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PubMed1986

Rapid-eye movement sleep and muscarinic receptor binding in rats are augmented during withdrawal from chronic scopolamine treatment.

The purpose of this study was to determine whether a seven day, once-daily morning administration of scopolamine produces upregulation of muscarinic receptors and augments REMS during withdrawal. After obtaining two, six-hour baseline sleep recordings, beginning at 0900, independent groups of rats were administered either scopolamine or saline every morning for seven days. Six hour sleep recordings were obtained following the first and seventh day of injection and during the two subsequent withdrawal days. After obtaining the last sleep recording the rats were sacrificed and the following brain areas removed: cerebral cortex, hippocampii, caudate nuclei, brainstem, and cerebellum. 3H-QNB was used as the ligand to assess for changes in muscarinic receptor binding. Compared to baseline, scopolamine produced a significant decrease in REMS during the period of drug administration. During the withdrawal days, however, REMS increased during the morning period. Compared to the saline group, the scopolamine treated animals had increased muscarinic receptor binding in the caudate and hippocampus; no significant change in receptor density was observed in the cortex, brainstem or cerebellum.

Animals↗
PubMed1995

Choline enhances scopolamine-induced acetylcholine release in dorsal hippocampus of conscious, freely-moving rats.

We examined the effects of exogenous choline (30, 60, 120 mg/kg, i.p.) on basal and scopolamine-evoked acetylcholine (ACh) release in awake animals, using in vivo microdialysis. After collection of 3-4 baseline dialysate samples (15 min each), rats received either saline or choline chloride and 4 additional samples were collected. All animals then received scopolamine hydrochloride (0.5 mg/kg, i.p.) and 6 additional samples were collected. Basal ACh release in animals receiving choline did not differ from that in rats given saline, nor from ACh release prior to choline administration. Scopolamine alone increased average ACh levels in dialysates from 1.22 +/- 0.54 to 11.18 +/- 3.07 pmol/15 min (mean +/- SD; p = 0.001); administration of 60 mg/kg or 120 mg/kg of choline chloride significantly enhanced maximal scopolamine responses by about 55%. These results suggest that supplemental choline enhances evoked ACh release in hippocampus of freely-moving rats.

Acetylcholine↗
PubMed1995

Ameliorating effects of histidine on scopolamine-induced learning deficits using an elevated plus-maze test in mice.

We investigated the effects of histidine on scopolamine-induced learning deficits in the elevated plus-maze test in mice. In this test, transfer latency (TL), the time mice took to move from the open arm to the enclosed arm, was used as an index of learning and memory. Intraperitoneal administration of scopolamine (0.5 mg/kg) prolonged the TL on day 2 compared with that in the saline-treated group. Histidine loading (500, 800 and 1600 mg/kg) reversed the prolongation of the TL induced by scopolamine. This ameliorating effect of histidine was abolished by alpha-fluoromethylhistidine, an inhibitor of histidine decarboxylase, suggesting that histidine itself has no such ameliorating effect. Moreover, the ameliorating effect of histidine was antagonized by a histamine H1 receptor antagonist, pyrilamine. However, zolantidine, a histamine H2 receptor antagonist, showed no antagonism of the effect of histidine. Thus, histamine, a decarboxylated product of histidine, elicited an ameliorating effect on scopolamine-induced learning deficit via histamine H1 receptors in mice. These findings clearly indicated that there is a close relationship between histaminergic and cholinergic systems in the brain, and that histamine may play certain important roles in learning and memory.

Animals↗
PubMed1986

Centrally administered neurotensin suppresses locomotor hyperactivity induced by d-amphetamine but not by scopolamine or caffeine.

