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At least 685 records · Page 38Linked to original sources
PubMed1994

Behavioral effects of the dopamine autoreceptor agonist PD 128483 alone and in combination with cocaine.

Many of the behavioral effects of cocaine are thought to be mediated via dopamine (DA) reuptake inhibition and a subsequent increase in DA activity. As a DA agonist with selectivity for autoreceptors, PD 128483 has behavioral effects consistent with decreased DA neurotransmission and might be expected to attenuate the behavioral effects of cocaine. The present study was designed to evaluate PD 128483 ((+)-4,5,5a,6,7,8-hexahydro-6-methyl-thiazolo[4,5-f]quinoline-2-amine) alone and in combination with cocaine in three behavioral paradigms. One group of rhesus monkeys (n = 7) was allowed to self-administer cocaine (0.03 or 0.1 mg/kg/injection i.v., fixed-ratio 10, 2 hr/day) in baseline sessions. When behavior was stable, PD 128483 (0.01-0.3 mg/kg/injection i.v.) was made available for self-administration, and failed to maintain responding in three of four monkeys tested. PD 128483 (1.0-10.0 mg/kg i.m.) decreased cocaine self-administration in all four monkeys tested when given before cocaine availability. Another group of monkeys (n = 4) was trained to discriminate cocaine (0.2 or 0.4 mg/kg i.m.) from saline in a two-lever, food-reinforced drug discrimination paradigm. High doses of PD 128483 (3.2-12.8 mg/kg i.m.) substituted for cocaine as a discriminative stimulus in three of four monkeys. Administered in combination with cocaine, PD 128483 had little effect on the cocaine discriminative stimulus up to doses which decreased response rate. PD 128483 (1.0-2.0 mg/kg i.p.) decreased milk intake in rats (n = 9) and, when given in combination with cocaine, shifted the cocaine dose-response function (4.0-16.0 mg/kg i.p.) to the left.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoquinolines↗
PubMed1992

Effect of chronic treatment with dizocilpine (MK-801) on the behavioral response to dopamine receptor agonists in the rat.

The D2 or D1 dopamine receptor blockers (-)-sulpiride or SCH 23390 antagonized, in a dose dependent manner, the hypermotility induced by the N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (0.25 mg/kg IP). MK-801 induced hyperactivity was not detected when rats were observed on days 7, 14 or 21 of 21 daily injections of MK-801. This lack of hyperactivity was also noted 5 days after the last administration of the repeated treatment with MK-801. The hypermotility induced by the D2 dopamine receptor agonist LY 171555 (0.3 mg/kg IP) was reduced 5 days following repeated treatment (21 days) with MK-801, while no change in the behavioral responses to the selective D1 agonist, SKF 38393, or the mixed D1/D2 agent apomorphine was detected. The results, although suggesting the involvement of dopaminergic pathways in the behavioral effect of MK-801, are conflicting with regard to the underlying mechanisms and to the adaptive changes of dopaminergic system following repeated NMDA receptor blockade.

Animals↗
PubMed2003

Effects of a partial dopamine D2-like agonist on the cocaine-induced behavioral sensitization of preweanling rats.

Partial D(2)-like receptor agonists act as functional antagonists when given during periods of high dopaminergic tone (e.g., when self-administering cocaine or amphetamine). For this reason, we determined whether pretreatment with the partial D(2)-like agonist terguride would block the induction and/or expression of cocaine-induced behavioral sensitization in preweanling rats. More specifically, we examined (a). whether repeated administration of terguride alone (0.4-1.6 mg/kg) would support behavioral sensitization (Experiment 1); (b). whether injecting preweanling rats with terguride (0.1-1.6 mg/kg) during the pretreatment phase would block the induction and ultimate expression of cocaine-induced behavioral sensitization (Experiment 2); and (c). whether injecting rats with terguride (0.2-0.8 mg/kg) on the test day would block the expression of cocaine sensitization (Experiment 3). Results showed that repeated terguride administration did not induce behavioral sensitization by itself, nor did it block the induction of cocaine sensitization in preweanling rats. Interestingly, terguride reduced, but did not fully attenuate, the locomotor activity of cocaine-treated rats during the pretreatment phase. When given on the test day, terguride also depressed cocaine-induced locomotor activity, but rather than blocking the expression of behavioral sensitization, terguride seemed to cause a general reduction in locomotion. Because partial D(2)-like agonists attenuate cocaine- and amphetamine-induced reward, it has been proposed that this class of drug might serve as an effective pharmacotherapy for psychostimulant abuse. Although partial D(2)-like agonists may prove useful in this regard, results from the present study suggest that terguride would not block sensitization components of the addiction process.

