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At least 1,387 records · Page 77Linked to original sources
PubMed1992

BMY-14802 protects against ischemia-induced neuronal damage in the gerbil.

BMY-14802, a selective sigma ligand currently under investigation as an atypical antipsychotic agent, was tested for potential anti-ischemic activity. BMY-14802 (10, 30 and 50 mg/kg) did not produce any stereotyped behavior, ataxia or seizures. When gerbils were pretreated with 10, 30 or 50 mg/kg of BMY-14802 30 min prior to bilateral occlusion of carotid arteries for 5 min, BMY-14802 significantly protected against ischemia-induced neuronal loss in the hippocampus. Thus, BMY-14802 may also be useful as an anti-ischemic agent that does not produce psychotomimetic effects.

Animals↗
PubMed1995

CCB, a novel specific kappa opioid agonist, which discriminates between opioid and sigma 1 recognition sites.

CCB, 6,11-Dimethyl-1,2,3,4,5,6-hexahydro-3-([2'-methoxycarbonyl-2'-(4- chlorophenyl)cyclopropyl]methyl)-2,6-methano-3-benzazocin-8-ol, displays specificity and very high affinity for kappa opioid receptor types (Ki = 0.41 +/- 0.19 nM). In contrast to other kappa opioid agonists, CCB is also selective with respect to sigma 1 sites (Ki = 1,050 +/- 55 nM). CCB displays antinociceptive and sedative effects in the mouse comparable to those of U50,488H and morphine. Naltrexone fully antagonizes these effects. The sedative effects of CCB are blocked in mice pretreated with naltrexone or nor-BNI. CCB and U50,488H produce a superimposable diuresis in rats. Naltrexone and nor-BNI, both are effective in antagonizing the effect. CCB does not produce any stereotyped behavior or ataxia in the behavioral assay in doses up to 40 mg/kg s.c. These findings suggest that CCB might be a useful tool to investigate the physiological role of kappa opioid receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1988

Receptor specific inhibition of N-methyl-D-aspartate stimulated 22Na flux from rat hippocampal slices by phencyclidine and other drugs.

Phencyclidine inhibited the flux of 22Na from hippocampal slices of the rat stimulated by N-methyl-D-aspartate (NMDA) in a concentration-dependent manner and consistent with the subclass of excitatory amino acid receptors, with a close interaction between NMDA and phencyclidine receptors. The inhibition by phencyclidine of the NMDA-stimulated flux of 22Na was non-competitive, in contrast to that produced by D-2-amino-5-phosphonovalerate. Other compounds which produce stereotyped behavior in vivo also inhibited the NMDA-stimulated flux of 22Na and the rank of the percentage inhibition of the NMDA-stimulated flux correlated with the affinities at the phencyclidine receptor with 97% confidence. The structural diversity and selectivity for the phencyclidine receptor of those compounds which inhibited the NMDA-stimulated flux of 22Na argue that the interaction was at the phencyclidine receptor. The presence of magnesium did not alter the relative magnitude of inhibition by phencyclidine, suggesting that the phencyclidine site is separate from the pressumably, channel-blocking magnesium site. Thus, the data of the present study support a model where the phencyclidine site is separate from the NMDA recognition site and from the presumed channel-blocking site of magnesium within the NMDA-associated ion channel.

Animals↗
PubMed1994

Effects of neonatal decortication on the social play of juvenile rats.

The effects of radical neonatal decortication on the social play of juvenile rats, as well as the effects of neonatal ablation of frontal or parietal cortex, were examined in this series of experiments. When total decorticates were tested in like-lesioned pairs, the frequency of pinning was reduced by about 50% and their average pin durations were shorter. Nevertheless, the play of decorticates appeared essentially normal in general appearance, and did not differ from controls in a measure of overall play vigor using an electronic activity platform. Further, there were no differences in pin frequencies when controls and decorticates were paired together in cross-lesion testing. Separate tests of play solicitation behaviors did not detect any differences between controls and decorticates suggesting that play motivation was essentially intact after decortication. No deficits in pinning resulted from frontal ablations; however, pin durations were shorter in like-lesion testing. In cross-lesion testing, there was an increase in dorsal contacts and a trend toward shortening of pin durations. Parietal aspirations resulted in a 65% reduction in pin frequency, without substantially altering dorsal contacts. Anesthetization of the anterior surface of the animal's back with xylocaine reduced pinning in controls but eliminated pinning in parietals. Although the results generally indicate little participation of the neocortex in the instigation of rough-and-tumble play, the reliable numerical changes that were observed may be explained by apparent motor changes as well as reduced somatosensory sensitivity.