The effects of intracisternally (i.c.) administered neurotensin (NT) on locomotor responses to scopolamine and caffeine, two psychomotor stimulants which do not depend on an intact mesolimbic dopamine (DA) system, were compared with the effects of the peptide on locomotion induced by d-amphetamine, which does depend on this DA system. Adult rats were injected intracisternally with 30 micrograms of neurotensin or vehicle. Immediately following these injections, the rats received intraperitoneal injections of either d-amphetamine (1, 2 or 3 mg/kg), scopolamine (0.25, 0.5, 1.0 or 2.0 mg/kg), caffeine (5, 15, 30 or 50 mg/kg) or the appropriate vehicle. After a 10 min recovery period, interruptions of photocells by ambulatory and non-ambulatory behavior were recorded every 30 min for 2 hr. Analyses of variance indicate that d-amphetamine and caffeine significantly elevated locomotor and non-locomotor activity at every dose tested. Scopolamine elevated locomotor activity at every dose and non-locomotor activity at 0.5, 1.0 and 2.0 mg/kg. Statistical analysis revealed that neurotensin significantly suppressed the locomotor response to 2 and 3 mg/kg of d-amphetamine but did not suppress the locomotor responses to any dose of scopolamine or caffeine or the non-locomotor responses to any of the three stimulants tested. Behavioral ratings of stereotyped responses indicated that neurotensin altered none of these responses to any stimulant tested. These findings are consistent with previous behavioral and biochemical data which indicate that neurotensin modulates the activity of the mesolimbic, but not nigroneostriatal, DA system and moreover, demonstrate that neurotensin does not simply induce a non-specific impairment of locomotor activity.

Animals↗
PubMed1992

Effects of cholinergic agonists on regional brain energy metabolism in the scopolamine-treated rat.

The effects of scopolamine, physostigmine, RS86 and U-80816B on regional energy metabolism were studied in rodents by means of the 2-deoxyglucose autoradiographic technique. Scopolamine depressed metabolism in an area of cerebral cortex, focused around the parietal region. Rats treated with cholinergic direct agonists (U-80816B, RS86) as well as with the indirect agonist (physostigmine) all showed decreases in cortical energy metabolism, similar to scopolamine. They also induced an increase in thalamic metabolism. When these drugs were given in conjunction with scopolamine, metabolism tended to change in the opposite direction from the values obtained with the drug alone. These results suggest that there are complex interactions between pre- and post-synaptic muscarinic receptors. Additionally, nicotinic receptors could also be involved in some of the effects of physostigmine.

Animals↗
PubMed1993

Suppression of eltoprazine-induced REM sleep rebound by scopolamine.

Previous studies have demonstrated that REM sleep suppression produced by the serotonin1 agonist eltoprazine (1 mg/kg b.i.d., administered i.p.) is followed by a dramatic rebound in REM sleep. In the present study, cats were treated with scopolamine (2 mg/kg b.i.d.) after 3 days of eltoprazine-induced REM sleep suppression. During scopolamine treatment, the percentage of REM sleep (9.9 +/- 3.5%) was well below baseline levels (13.7 +/- 1.6%; P < 0.05). Even after the 3-day scopolamine treatment ended, the subsequent REM sleep rebound after the combined eltoprazine-scopolamine treatment (16.8 +/- 2.8% REM sleep during 3-day rebound; P < 0.10 compared to baseline) was less than a third of the rebound normally seen after eltoprazine. These results provide evidence for the reciprocal relationship between acetylcholine and serotonin and suggest a new set-point model for the mechanism of REM sleep regulation and rebound.

Analysis of Variance↗
PubMed1987

Effect of pyroglutamic acid stereoisomers on ECS and scopolamine-induced memory disruption and brain acetylcholine levels in the rat.

