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PubMed1988

Effects of the novel benzodiazepine agonist quazepam on suppressed behavior of monkeys.

Behavioral effects of the benzodiazepine agonist quazepam were compared with those of lorazepam in squirrel monkeys responding under a fixed-interval schedule of food presentation with a superimposed fixed-ratio schedule of response-produced shock. Low and intermediate i.v. doses of quazepam (0.1-1.0 mg/kg) and lorazepam (0.03-0.3 mg/kg) increased rates of suppressed responding, yet the maximal increases in rate were less after quazepam than after lorazepam. Higher doses of both drugs tended to increase responding less or decrease it and, with quazepam, frequent sleep was observed for 2-3 days afterwards. The dose-response curves for quazepam and lorazepam were shifted to the right following i.v. pretreatment with the benzodiazepine antagonists Ro 15-1788 (0.18-3.0 mg/kg) or AHR-11797 (1.0-5.6 mg/kg); in this regard, AHR-11797 was less potent than Ro 15-1788. Although the effects of quazepam on suppressed responding are likely due to actions at benzodiazepine receptors, these effects may be influenced by or reflect a more prominent sleep-promoting action of the drug.

Animals↗
PubMed1992

(-)-stepholidine: a dopamine receptor antagonist shows agonistic effect on rotational behavior in 6-hydroxydopamine-lesioned rats.

(-)-Stepholidine ((-)-SPD), a well demonstrated dopamine (DA) receptor antagonist in normal rats, could markedly induce contralateral rotational behavior in 6-hydroxydopamine (6-OHDA)-lesioned rats. This peculiar behavioral action of (-)-SPD, proposed to be an agonistic action on DA receptors, was further studied in this paper. The rotational behavior challenged by (-)-SPD (4 mg.kg-1, ip) or SKF-38393 (selective D1 agonist) had a gradually progressive process with a long latent period and a plateau response after 56-67 postlesion days. On the contrary, the action of apomorphine (APO) or D2 selective agonist N-0347, had a short latent period and a plateau response after d 21 of postlesion. In the latent period of rotation, (-)-SPD (4 mg.kg-1) was primed by pretreatment of APO (0.2 mg.kg-1, ip). In the period of steady contralateral rotation, a dose-dependent action of (-)-SPD was found in a range of 0.5-8 mg.kg-1 and a linear correlation (r = 0.77, P less than 0.01) between the rotation induced by (-)-SPD (4 mg.kg-1) and by APO (0.2 mg.kg-1) was also shown. These results suggest that the agonistic effect of (-)-SPD on rotation behavior in 6-OHDA-lesioned rats resembles that of D1 agonist SKF-38393. Taken together, the dual actions of (-)-SPD, antagonistic on normosensitive DA receptors and agonistic on supersensitive DA receptors, were proposed.

Animals↗
PubMed1992

Effects of LY163502, a D2 dopaminergic agonist, on the sexual behavior of male rats.

LY163502, a selective D2 receptor agonist, has been reported to stimulate sexual behavior in both copulating and noncopulating male rats. Three experiments were conducted to further characterize the role of dopamine on male sexual behavior. In the first experiment, quinelorane (LY163502) was directly infused into the medial preoptic area (MPOA) of castrated males either alone or in combination with subphysiological levels of testosterone (T) exposure. The results showed that male sexual behavior was not affected by infusion of LY163502 alone, subphysiological T levels alone, or the combination of LY163502 and subphysiological T levels. For the second experiment, all animals received physiological levels of T and MPOA infusions of LY163502 or saline. The results showed an earlier restoration of male sexual behavior in the LY163502 group when compared to the T-only group. In the third study, noncopulating, gonadally intact males received SC injections of either LY163502 or saline 30 min prior to copulatory testing. The results showed that LY163502 induced a significant decrease in mount and intromission latencies after 14 days of drug exposure. From these results, we conclude a) that D2 receptors play a role in the facilitation of male sexual behavior and b) that the action of dopamine at D2 receptors requires the presence of T.

Animals↗
PubMed1985

Dominant social status facilitates the behavioral effects of serotonergic agonists.

