Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GDEE, an antagonist of the AA2 or quisqualic acid category of excitatory amino acid receptor, decreases behavioral activity and locomotor stimulation induced by cocaine and amphetamine when locally injected into the nucleus accumbens. The present experiment was intended to examine the effects of systemic GDEE and other excitatory amino acid antagonists on stimulant-induced locomotor activity. GDEE markedly attenuated the stimulant effect of amphetamine, and partially blocked the effects of phencyclidine (PCP). Apomorphine-induced cage climbing behavior was partially decreased by lower dosages of GDEE, but was almost completely blocked by the highest dosage tested. Amphetamine-induced stimulation of locomotor activity was not decreased by any of the other excitatory amino acid antagonists that were tested, including MK-801, 2-amino-7-phosphonoheptanoic acid (APH), or CNQX. APH decreased stereotypy only at a high dosage (250 mg/kg), which also produces ataxia. Several other compounds, including L-glutamic acid gamma ethyl ester (GMEE), L-glutamic acid, glycine, and L-glutamine did not block amphetamine-induced stimulation in molar dosages equivalent to the highest dosage of GDEE (8 mmol/kg). It is concluded that the AA2 excitatory amino acid receptor is important in the expression of activating effects of stimulant drugs.
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PMID:A possible role of AA2 excitatory amino acid receptors in the expression of stimulant drug effects. 197 5

The recognition of an unfamiliar juvenile rat by an adult rat has been shown to imply short-term memory processes. In this study the effect of various psychotropic drugs on this investigatory behaviour was examined. The procedure was as follows: an unfamiliar juvenile rat was placed in the home cage of an adult rat for 5 min. The time spent by the adult rat in investigating the juvenile was recorded. The adult rat was then immediately treated with vehicle or test compounds, and was again exposed for 5 min to the same juvenile 2 h later. At this time point vehicle-treated rats no longer recognized the juvenile rat, i.e. the time of investigation was similar to that observed during the first presentation. Arecoline (1 and 3 mg/kg IP), physostigmine (0.05 and 0.1 mg/kg SC), RS86 (0.5 mg/IP) and nicotine (0.125 and 0.5 mg/kg IP) reduced in a dose-dependent fashion the time spent in investigating the juvenile during the second exposure. This result cannot be attributed to nonspecific effects, since it was not observed when a different juvenile was used for the second exposure. The effect of arecoline was reversed by scopolamine, but not by methylscopolamine. Aniracetam reduced investigatory behaviour at the dose of 50 mg/kg IP. FG 7142 (5 mg/kg IP) and beta-CCM (0.4 mg/kg IP) were also active and their effect was reversed by Ro 15-1788. DL-Amphetamine (0.5 and 1 mg/kg IP), nomifensine (1.25-10 mg/kg IP) and strychnine (0.25 and 0.5 mg/kg IP) were ineffective or reduced this behaviour unspecifically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specific modulation of social memory in rats by cholinomimetic and nootropic drugs, by benzodiazepine inverse agonists, but not by psychostimulants. 256 26

Pentobarbital was injected into rats 20 min after they were placed in an apparatus where heart rates were recorded. Amphetamine was injected after they were removed from the apparatus 29-30 min later. A Pavlovian conditioned response (CR) began after three or four such trials in the form of a failure of conditioned rats to show the same decline in heart rate obtained in controls after the pentobarbital injection. On later trials, the amphetamine was not injected until 50 min after the pentobarbital, and the CR was most obvious during the period 30-50 min after the pentobarbital injection, an effect characteristic of Pavlovian delay conditioning. The pharmacological effects of pentobarbital were necessary for conditioning because the CR was not obtained (a) when normal saline was substituted for the pentobarbital after successful conditioning or (b) when saline was used instead of pentobarbital throughout. Because of the speed and effectiveness of the conditioning, we believe the mechanism responsible for it has homeostatic regulation as its natural role. It was puzzling that environmental cues seemed to have a role in the conditioned stimulus complex, because conditioning was not apparent when the drug-drug pairings were administered in the home cage.
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PMID:Heart rate conditioning with pentobarbital as a conditioned stimulus and amphetamine as an unconditioned stimulus. 270 76