The acquisition of a passive avoidance conditioned response was disrupted in the rat by electroconvulsive shock (ECS) and scopolamine administration. D,L-pyroglutamic acid (D,L-PCA) 500 and 1000 mg/kg, administered as arginine salt 120 min before the retest, prevented both the ECS and scopolamine-induced amnesia. Arginine alone was ineffective. Scopolamine brought about a 52 and 39% decrease, respectively, in cortical and hippocampal acetylcholine (ACh) levels, measured by means of a gas-chromatographic method. D,L-PCA 500 and 1000 mg/kg also prevented the decrease in brain ACh level. When the two isomers were studied separately, D-PCA was more effective than L-PCA and antagonized scopolamine-induced amnesia at the doses of 250 and 500 mg/kg. In conclusion, D,L-PCA is active on cortical and hippocampal cholinergic mechanisms and, like other 2-oxopyrrolidone derivatives, shows cognition-enhancing properties.

Acetylcholine↗
PubMed1993

Scopolamine affects response-to-change test involving 20-min retention interval after locomotor exploration in rats.

The tendency to select the T-maze arm that has been changed in brightness between two successive trials (response-to-change) was investigated. Our previous findings indicated that scopolamine injections (1.0 mg/kg) impaired responding to change of brightness in a choice trial (trial II) following a 1-min retention interval, when in the first acquisition trial rats could only inspect the white-black T-maze arms through transparent partitions (the passive test). The drug was ineffective when rats were allowed locomotor exploration of the maze (the active test). The aim of the present experiment was to investigate the effect of the same dose of scopolamine on the active test involving a longer 20-min retention interval between the acquisition trial and the choice trial. The effect of cue salience also was examined by using grey-black arms. Rats injected with scopolamine (Scopo) 20 min before the acquisition trial performed in the white-black maze on the chance level, whereas saline-injected rats (Sal) showed significant preference for the changed arm. Decreasing the cue salience impaired response-to-change in Sal rats (50% of changed arm choices) but had no further effect on performance of Scopo rats, presumably because of a floor effect. The postacquisition injection had a somewhat stronger effect than the injections preceding acquisition, which most probably reflects the state dependency phenomenon. The deficient performance due to scopolamine treatment that appeared in the present study at a longer retention interval could be interpreted in terms of increased forgetting.

Animals↗
PubMed1991

A monoclonal antibody to scopolamine and its use for competitive enzyme-linked immunosorbent assay.

A hybridoma clone producing a monoclonal antibody (SC78.H81) against scopolamine was established. The monoclonal antibody was an IgG1 (k) antibody with high affinity (1.6 x 10(9) M-1 for methylscopolamine). The monoclonal antibody was cross-reactive with methylscopolamine and butylscopolamine, and showed weak cross-reactivity with 6 beta- and 7 beta-hydroxyhyoscyamine. The cross-reaction with L-hyoscyamine, atropine, scopine and DL-tropic acid was very weak. A competitive enzyme-linked immunosorbent assay using SC78.H81 was established to quantify scopolamine. The sensitivity of the assay allowed detection of 20 pg assay-1 (0.2 ng ml-1) of scopolamine. The assay was applied to the estimation of scopolamine content in hairy root cultures of a Duboisia hybrid.

Antibodies, Monoclonal↗
PubMed1978

Scopolamine interacts with reactions to cat and genotypic emotional reactivity in rat.

In the presence or absence of a cat the effects of scopolamine hydrobromide were investigated on approach, freezing and defecation behaviors of the bidirectionally selectively bred rat strains for emotional reactivity. Compared to the baseline behavior (absence of cat and scopolamine), both the genetic lines showed decrease in approach and increase in freezing in the presence of cat. Scopolamine in the absence of cat did not affect any of the behaviors of the nonreactive strain but increased approach and decreased freezing in the reactive strain. The presence of both cat and scopolamine affected both the strains but differently, i.e., showing no significantly change in the nonreactive, but increase in freezing and decrease in approach in the reactive strain, as compared to the respective baselines.

Animals↗
PubMed1978

Scopolamine does not affect footshock sensitivity in the rat.