The effects of dominance rank on the behavioral responses to drugs that enhance central serotonergic function were examined in 45 adult male vervet monkeys living in 15 stable social groups. Each group contained 3 adult males, 3 adult females, and their immature offspring. Dominance rank was assessed by measuring success in intermale agonistic encounters. In every group one male was clearly the dominant, or alpha male, and the other two males were subordinate. Males from 5 groups received 3 doses of the serotonin reuptake inhibitor fluoxetine (0.5, 1.0 and 2.0 mg/kg/day); those from a second set of 5 groups received 3 doses of the receptor agonist quipazine (0.25, 0.50 and 1.0 mg/kg/day); those from a third set of 5 groups received the serotonin precursor tryptophan (10, 20 and 40 mg/kg/day). The 3 drug treatments produced strikingly similar behavioral effects. Each produced dose-dependent increases in approaching, grooming, resting and eating and decreases in locomoting, avoiding, being vigilant and being solitary. Dominant males were significantly more responsive behaviorally to all 3 drugs than were subordinate males: the increase or decrease in each behavioral measure was larger in dominant than in subordinate males. In combination with previous studies, these data suggest that dominant and subordinate males differ in the drug sensitivity of their serotonergic systems.

Age Factors↗
PubMed1987

Effects of clenbuterol and prenalterol on behavior maintained under a multiple fixed-interval, fixed-ratio schedule.

The results of a number of studies have implicated beta adrenergic receptors in the brain in the actions of proven antidepressant drugs. This suspected involvement of central beta adrenergic receptors made it of interest to characterize the behavioral effects of centrally acting beta adrenergic agonists. Clenbuterol and prenalterol, unlike most beta adrenergic agonists, penetrate into the central nervous system after peripheral administration. In the present study, the effects of these agonists on behavior maintained under a multiple fixed-interval 5-min, fixed-ratio 30-response schedule were determined. Both compounds, in a dose-dependent manner, reduced response rate under both components of the multiple schedule. Under the fixed-interval component, clenbuterol and prenalterol altered the temporal pattern of responding. At no dose tested was there evidence for any stimulant action of either of the drugs. The effects of clenbuterol and prenalterol on behavior maintained under the multiple schedule appeared to be a result of an interaction of the agonists with beta adrenergic receptors. This was evidenced by the ability of the beta adrenergic antagonist propranolol to block the effects of the agonists. The behavioral effects of clenbuterol and prenalterol appear, in general, to be similar to effects reported previously for tricyclic and monoamine oxidase inhibiting antidepressant drugs.

Adrenergic beta-Agonists↗
PubMed1987

Behavioral effects of GABA agonists in relation to anxiety and benzodiazepine action.

A considerable body of biochemical and neurophysiological evidence implicates GABA in anxiety and in benzodiazepine action. The present article surveys the behavioral effects of GABA agonists and their interactions with drugs acting at the benzodiazepine receptor in animal anxiety paradigms. Certain GABA agonists, notably valproate, simulate many behavioral actions of benzodiazepines. Moreover, several behavioral studies of the interaction of GABA agonists with benzodiazepines support the hypothesis of a benzodiazepine receptor complex with one or more GABA, benzodiazepine and probably other binding sites. However, there are also a number of anomalous findings of GABA agonist action alone and in combination with benzodiazepines. It is argued that these paradoxical results can better be accounted for in terms of the receptor complex and the distribution of the drugs, rather than by suggesting that the anxiolytic actions of benzodiazepines are not mediated by GABA systems. The potential clinical usefulness of GABA agonists in anxiety is commented upon.

Animals↗
PubMed1983

Effects of three dopamine agonists on cage climbing behavior.

The effects of three structurally related dopamine (DA) agonists (pergolide, lergotrile, bromocriptine) on motor activity and induction of cage climbing behavior were compared in mice. Pergolide stimulated activity and induced cage climbing that persisted for at least 5 h. Lergotrile depressed activity and failed to induce climbing over a wide range of doses. Bromocriptine produced stimulation and climbing, but only after a 2-3 h delay following injection. The qualitative differences among these drugs may represent an action involving different DA receptor subjects.

Animals↗
PubMed1993

Effects of the beta-2 adrenergic agonist zinterol on DRL behavior and locomotor activity.