Aging↗
PubMed1980

The spacing of rhesus monkey troops changes when a few group members receive delta 9THC or D-amphetamine.

Free ranging troops of 18--25 rhesus macaques were housed in large enclosures where a few higher-ranking monkeys were given psychotropic agents (delta 9THC: 4 mg/kg or d-amphetamine: 2 mg/kg). Measures of group spacing were (1) mean distance between all animals. (2) daily variance in mean distance, (3) nearest neighbor distance, (4) daily variance in nearest neighbor distance, (5) index of clumping (S2/mean ratio), (6) % touching, and (7) % movement/2 sec. When 3--4 animals were drugged, the entire group moved closer together and distances were more variable. Acute changes after the first week of delta 9THC and effects after delta 9THC withdrawal were seen in two experiments. Chronic behavioral changes were found for d-amphetamine and in one delta 9THC experiment.

Animals↗
PubMed1980

Effect of neuroleptics and tricyclic antidepressants upon d-amphetamine discrimination.

After rats were trained to differentiate between the effects of intraperitqoneal administration of 0.6 mg/kg d-amphetamine and saline, pretreatment with various neuroleptic drugs was observed to significantly inhibit d-amphetamine discrimination. Thus, trifluoperazine, haloperidol, fluphenazine, chlorpromazine and thioridazine, but not clozapine, decreased d-amphetamine-induced control of discriminative performance. The ED50s of the effective neuroleptics for this inhibition were similar to those reported for antagonism of amphetamine-induced stereotypic behavior in the rat and the slopes of the dose-response curves were parallel indicating a common site and mechanism of action, presumably blockade of postsynaptic dopaminergic receptors. In contrast, pretreatment with the tricyclic antidepressant agents, imipramine, nortryptiline and desipramine had no significant effect on the discrimination of a dose of d-amphetamine which produced a low degree of discriminative control. The results are viewed in relation to the "dopamine hypothesis" of schizophrenia and affective disorders and the use of this animal behavioral method for determining brain dopamine interactions is discussed.

Animals↗
PubMed1984

The effect of apomorphine on the open-field behavior of rats: alone and in pairs.

Male rats were observed in the open-field while alone and while in pairs in an alternating series of trials. The trials extended over a 78 min session following injections of either saline (0.9%) or apomorphine (5.0 mg/kg, IP) into the observed member of each pair. Contrary to the literature on apomorphine stereotypy, apomorphine did not induce continuous sniffing of the environment and continuous gnawing in most rats. Sniffing of the environment remained at normal levels but there was an increase in nodding the head in the vertical plane while keeping the snout close to the floor. Apomorphine-induced hyperactivity was attributed to two factors: a sustained increase in the duration of bouts of locomotion and a failure of the frequency of bouts of locomotion to habituate to novelty. Apomorphine eliminated all social behavior directed toward the other rat, however apomorphine rats showed they were sensible to the presence of the other by increasing their locomotion and rearing when the partner was introduced.

Animals↗
PubMed1984

p-Chlorophenylalanine alters pacing of copulation in female rats.

When tested in apparatus that allowed them to determine their contacts with conspecifics, including sexually active male rats, estrogen- and progesterone-treated female rats systemically treated with para-chlorophenylalanine (PCPA), a tryptophan hydroxylase inhibitor, showed reduced frequency of coital contacts and reduced duration of interactions with sexually active males. PCPA administration did not alter contacts with noncopulating males or other females nor did treated females differ from controls in ability to display lordosis or posing, both stereotyped behaviors characteristic of female rats in behavioral estrus. It is suggested that the alteration of temporal pacing of copulation in the PCPA-treated females is a result of drug-induced changes in the processing of exteroceptive stimuli.

Animals↗
PubMed1988

Behavioral effects of acute and chronic administration of caffeine in the rat.