To test the generality of the finding of Feigley, et al. [8] that scopolamine increases sensitivity/reactivity to footshock, rats were tested under either scopolamine or saline conditions for sensitivity to footshock in an automated version of the flinch-jump paradigm. There was no significant trend toward increased sensitivity following scopolamine injection at any of the response magnitudes assessed. Since the previous study included an operant response in the measure of sensitivity, it was suggested that apparent effects of scopolamine on reactivity to footshock are dependent on the inclusion of an operant response in the measure of reactivity, and are not due to changes in sensory thresholds.

Animals↗
PubMed1978

A reappraisal of scopolamine effects on inhibition.

A series of related experiments was conducted to examine the effects of scopolamine on discrimination performance in the presence or absence of a stimulus signalling non-reinforcement. In Experiment 1, rats trained to respond on 1 of two levers in the presence of a 1000-Hz tone and on the other lever in the presence of a 3000-Hz tone were not reinforced when white noise was added to 1 of the tones. Pairing white noise with the other tone during an extinction session demonstrated that the white noise had become a conditioned inhibitory stimulus. In Experiment 2, scopolamine decreased responding and discrimination accuracy on the excitatory (reinforced) trials, and increased responding on the inhibitory (non-reinforced) trials. The magnitude of the drug's effect was similar on excitatory and inhibitory trials. Using combination of visual and auditory discriminative stimuli, Experiment 3 confirmed the results of Experiment 2. These experiments show that scopolamine disrupts animals' ability to discriminate, and that scopolamine-induced increases in non-rewarded responses cannot be attributed solely to a disinhibitory effect of the drug as Carlton (1969) and others have claimed.

Animals↗
PubMed1981

The effect of para-chlorophenylalanine and scopolamine on passive avoidance in chicks.

Four-day-old Vantress x Arbor Acre chicks were treated for key-peck passive avoidance (PA) learning following intraperitoneal injections of parachlorophenylalanine (PCPA) and/or scopolamine. In Experiment 1, chicks were pre-treated with either three or five injections of PCPA (150 mg/kg) or saline across th first three posthatch days and then tested for PA learning on the fourth posthatch day. In Experiment 2, chicks were first pre-treated with three injections of PCPA (150 mg/kg) or saline, and then injected with either scopolamine (0.5 mg/kg) or saline 20 min prior to PA testing on the fourth posthatch day. Major findings were: (a) Chicks pre-treated with PCPA did not significantly differ from saline control chicks in either the acquisition or maintenance of response suppression during PA testing; (b) chicks injected with scopolamine were significantly disrupted in PA learning as compared to saline control chicks; and (c) PCPA pre-treatment did not significantly affect the scopolamine-induced disruption of PA learning. These findings, therefore, suggest that cholinergic, but not serotonergic, mechanisms are involved in PA learning of the young chick.

Animals↗
PubMed1981

Aversive stimulus properties of scopolamine.

The drug state produced in rats by intraperitoneal injections of scopolamine hydrobromide (1.2 mg/kg) was treated as a putative aversive US. This US was paired with a distinctive spatial location in a shuttle box for 6 of 12 daily sessions by confining the subject to one side following scopolamine and to the other side following saline (6 sessions). Two groups of 8 subjects each received zero and 20 min post-injection delays respectively. Following zero delay, but not 20 min delay, subjects avoided the side associated with scopolamine in drug-free, free choice tests. This is evidence that the immediate post-injection drug state induced by scopolamine is aversive.

Animals↗
PubMed1982

Lesions of cholinergic forebrain nuclei: changes in avoidance behavior and scopolamine actions.