Animals↗
PubMed2002

The nest as fortress: defensive behavior of Polybia emaciata, a mud-nesting eusocial wasp.

The swarm-founding wasp Polybia emaciata is unusual among eusocial Vespidae because it uses mud, rather than wood pulp, as its primary nest construction material. Polybia emaciata nests are more durable than similarly sized paper nests. We tested the hypothesis that the defensive behavior of this wasp may have been modified to take advantage of their strong nests in defense against vertebrate attacks. We simulated vertebrate disturbances by tapping on, and breathing in, P. emaciata nests and similarly sized P. occidentalis paper nests in the same location at the same time. Polybia emaciata responses to disturbance were qualitatively different from those of P. occidentalis. The latter exit the nest and attack, while P. emaciata workers typically fled or entered the nest, attacking only after repeated and extended disturbances. We conclude that durable nest material may permit predator avoidance behavior in P. emaciata. We compare the defensive responses of P. emaciata workers with those of other swarm-founding Vespidae, and discuss several selective forces that could cause the evolution of species variation in nest defense behavior.

Agonistic Behavior↗
PubMed1983

Organization and expression of agonistic and socio-sexual behavior in golden hamsters over the estrous cycle and after ovariectomy.

Pairs of hamsters were housed in large enclosures that contained separate male and female living areas and observed over the 4-day estrous cycle and after ovariectomy. Agonistic elements exhibited frequently by females included on-back, boxing, lateral posturing, and biting, whereas males engaged frequently in boxing and on-back patterns of behavior. Furthermore, on-back and boxing by females were significantly higher on estrus than on any other day of the estrous cycle. Agonistic acts performed after ovariectomy did not differ in occurrence from those shown by animals on diestrus and proestrus. Vaginal marking increased during diestrus and attained a peak 24 hr prior to sexual receptivity. Both vaginal marking and mating occurred more frequently in the female's than male's home area suggesting that vaginal marking and mating occurred serve to attract males to the nest of females. Males also organized their marking patterns by location as shown by more flank marking in their own than their partner's area, albeit the significance for this difference in location is not known. The results demonstrate that when heterosexual pairs of hamsters are tested in large and partially familiar habitats, a wide range of behavior is exhibited and organized in a manner that is not observed in small and unfamiliar cages.

Aggression↗
PubMed1995

Differential effects of CGS 12066B and CP-94,253 on murine social and agonistic behaviour.

Although it has been previously proposed that 5-HT1B agonism specifically attenuates rodent agonistic behaviour, more recent investigations have indicated that such influences may be ancillary to an anxiogenic effect. The present study examined the influences of two 5-HT1B agonists, CGS 12066B and CP-94,253, on murine agonistic behaviour. In a resident-intruder paradigm, CGS 12066B (0.5-5.0 mg/kg) decreased resident offensive aggression, social interest, and exploration while dose-dependently enhancing defensive behaviours across the dose range tested. CP-94,253 (2.5-10.0 mg/kg) also reduced elements of resident offensive behaviour whereas defensive behaviours were largely unchanged. Some elements of resident nonsocial and social behaviour were enhanced at 2.5 and 5.0 mg/kg but decreased at 10.0 mg/kg. The behavioural profile of CP-94,253, but not CGS 12066B, supports the proposal that 5-HT1B receptors inhibit agonistic behaviour without concomitant sedative or anxiogenic effects. Findings are discussed in relation to 5-HT1A/1B/2C receptors involved in agonistic behaviour and anxiety.

Agonistic Behavior↗
PubMed1989

Effects of centrally acting beta adrenergic agonists on discrete trial conditioned avoidance behavior in rats.

The acute effects of centrally acting beta adrenergic agonists on discrete trial conditioned avoidance responding in rats were examined. Clenbuterol (0.01-3.0 mg/kg), salbutamol (0.01-30 mg/kg), and prenalterol (30-300 mg/kg) suppressed avoidance responding in a dose-dependent manner at doses that did not produce escape failures. For comparative purposes, the effects of the tricyclic antidepressant desipramine (1.0-30 mg/kg) and the antipsychotic haloperidol (0.03-0.3 mg/kg) were similarly assessed. Both compounds suppressed avoidance responding in a dose-dependent manner. Only haloperidol (0.3 mg/kg) produced escape failures. Administered alone, the beta adrenergic antagonist propranolol (1.0 and 10 mg/kg) did not affect avoidance behavior. When administered prior to clenbuterol (0.1 mg/kg), salbutamol (1.0 mg/kg), or prenalterol (100 mg/kg), propranolol antagonized the beta adrenergic agonist-induced suppression of avoidance responding. The suppressive effect of desipramine (3.0 mg/kg) on avoidance performance only tended to be attenuated by propranolol. Propranolol had no effect on the ability of haloperidol (0.1 mg/kg) to reduce avoidance responding. These results suggest that the effects of the beta adrenergic agonists clenbuterol, salbutamol, and prenalterol on discrete trial avoidance behavior are mediated, in part, through agonist interactions with beta adrenergic receptors.

