to determine if MSF (1.5 mg/kg) would be effective in reducing or blocking amnesia induced by various doses of scopolamine (0.2, 0.6, and 2.0 mg/kg). One hundred and twenty-two female Sprague-Dawley albino rats were trained and retention tested in a Y-maze brightness discrimination task. MSF was highly effective in reducing scopolamine-induced amnesia.

Amnesia↗
PubMed1984

Use of scopolamine for dental anesthesia and analgesia techniques.

A review of the English literature on the pharmacologic effects of scopolamine is presented and indications for the current use of the drug in dental anesthesia and analgesia are evaluated. The authors conclude that the role of scopolamine in the production of conscious sedation for outpatient dental surgery should be reevaluated in the light of contemporary findings.

Amnesia↗
PubMed1995

Scopolamine-physostigmine combination does not substitute for nicotine.

1. Male Sprague-Dawley rats were trained to discriminate 0.4 mg/kg nicotine subcutaneously administered from its saline vehicle in a food-motivated operant discrimination task. Once trained, the discriminative performance was observed to be dose-responsive with an ED50 = 0.11 mg/kg. 2. The co-administration of 0.1 or 0.2 mg/kg physostigmine with either 0.1, 0.15 or 0.2 mg/kg scopolamine produced intermediate discriminative effects, i.e., neither nicotine- nor saline-like responding. However, the physostigmine-scopolamine combination neither substituted for nor increased the discriminative effects of co-administered nicotine. 3. The theoretical/mechanistic possibility that a combination of a cholinesterase inhibitor to increase available acetylcholine plus a specific anti-muscarinic to allow that increased acetylcholine to stimulate nicotinic receptors was investigated. Results indicate that the combination does not produce nicotine-like discriminative effects and evidence the possibility that nicotine discrimination may involve non-cholinergic mechanisms.

Animals↗
PubMed1989

Effect of scopolamine and HP 029, a cholinesterase inhibitor, on long-term potentiation in hippocampal slices of the guinea pig.

The effect of scopolamine and a cholinesterase inhibitor on long-term potentiation (LTP) of population spikes was studied in a guinea pig hippocampal slice preparation. After brief application of each drug (10 min), LTP in CA1 and CA3 was induced by tetanus stimulation delivered to commissural/associational fibers and mossy fibers, respectively. Scopolamine at concentration of 10 microM had no effect on LTP in CA1 but significantly suppressed LTP in CA3. The cholinesterase inhibitor, 9-amino-1,2,3,4-tetrahydroacridine-1-ol maleate (HP 029) at concentration of 10 microM significantly enhanced LTP both in CA1 and CA3. These results suggest that the cholinergic system is involved in producing LTP in CA3. Another mechanism of the effect of HP 029 on LTP in CA1 is discussed.

Action Potentials↗
PubMed1995

Basal and scopolamine-evoked release of hippocampal acetylcholine following traumatic brain injury in rats.

This study employed in vivo microdialysis in awake, freely-moving Sprague-Dawley rats to examine acetylcholine (ACh) release in the dorsal hippocampus at 14 days following lateral controlled cortical impact. Extracellular levels of ACh were measured prior to and after an intraperitoneal administration of scopolamine (1 mg/kg), which evokes ACh release by blocking autoreceptors. At 14 days post injury there were no differences in basal ACh levels. However, injury produced a significant reduction in scopolamine-evoked ACh release. The data suggest that cholinergic neurotransmission remains chronically compromised, and thus may contribute to previously documented post traumatic spatial memory deficits.

Acetylcholine↗
PubMed1995

Glutamate decarboxylase messenger RNA in rat pallidum: comparison of the effects of haloperidol, clozapine and combined haloperidol-scopolamine treatments.

We have investigated the effects of neuroleptic treatments which do, or do not, induce catalepsy on the level of expression of glutamate decarboxylase, the rate limiting enzyme in GABA synthesis, in efferent neurons of the pallidum in adult rats. Different regimens of haloperidol (1 mg/kg s.c., three, seven or 14 days; 2 mg/kg, s.c., 10 days) induced catalepsy in a majority of rats and increased glutamate decarboxylase messenger RNA levels in the globus pallidus (external pallidum) in those rats exhibiting catalepsy. Levels of glutamate decarboxylase messenger RNA were also increased in the entopeduncular nucleus (internal pallidum), but only after 14 days of treatment with haloperidol. The atypical antipsychotic clozapine (seven days, 20 mg/kg, s.c.), which did not induce catalepsy, slightly decreased glutamate decarboxylase messenger RNA levels in the globus pallidus. When co-administered with haloperidol (seven days, 1 mg/kg s.c.), the muscarinic antagonist scopolamine (1 mg/kg, s.c.) completely blocked both haloperidol-induced catalepsy and increases in glutamate decarboxylase messenger RNA levels in the globus pallidus. In contrast, scopolamine was not able to block increased glutamate decarboxylase and enkephalin messenger RNA expression induced by haloperidol in the striatum. These results reveal a good correlation between increases in glutamate decarboxylase messenger RNA levels in the globus pallidus and catalepsy after these drug treatments and suggest that anticholinergic blockade of the behavioral and molecular effects of neuroleptics may involve non-striatal mechanisms.

Animals↗
PubMed1996

Electrical stimulation of the cholinergic laterodorsal tegmental nucleus elicits scopolamine-sensitive excitatory postsynaptic potentials in medial pontine reticular formation neurons.

A large and consistent body of data implicates mesopontine cholinergic neurons in the production of rapid eye movement sleep, and indicates that many rapid eye movement sleep events are mediated by activation of pontine reticular formation neurons. There is anatomical evidence for projections from the mesopontine cholinergic nuclei to the pontine reticular formation, but no study has shown that stimulation of this cholinergic zone produces excitatory postsynaptic potentials in pontine reticular formation neurons. In the present study, intracellular recording were made from 168 pontine reticular formation neurons, identified by antidromic activation from the bulbar reticular formation and by neurobiotin intracellular labeling, in acutely anesthetized cats. The effects of single-pulse electrical stimulation of the laterodorsal tegmental nucleus portion of the ipsilateral mesopontine cholinergic zone were evaluated in these neurons. Under urethane anesthesia this stimulation produced, in 21 of 22 recorded neurons, long-latency excitatory postsynaptic potentials (mean = 3 ms), consistent with the conduction velocity of unmyelinated cholinergic fibers (measured conduction velocity was 2 m/s). This excitatory postsynaptic potential was virtually abolished by intravenous administration of the muscarinic cholinergic receptor blocker scopolamine (n = 40 neurons), and by acute cuts separating the laterodorsal tegmental nucleus and the recorded neurons (n = 40). In contrast, a short-latency excitatory postsynaptic potential (0.7-1.5 ms) was not reduced in amplitude by scopolamine and could still be elicited following acute transverse cuts. Unlike the longer-latency excitatory postsynaptic potential, its amplitude was not reduced by barbiturate anesthesia. These data, suggesting the presence of an excitatory, cholinergic laterodorsal tegmental nucleus projection to the pontine reticular formation, provide further support to other lines of evidence implicating mesopontine cholinergic neurons in the production of rapid eye movement sleep, and are compatible with a model of rapid eye movement sleep generation in which a key element is mesopontine cholinergic input depolarizing and increasing the excitability of reticular core neurons.

Animals↗