The purpose of the present study was to assess the behavioral effects of the beta adrenergic agonist zinterol and to determine whether its actions were mediated by beta adrenergic receptors. Zinterol reduced response rate and increased reinforcement rate of rats under a differential-reinforcement-of-low-rate schedule in a dose-dependent manner; significant decreases in response rate and increases in reinforcement rate were observed at doses of 0.1-1 mg/kg. The effect of 0.3 mg/kg zinterol on this behavior was blocked by pretreatment with the beta adrenergic antagonist propranolol. Zinterol also reduced locomotor activity in a dose-dependent manner; significant reductions were observed at doses of 0.3-10 mg/kg. Similarly, the effect of 1 mg/kg zinterol on locomotor activity was antagonized by propranolol. These effects of zinterol were similar to those of other beta adrenergic agonists as well as those of antidepressant drugs. Although the site of action (central versus peripheral) of zinterol was not determined in the present study, an experiment was carried out to determine if zinterol could act centrally after peripheral administration. The ability of repeated, systemic administration of zinterol to reduce the density of beta adrenergic receptors in cerebral cortex and cerebellum was determined. Repeated treatment with a high dose of zinterol (10 mg/kg, IP) reduced the density of beta adrenergic receptors in these brain regions, suggesting that, at least under certain conditions, systemically administered zinterol did have access to the central nervous system.

Adrenergic beta-Agonists↗
PubMed1992

Mu-, delta-, and kappa-opioid receptor agonists selectively modulate sexual behaviors in the female rat: differential dependence on progesterone.

Previous studies suggested that opioid receptor agonists infused into the lateral ventricles can inhibit (through mu receptors) or facilitate (through delta receptors) the lordosis behavior of ovariectomized (OVX) rats treated with estrogen and a low dose of progesterone. The present study investigated the behavioral and hormonal specificity of those effects using more selective opioid receptor agonists. Sexually experienced OVX rats were implanted stereotaxically with guide cannulae aimed at the right lateral ventricle. One group of rats was treated with estradiol benzoate (EB, 10 micrograms) 48 hr and progesterone (P, 250 micrograms) 4 hr before testing, whereas the other group was treated with EB alone. Rats were infused with different doses of the selective mu-receptor agonist DAMGO, the selective delta-receptor agonist DPDPE, or the selective kappa-receptor agonist U50-488. The females were placed with a sexually vigorous male in a bilevel chamber (Mendelson and Gorzalka, 1987) for three tests of sexual behavior, beginning 15, 30, and 60 min after each infusion. DAMGO reduced lordosis quotients and magnitudes significantly in rats treated with EB and P, but not in rats treated with EB alone. In contrast, DPDPE and U50-488H increased lordosis quotients and magnitudes significantly in both steroid-treatment groups. Surprisingly, measures of proceptivity, rejection responses, and level changes were not affected significantly by mu or kappa agonists, although proceptivity and rejection responses were affected by DPDPE treatment. These results suggest that the effects of lateral ventricular infusions of opioid receptor agonists on the sexual behavior of female rats are relatively specific to lordosis behavior. Moreover, the facilitation of lordosis behavior by delta- or kappa-receptor agonists is independent of progesterone treatment, whereas the inhibitory effect of mu-receptor agonists on lordosis behavior may require the presence of progesterone.

Animals↗
PubMed1992

Selective effects of the D1 dopamine receptor agonist, SKF 38393, on behavior maintained by cocaine injection in squirrel monkeys.

The effects of the dopamine receptor D1 partial agonist, SKF 38393, on behavior maintained by cocaine was assessed in squirrel monkeys (Saimiri sciureus). One group of subjects was trained to press a key under a fixed-ratio 30-response schedule of cocaine injection; when green stimulus lamps were illuminated each 30th response produced an injection (17 micrograms/kg) followed by a 1-min period during which the lights were out and responses had no scheduled consequences. Another group of squirrel monkeys was trained under an identical schedule with food reinforcement. SKF 38393 produced dose-related decreases in rates of responding maintained by either cocaine injection or food presentation. Rates of responding maintained by cocaine were decreased to a greater extent than those maintained by food. The ED50 value for SKF 38393 for responding maintained by cocaine was 2.53 mg/kg (95% CL: 1.22-5.23), whereas that value was 15.63 mg/kg (95% CL: 2.83-86.33) for responding maintained by food. Rates of responding maintained by cocaine were an inverted-U-shaped function of dose. Pretreatment with 3.0 mg/kg SKF 38393 shifted the ascending limb of the cocaine dose-effect curve to the right. These findings suggest that indirect D1-receptor activation plays a role in the reinforcing effects of cocaine, and that drugs acting at D1 receptors may show promise as therapeutic agents in the treatment of cocaine abuse.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Comparison of the behavioral effects of adenosine agonists and dopamine antagonists in mice.