This study investigated the effects of acute and chronic caffeine treatment on behavior in the social interaction, holeboard and home-cage aggression tests and on proconvulsant actions with pentylenetetrazol. Acutely-treated rats received an IP injection of caffeine (20 or 40 mg/kg). Chronically-treated rats received caffeine in their drinking water for 21 days (50 or 100 mg/kg/day) followed by an injection of caffeine on the test day (20 or 40 mg/kg respectively). Acutely, the higher dose of caffeine (40 mg/kg) decreased levels of social interaction. In the holeboard test, 20 mg/kg of acute caffeine increased motor activity whilst 40 mg/kg reduced head-dipping behavior. In the home-cage aggression test, acute caffeine (40 mg/kg) reduced offensive aggressive behaviors. After chronic treatment with caffeine none of these behaviors differed significantly from controls. After both acute and chronic treatment, caffeine (20 and 40 mg/kg) was proconvulsant with pentylenetetrazol.

Aggression↗
PubMed1993

The role of dopamine and AMPA/kainate receptors in the nucleus accumbens in the hypermotility response to MK801.

The purpose of this study was to evaluate the role of endogenous dopamine in the hypermotility response to MK801. The administration of MK801 (0.1 mg/kg, SC) to rats produced an intense stimulation of coordinated locomotor activity, which was not associated with stereotyped behavior. This stimulatory response was inhibited by pretreatment with either reserpine (5 mg/kg, IP) or alpha-methyl-p-tyrosine (2 doses of 250 mg/kg, IP). Similarly, pretreatment with the D2 antagonist eticlopride (0.03 mg/kg, SC) or the D1 antagonist SCH23390 (0.1 mg/kg, SC) produced a marked inhibition of MK801-stimulated hypermotility, and the combination of eticlopride (0.03 mg/kg, SC) and SCH23390 (0.03 mg/kg, SC) produced a greater inhibition of MK801-stimulated locomotion than either agent alone. The administration of SCH23390 or eticlopride directly into the nucleus accumbens inhibited the locomotor response to MK801, with the combination of both drugs producing a greater inhibition than either agent alone. The intra-accumbens administration of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate receptor antagonists DNQX or GAMS also inhibited the locomotor response produced by MK801. These data suggest that the activation of D1 and D2 dopaminergic receptors and AMPA/kainate excitatory amino acid receptors in the nucleus accumbens is required for the stimulation of locomotor activity produced by MK801.

Animals↗
PubMed1996

Measurement issues in curve-shift analysis of apomorphine effects on rewarding brain stimulation.

The direct dopamine agonist apomorphine has been reported to reduce the rewarding efficacy of lateral hypothalamic (LH) self-stimulation. This effect has been claimed to support the notion that dopamine mediates the rewarding effects of LH self-stimulation. Using a standard rate-frequency curve-shift paradigm with ascending order of frequency presentation, we also found that apomorphine (0.1-0.8 mg/kg, SC) appeared to decrease LH self-stimulation reward. These apparent rightward curve shifts were exacerbated by shortening the test duration, which also produced a number of sessions in which the subjects did not respond at all. When the presentation order of stimulation frequencies was reversed, apomorphine did not produce large reward decreases. These results suggest that the previously reported effects of apomorphine on LH self-stimulation were the result of artifact, perhaps related to apomorphine-induced stereotypical behavior combined with rapid pharmacological recovery.

Animals↗
PubMed1996

Effects of antimuscarinic antiparkinsonian drugs on brightness discrimination performance in rats.