The acquisition of active (shuttle-box) and passive avoidance conditioned responses and the effects of scopolamine on acetylcholine (ACh) output in freely moving rats and on conditioned responses were investigated 20 days after placing a unilateral lesion in the magnocellular forebrain nuclei (MFN). In the lesioned rats spontaneous ACh output from the cerebral cortex ipsilateral to the lesion was slightly decreased, while on the other hand the increase in ACh output elicited by scopolamine was strongly reduced. Sham operated rats always performed more active avoidance responses than MFN lesioned rats in the daily training shuttle-box sessions, and the facilitating effect of scopolamine (1 mg/kg IP) on the shuttle-box performance was suppressed. However the lesion did not disrupt the shuttle-box performance whenever training had taken place before the lesion. In the lesioned rats retested 30 min after the training trial, an impairment of the passive avoidance response was found. The effect of the lesion was potentiated by scopolamine. The results show therefore that MFN lesions impair the cortical cholinergic mechanisms, whose activity seems to play an important role in cognitive functions.

Animals↗
PubMed1984

Chronic scopolamine treatment and brain cholinergic function.

Scopolamine was either continuously infused or injected once daily into C3H mice. Chronic infusion resulted in mice that were supersensitive to the hypothermia and tremor produced by the muscarinic agonist, oxotremorine. Chronic scopolamine infusion did not alter brain acetylcholinesterase (AChE) or choline acetyltransferase (ChAT) activities but it did produce an increase in brain muscarinic receptors, as measured by quinuclidinyl benzilate (QNB) binding. The maximal increase in QNB binding was seen at the 0.2 mg/kg/hr dose. Further increase in dose resulted in a return to control QNB binding in all brain regions studied except cortex. These animals were still supersensitive to oxotremorine, suggesting a dissociation between receptor number and response to agonist. Animals injected once daily for 10 days with 5 mg/kg exhibited an increase in QNB binding while no increase was seen at 20 mg/kg/day. Chronic oxotremorine infusion resulted in tolerance to the hypothermia-producing effects of oxotremorine. This was accompanied by a decrease in brain QNB binding. Coinfusion of scopolamine with oxotremorine blocked both the tolerance development and receptor changes. These experiments demonstrate that chronic scopolamine treatment can elicit an increase in brain muscarinic receptors which is accompanied by supersensitivity to agonists. However, this effect is not clearly dose related, and a strict relationship between receptor number and agonist response does not exist.

Acetylcholine↗
PubMed1986

Scopolamine impairs learning performance of rats in a 14-unit T-maze.

To assess involvement of muscarinic cholinergic systems in performance of a shock-motivated 14-unit T-maze task, 3-month old Fischer-344 rats were given an IP injection of scopolamine (0.1, 0.3, 1.0 or 3.0 mg/kg), methylscopolamine (1.0 mg/kg), or saline 30 min prior to maze training on 2 consecutive days. Scopolamine, but not methylscopolamine, impaired all components of acquisition performance. Measures of error performance, run time, shock duration, and number of shocks received were significantly increased but only at the 1.0 and 3.0 mg/kg scopolamine doses. The cognitive component of the task, measured by error performance, appeared most affected. Cognitive performance deficits observed following scopolamine administration in the present study resembled age-related impairments in rats and mice previously observed in this task. The cholinergic hypothesis of geriatric memory dysfunction appears to be implicated by these findings; however, the degree to which memory systems are involved remains unclear. Other performance variables such as discriminative control of stimuli or mechanisms of attention are implicated and discussed.

Animals↗
PubMed1988

Alleviation of scopolamine amnesia by different retrieval enhancing treatments.

Mice were trained in a one-way active avoidance task to a criterion of 9/10 avoidances. Immediately following training they were injected with scopolamine hydrochloride (1 mg/kg SC) or with saline. Retention was assessed 3 days after training by 5 test trials on which the UCS was not present. Thirty min prior to the test, groups were injected with different doses of arecoline, d-amphetamine sulphate or with saline. Other scopolamine-treated mice were exposed to the CS or the UCS 24 hr prior to the test. The scopolamine-induced amnesia was attenuated by both 0.5 and 1.0 mg/kg arecoline and by 2.0 mg/kg d-amphetamine. Retention was also improved by exposure to the CS and the UCS. These data show that scopolamine amnesia can be alleviated by treatments which activate retrieval processes.

Amnesia↗