The adenosine agonists 5'-N-ethylcarboxamideadenosine (NECA), 2-chloroadenosine (2-CLA), N6-cyclohexyladenosine (CHA), N6-cyclopentyladenosine (CPA), 2-(phenylamino)adenosine (CV-1808) and R and S isomers of N6-phenylisopropyladenosine (R-PIA and S-PIA) decreased spontaneous locomotor activity in mice and, except for CPA, did so at doses that did not impair motor coordination, a profile shared by dopamine antagonists. CV-1808, the only agent with higher affinity for A2 as compared with A1 adenosine receptors, displayed the largest separation between locomotor inhibitory and ataxic potency. Like dopamine antagonists, NECA and CV-1808 also decreased hyperactivity caused by d--amphetamine at doses that did not cause ataxia whereas A1-selective adenosine agonists reduced amphetamine's effects only at ataxic doses. Unlike dopamine antagonists, adenosine agonists inhibited apomorphine-induced cage climbing only at doses that caused ataxia. Involvement of central adenosine receptors in these effects was suggested by the significant correlation obtained between potency for locomotor inhibition after IP and ICV administration. Affinity for A1 but not A2 adenosine receptors was significantly correlated with potency for inducing ataxia. These results suggest that the behavioral profile of adenosine agonists in mice is related to their affinity for A1 and A2 adenosine receptors and indicate that adenosine agonists produce certain behavioral effects that are similar to those seen with dopamine antagonists.

Adenosine↗
PubMed1996

Agonist efficacy and the behavioral effects of dopamine D1 receptor ligands: drug interaction studies in squirrel monkeys.

Dopamine agonists that reportedly differ in intrinsic activity at dopamine D1 receptors were compared for their behavioral effects in squirrel monkeys responding under a fixed-ration schedule of reinforcement. When administered alone, all drugs produced dose-related decreases in fixed-ratio response rates. Pretreatment with the dopamine D1 receptor blocker SCH 39166, but not the dopamine D2 receptor blocker eticlopride, produced rightward shifts in the dose-effect functions for the high-efficacy dopamine D1 agonists SKF 82958 (R,S-6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro- 1H-3-benzazepine) SKF 81297 (R,S-6-chloro-7,8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine ) and dihydrexidine, indicative of surmountable antagonism at dopamine D1 receptors. Pretreatment with SCH 39166, however, did not antagonize the effects of the low-efficacy dopamine D1 agonists SKF 75670 (R,S-7,8-dihydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine ), SKF 77434 (R,S-7,8-dihydroxy-3-allyl-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine) or R-SKF 38393 (R-7,8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine); instead, dose-effect functions for each of these drugs were shifted downward and to the left. In additional experiments, pretreatment with SKF 75670 produced overall rightward shifts in the dose-effect functions for dihydrexidine and SKF 81297; pretreatment with R-SKF 38393 produced an overall rightward shift in the dose-effect function for dihydrexidine, but not SKF 81297; and pretreatment with SKF 81297 failed to produce a rightward shift in the dose-effect function for dihydrexidine. These findings provide further evidence that the behavioral effects of dopamine D1 agonists in monkeys are mediated primarily by their actions at dopamine D1 receptors. The differing susceptibility of dopamine D1 agonists to antagonism by SCH 39166 and their differing interactions provide functional evidence for differences in their dopamine D1 agonist efficacy.

Animals↗
PubMed1984

The effect of olfactory bulb lesions on agonistic, locomotory and social behavior in mice housed in aggregate.

Eleven Dublin ICR mice sustaining nearly complete bilateral aspiration lesions of the olfactory bulbs were compared to 16 sham-operated mice on the frequency of agonistic, locomotory, social, and maintenance behaviors. The animals were housed in aggregate with two cages of bulbectomized mice and two cages of shams. A time sampling technique was used to quantify the frequency of the various behaviors three times per week during one preoperative and four postoperative weeks. During the first two postoperative weeks the bulbectomized mice were observed to make frequent single bites of the head incision and tail of mice passing directly in front of them, with the bites resulting in mild to severe lesions. Following surgery, the bulbectomized mice also showed a temporary increase in locomotory responses and permanent suppression of social responses.

Aggression↗
PubMed1995

Induction or protection of limbic seizures in mice by mGluR subtype selective agonists.