Biperiden (BPR) and trihexyphenidyl (THP), the current antimuscarinic drugs of choice in the management of parkinsonism, have been shown to exert anticonvulsant effects induced by poisoning by the organophosphorus compound soman. The present study was undertaken to evaluate the effects of these drugs on performance of a simple light-intensity discrimination task in rats under a tandem schedule of fixed-ratio (FR) reward/ differential-reinforcement-of-low-rate (DRL) nonreward contingencies, for water reinforcement in 2-h experimental sessions. Both BPR (0.125-2.0 mg/kg, SC) and THP (0.25-8.0 mg/kg, SC) in general decreased overall reinforcement rates in a similar dose dependent and parallel manner, concurrent with increased overall nonreinforced responses in an inverted U-shaped dose-response relationship. Lower doses of BPR (0.125-0.5 mg/kg) and and THP (0.25-2.0 mg/kg) produced a moderate reduction in reinforcement (> or = 50% of baseline controls), which was correlated well with increases in nonreinforced responses emitted, whereas, higher doses of BPR (> 0.5 mg/kg) and TPH (> or = 2.0 mg/kg) markedly decreased reinforcements, which mainly resulted from the pausing of responding in the presence of stereotyped behavior. The behavioral disruption induced by BPR was much more rapid than that induced by THP. The ED50 values (0.6 mg/kg vs. 1.3 mg/kg, respectively) and parallel dose-effect curves suggest that these drugs have similar efficacy, and that BPR is about twice as potent as THP, a ranking that corresponds with their binding affinity at M-1 muscarinic acetylcholine receptors in rat cerebral cortex. Based on the similarity between the anticonvulsant doses of these drugs and the maximal doses that in this study did not disrupt operant responses (0.125 mg/kg vs. 0.25 mg/kg, respectively), it is suggested that both drugs may be useful in protection against seizures produced by the cholinesterase inhibitor soman. Overall, these results suggest that this multiple schedule operant contingency may have promise as a behavioral model to identify the therapeutic or toxic potentials of centrally acting antimuscarinic antiparkinsonian drugs based on their congnitive side effects.

Animals↗
PubMed1996

Low-dose apomorphine attenuates morphine-induced enhancement of brain stimulation reward.

Thresholds for brain stimulation reward (BSR) delivered to the medial forebrain bundle-lateral hypothalamus were determined by means of a rate free psychophysical method. Lower doses of apomorphine (0.5 to 0.2 mg/kg) produced modest elevations in BSR thresholds. A 0.4 mg/kg dose of apomorphine resulted in emergence of stereotypic behaviors and the loss of stimulus control. Morphine's BSR threshold lowering effects were significantly blocked by the concurrent administration of a 0.1 mg/kg dose of apomorphine. These results support the hypothesis that presynaptic dopamine neurons are involved in the mediation of morphine's reinforcing effects and that dopamine autoreceptor agonists may be of some use in the pharmacotherapy of opiate abuse.

Animals↗
PubMed1986

Naltrexone inhibits the persistent spasmodic dyskinesia induced by chronic intraperitoneal administration of iminodipropionitrile (IDPN).

The effects of naltrexone on the persistent movement disorder induced in mice by the neurotoxic substance IDPN were examined. Naltrexone (2-4 mg/kg, IP) significantly reduced the hyperactivity and the stereotypic behaviors induced by IDPN. Fifteen minutes after the injection of naltrexone, the dyskinetic neck movements were almost completely inhibited at the higher dose. Thus, blockade of opiate receptors can significantly affect drug-induced persistent dyskinesia.

Animals↗
PubMed1985

Animal models for the study of anti-anxiety agents: a review.

Animal models for the study of anxiolytic agents are reviewed and evaluated according to pharmacological and behavioral criteria. Although there are important exceptions, in general, most early animal models have not provided a reliable basis for identifying compounds with potential anxiolytic action, or for delineating the mechanisms of anxiolytic drug action. The possibility that phylogenetically 'prepared' forms of defensive learning might serve as a basis for the study of anxiolytic agents is introduced.

Aggression↗
PubMed1991

Corticotropin-releasing hormone is a rapid and potent convulsant in the infant rat.

Corticotropin-releasing hormone (CRH) administered into the cerebral ventricles of rats during the first postnatal week caused a specific and stereotyped behavior sequence: rhythmic chewing and licking (jaw myoclonus) were followed by 'limbic'-type seizures. The onset of the seizures was much more rapid (2-45 min vs 3-7 h) than in adult rats, and the convulsant doses were much lower (50 x 10(-12) mol per gram brain weight vs 750 x 10(-12) mol per gram brain weight in adults). CRH potency in inducing seizures varied inversely with age. CRH-induced seizures occurred prior to any changes in serum corticosterone, and were eliminated by the administration of a CRH antagonist, as well as of phenytoin. Electrocorticographic correlates of CRH-induced behaviors in the infant rat were inconsistent, suggesting a subcortical origin of CRH-induced paroxysmal events in the immature brain.

Aging↗