Adrenergic beta-Agonists↗
PubMed1990

Behavioral effects of beta adrenergic agonists and antidepressant drugs after down-regulation of beta-2 adrenergic receptors by clenbuterol.

Acute treatment with the centrally active beta-2 adrenergic agonist clenbuterol reduced response rate and increased reinforcement rate of rats responding under a differential-reinforcement-of-low-rate (DRL) 72-sec schedule in a dose-dependent manner (ED50 value of about 0.1 mg/kg). With repeated treatment, rapid tolerance developed to this effect of clenbuterol. Redetermination of the dose-response function for clenbuterol, following 2 weeks of repeated daily administration, showed that clenbuterol no longer affected DRL behavior at doses up to 3 mg/kg. Interestingly, tolerance developed to clenbuterol even when it was administered after each daily session. This suggests that behavioral factors did not contribute, in an appreciable manner, to the development of tolerance to clenbuterol, and that neuropharmacological changes were sufficient for tolerance development. Such an interpretation is supported by the finding that the density of beta-2 adrenergic receptors in the cerebral cortices and cerebella of rats receiving the same repeated-treatment regimen was reduced with a time course similar to the loss of behavioral responsiveness. The effects of two additional beta-2 selective agonists, SOM-1122 and zinterol, on DRL behavior also were attenuated after repeated treatment with clenbuterol. By contrast, the effects of the beta-1 selective agonists dobutamine and prenalterol and the antidepressants desipramine, phenelzine and fluoxetine on DRL behavior were unaltered after repeated treatment with clenbuterol. These findings suggest functional independence of the beta adrenergic receptor subtypes and further suggest that, consistent with neuropharmacological data, the behavioral effects of the antidepressants do not depend on functionally responsive beta-2 adrenergic receptors.

Adrenergic beta-Agonists↗
PubMed1997

The effects of mixing on behavior and circadian parameters of salivary cortisol in pigs.

The present study describes an experiment that was carried out to study the effects of mixing pigs once at 25 kg, preceded by transportation for 1.5 h, on the behavior and the circadian rhythmicity of salivary cortisol. The frequency of agonistic interactions was higher for mixed pigs. This was not only the case immediately after mixing, when pigs started to fight to establish a new social rank (p < 0.05), but also 5 to 6 weeks later; still more headknocks and bites towards other pigs were seen at that time among mixed pigs (p < 0.01). However, neither the basal cortisol concentration, assessed as the MESOR of the circadian rhythm of salivary cortisol, nor the amplitude of that rhythm was different between the groups.

Aggression↗
PubMed2003

Altered behavioral response to dopamine D3 receptor agonists 7-OH-DPAT and PD 128907 following repetitive amphetamine administration.

Behavioral sensitization, the progressive and enduring enhancement of certain behaviors following repetitive drug use, is mediated in part by dopaminergic pathways. Increased locomotor response to drug treatment, a sensitizable behavior, is modulated by an opposing balance of dopamine receptor subtypes, with D1/D2 dopamine receptor stimulation increasing and D3 dopamine receptor activation inhibiting amphetamine-induced locomotion. We hypothesize that tolerance of D3 receptor locomotor inhibition contributes to behavioral sensitization. In order to test the hypothesis that expression of behavioral sensitization results in part from release of D3 receptor-mediated inhibition, thereby resulting in decreased response to D3 receptor agonists, we examined the effect of repetitive amphetamine administration on the behavioral response to the D3 receptor preferring agonists 7-OH-DPAT and PD 128907. D3-selective effects have recently been described for both drugs at a low dose. At 1 week following completion of a repetitive treatment regimen, amphetamine-pretreated rats displayed a decreased response to D3-selective doses of both 7-OH-DPAT and PD 128907, when compared to animals receiving saline pretreatment. Moreover, in addition to the quantitative alteration in response, there was a change in the inter-relation between response to amphetamine and D3 agonist. A highly significant inverse relation between locomotor inhibitory response to PD 128907 and the locomotor-stimulant response to amphetamine was observed prior to amphetamine treatment. In contrast, 10 days following repetitive amphetamine treatment, the relation between response to PD 128907 and amphetamine was not detected. The observed behavioral alteration could not be accounted for by changes in D3 receptor binding in ventral striatum. These findings suggest a persistent release of D3 receptor-mediated inhibitory influence contributes to the expression of behavioral sensitization to amphetamine.

Amphetamine↗