Animals with a history of receiving psychomotor stimulants in a specific environment show enhanced activity when injected with saline and placed there. In the present study, a Pavlovian paradigm was used to compare the unconditioned and conditioned activity effects of (+)-amphetamine (0.1, 0.5, 1.0, and 5.0 mg/kg), caffeine (0.1, 1.0, 10.0, and 30.0 mg/kg), and a saline group (n's = 6-12). Rats experienced conditioning days with either drug or saline injected IP prior to a 60-min session in the activity monitor and the alternate saline or drug injected in the home cage following the session. On test days, all animals received saline in the activity monitors. Results revealed that amphetamine produced environment-specific conditioning in a dose-dependent manner; previous experience with 0.5, 1.0, and 5.0 but not 0.1 mg/kg in the activity monitor resulted in conditioned activity. A caffeine dose of 10.0 mg/kg produced stimulant effects on conditioning days and previous experience with the 1.0, 10.0, or 30.0 mg/kg dose in the activity monitor led to conditioned activity on test days. However, on test days the control groups as well as the 30.0 mg/kg experimental group showed significantly reduced activity as compared to the saline group. Thus, it appeared that caffeine produced hypoactivity 23 h after injection. Amphetamine produced conditioning in a dose-dependent manner, and the appearance of significant unconditioned activity during conditioning sessions was not necessary or sufficient to produce a conditioned effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the ability of (+)-amphetamine and caffeine to produce environment-specific conditioning. 311 89

Saline-treated and amphetamine-treated (7 mg/kg, ip, immediate) male rats from a Sprague-Dawley substrain were observed in two test environments designed to elicit different investigative responses in normal rats. Snout contact with the substrate was generated by placing the rat in a small enclosed cage. Absence of snout contact was induced by placement of the rat on a square elevated platform. Detailed ethological records were kept of locomotion, rearing, sitting, grooming, gnawing, and sleeping throughout the 90-min session. Amphetamine-treated rats incorporated environmentally contingent bodily postures into their forms of stereotyped behavior. The postures were characteristic of those evinced initially by the saline-treated rats in the same test environment. The control rats showed appropriate changes in their investigative behavior when the apparatus was changed at 10 and at 30 min postinjection. The amphetamine-treated rats, however, were completely unresponsive to such changes at 30 min and only partially so at 10 min postinjection. It was concluded that there is a temporal gradient of decreasing readiness to modify repetitive behavior after a single, large dose of amphetamine.
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PMID:Initial environment influences amphetamine-induced stereotypy: subsequently environment change has little effect. 381 44

beta-/Tyr9/melanotropin-/9-18/ significantly increased apomorphine-induced cage-climbing, while only a tendency towards an increase was observed after supersensitization with haloperidol. Amphetamine also enhanced apomorphine-induced climbing behavior. The peptide showed only a tendency to increase dopamine release from striatal slices, while amphetamine elevated this significantly. The results suggest that the striatal dopamine system is involved in the behavioral action of beta-/Tyr9/melanotropin-/9-18/.
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PMID:Effects of beta-/Tyr9/melanotropin-/9-18/ on apomorphine-induced stereotyped cage-climbing and on striatal dopamine release in mice. Comparative studies with amphetamine. 689 51

Three-month old Long-Evans female rats were submitted to aspirative lesions of the fimbria-fornix and intrahippocampal grafts of a cell suspension prepared from a region of the fetal brain including the septum and the diagonal band of Broca (rich in cholinergic neurons) or the raphe (rich in serotonergic neurons). A group of lesioned rats was grafted with both suspensions mixed. Lesion-only and sham-operated rats served as controls. Four months after the lesions, all rats were tested daily for locomotor activity in their home cage, 1 day without being injected, 2 days with an injection of NaCl and 5 days with an injection of 1 mg/kg (i.p.) d-amphetamine. The effects of the lesions and grafts were assessed by measuring the accumulation of [3H]-choline or [3H]-5-hydroxytryptamine (5-HT) by hippocampal slices, and the electrically-evoked release of tritium. Amphetamine injections produced hyperlocomotion which was potentiated by the lesion. This lesion-induced potentiation was also found in rats with septal grafts, but not in those with raphe or co-grafts. The uptake and electrically-evoked release of [3H]-acetylcholine or [3H]-5-HT were reduced in hippocampal slices from lesion-only rats. In rats which received grafts of septal cells or co-grafts, but not in those with raphe grafts, uptake and release of [3H]-acetylcholine were close to normal. Uptake and release of [3H]-5-HT were close to normal in rats with raphe grafts or with co-grafts, but not in those with septal grafts. Altogether, these data suggest that damage to the serotonergic afferents of the hippocampus might play some role in the potentiation of amphetamine-induced hyperlocomotion associated with fimbria-fornix lesions.
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PMID:The potentiation of amphetamine-induced hyperlocomotion by fimbria-fornix lesions in rats is abolished by intrahippocampal grafts rich in serotonergic neurons. 1032 73

The environmental context in which psychostimulant drugs are administered can have a large effect on both their acute psychomotor activating effects and their ability to induce the psychomotor sensitization associated with repeated drug administration. For example, the acute effects of amphetamine and the development of psychomotor sensitization to amphetamine and cocaine are enhanced when they are administered in a distinct and relatively novel test environment, relative to when they are given in the home cage, in the absence of any environmental stimuli predictive of drug administration. The experiments reported here were designed to further examine this phenomenon and to test the hypothesis that the ability of a distinct context to promote robust psychomotor sensitization is due to its ability to reliably signal (cue) drug administration. Specifically, we compared the ability of contextual cues (a distinct test environment) and discrete cues (light, tone and/or odor), which both reliably predict drug administration, to promote the induction of sensitization. The psychomotor stimulant effects (rotational behavior) of repeated intravenous infusions of 0. 5 mg/kg amphetamine were assessed in rats for whom drug treatments were signaled either: (1) by placement into a distinct test environment; (2) by presentation of discrete cues; or (3) rats for whom drug treatments were given in the home environment in the absence of any environmental cues. Amphetamine produced robust sensitization when given in association with placement into a distinct test environment. The same treatment failed to produce sensitization when the drug was given unsignaled in the animal's home cage. Most importantly, signaling drug administration by presenting discrete cues was not sufficient to promote the robust sensitization seen when treatments were given in a distinct test environment. These results confirm that the induction of psychomotor sensitization can be powerfully modulated by environmental context and further establish that, although contextual stimuli associated with a distinct test environment promote robust sensitization, discrete cues that merely predict drug administration do not have this property. Possible reasons for the difference in the ability of contextual versus discrete environmental cues to promote sensitization are discussed.
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PMID:The role of contextual versus discrete drug-associated cues in promoting the induction of psychomotor sensitization to intravenous amphetamine. 1109 Aug 82

The automated measurement of rodent behaviour is crucial to advance research in neuroscience and pharmacology. Rats and mice are used as models for human diseases; their behaviour is studied to discover and develop new drugs for psychiatric and neurological disorders and to establish the effect of genetic variation on behavioural changes. Such behaviour is primarily labelled by humans. Manual annotation is labour intensive, error-prone and subject to individual interpretation. We present a system for automated behaviour recognition (ABR) that recognises the rat behaviours 'drink', 'eat', 'sniff', 'groom', 'jump', 'rear unsupported', 'rear wall', 'rest', 'twitch' and 'walk'. The ABR system needs no on-site training; the only inputs needed are the sizes of the cage and the animal. This is a major advantage over other systems that need to be trained with hand-labelled data before they can be used in a new experimental setup. Furthermore, ABR uses an overhead camera view, which is more practical in lab situations and facilitates high-throughput testing more easily than a side-view setup. ABR has been validated by comparison with manual behavioural scoring by an expert. For this, animals were treated with two types of psychopharmaca: a stimulant drug (Amphetamine) and a sedative drug (Diazepam). The effects of drug treatment on certain behavioural categories were measured and compared for both analysis methods. Statistical analysis showed that ABR found similar behavioural effects as the human observer. We conclude that our ABR system represents a significant step forward in the automated observation of rodent behaviour.
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PMID:An automated system for the recognition of various specific rat behaviours. 2376 69

Several studies suggest that 50-kHz ultrasonic vocalizations (USVs) may indicate a positive affective state in rats, and these vocalizations are increasingly being used to investigate the properties of psychoactive drugs. Previous studies, however, have focused on dopaminergic psychostimulants and morphine, whereas little is known about how other drugs modulate 50-kHz USVs. To further elucidate the neuropharmacology of 50-kHz USVs, the present study characterized the direct and long-lasting effects of different drugs of abuse, by measuring the number of 50-kHz USVs and their 'trill' subtype emitted by adult male rats. Rats received repeated administrations of amphetamine (2 mg/kg, i.p.), 3,4-methylenedioxymethamphetamine (MDMA, 7.5 mg/kg, i.p.), morphine (7.5 mg/kg, s.c.), or nicotine (0.4 mg/kg, s.c.), on either consecutive or alternate days (five administrations in total) in a novel environment. Seven days later, rats were re-exposed to the drug-paired environment, subjected to USVs recording, and then challenged with the same drug. Finally, 7 d after the challenge, rats were repeatedly exposed to the drug-paired environment and vocalizations were measured. Amphetamine was the only drug to stimulate 50-kHz USVs and 'trill' subtype emission during administration and challenge. Conversely, all rats emitted 50-kHz USVs when re-exposed to the test cage, and this effect was most marked in morphine-treated rats, and less evident in nicotine-treated rats. This study demonstrates that the direct and long-lasting effects of drugs on 50-kHz USVs are regulated differently, providing a better understanding of the usefulness of these vocalizations in the study of psychoactive drugs.
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PMID:Direct and long-lasting effects elicited by repeated drug administration on 50-kHz ultrasonic vocalizations are regulated differently: implications for the study of the affective properties of drugs of abuse. 2413 7


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