The behavioral consequences of metabotropic glutamate receptor (mGluR) activation were investigated following intracerebral administration of the mGluR selective agonists (RS)3,5-dihydroxyphenyl-glycine (3,5-DHPG), (1S,3R)-1-aminocyclopentane-1,3-dicarboxylate (1S,3R-ACPD), (1R,3S)-1-aminocyclopentane-1,3-dicarboxylate (1R,3S-ACPD), L-2-amino-4-phosphonobutyrate (L-AP4), L-serine-O-phosphate (L-SOP) and (2S,3S,4S)alpha-(carboxycyclopropyl)glycine (L-CCGI) into the thalamus in mice. Injections of 3,5-DHPG, 1S,3R-ACPD and L-CCGI produced dose-dependent increases in limbic seizures with a potency order of 3,5-DHPG = 1S,3R-ACPD > L-CCGI. This effect of 1S,3R-ACPD was stereoselective, since the inactive isomer (1R,3S-ACPD) did not elicit seizure activity. Limbic seizures induced by the phosphoinositide-coupled mGluR subtype selective agonist 3,5-DHPG were attenuated by the mGluR antagonist L-2-amino-3-phosphonopropanoic acid (L-AP3) and dantrolene, inhibitors of mGluR-mediated intracellular calcium mobilization. Interestingly, L-AP4, L-SOP and low doses of L-CCGI also protected against 3,5-DHPG seizures. These data indicate that mGluR agonist-induced limbic seizures in mice are mediated by activation of phosphoinositide-coupled mGluRs. Furthermore, these seizures can be protected against by activation of mGluRs that are negatively-linked to cAMP formation.

Animals↗
PubMed1995

Differential effects of dopamine D1 and D2 receptor agonists on schedule-controlled behavior of squirrel monkeys.

The effects of dopamine agonists differing in affinity and selectivity at D1 and D2 types of dopamine receptors were compared in squirrel monkeys responding under two different schedules of reinforcement: a fixed-interval (FI) schedule of stimulus-shock termination and a fixed-ratio (FR) schedule of food presentation. Dopamine D1 family agonists included dihydrexidine, SKF 81297, SKF 82958, R-6-Br-APB, SKF 83189, SKF 77434, SKF 75670 and R- and R, S-SKF 38393. Dopamine D2 agonists included (+)-PHNO, quinpirole and N-0434; nonselective DA agonists included R(-)-apomorphine and CY 208-243. The behavioral effects of D1 agonists differed qualitatively from those of D2 and nonselective DA agonists. D1 agonists produced dose-related decreases in both FI and FR responding, with comparable doses being effective under the two schedules. The rank order of potency for the rate-decreasing effects of these drugs was R(+)-6-Br-APB > SKF 75670 > SKF 82958 > R-SKF 38393 > SKF 81297 > SKF 77434 > SKF 83189 > dihydrexidine > R, S-SKF 38393. In contrast, D2 and nonselective DA agonists produced significant increases in rates of FI responding at doses that reduced FR response rates. The rank order of potency for the rate-increasing effects of these drugs under the FI schedule was (+)-PHNO > N-0434 > R-apomorphine > CY 208-243 > quinpirole.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1991

Behavioral studies of serotonin receptor agonists as antidepressant drugs.

Recent developments in the pharmacology of antidepressant drugs have focused on compounds that enhance the neurotransmission of serotonin (5-hydroxytryptamine; 5-HT), such as 5-HT uptake inhibitors. In addition, the 5-HT1A receptor partial agonist buspirone and other similarly structured compounds termed azapirones are also candidates for antidepressant therapy. The author reviews results from clinical and preclinical studies that support the efficacy of 5-HT1A receptor agonists as antidepressants. Initial clinical trials and animal behavior studies that predict clinical activity of antidepressant drugs have reported evidence favoring the antidepressant-like activity of 5-HT1A receptor partial agonists. Animal behavior studies have also examined the potential neurochemical mechanisms underlying the antidepressant effects of buspirone and related compounds. Evidence is reviewed that the antidepressant activity may be due to the activation of postsynaptic 5-HT1A receptors, although 5-HT1A receptor agonists also activate somatodendritic autoreceptors which diminish the release of 5-HT. Evidence does not support the involvement of a common metabolite 1-PP in the antidepressant activity of 5-HT1A receptor-selective azapirones. Few studies have examined the effects of chronic administration of 5-HT1A receptor agonists and their potential interaction with other receptors, such as 5-HT2 receptors.

Animals↗
PubMed1993

Behavioral effects of dopaminergic agonists and antagonists alone and in combination in the squirrel monkey.

The effects on schedule-controlled operant behavior of the D2 receptor agonist, quinpirole, and the D1 agonist, SKF 38393, were assessed alone and in combination with selective dopamine-receptor antagonists. Squirrel monkeys (Saimiri sciureus) were trained to press a response key under fixed-interval and fixed-ratio schedules of food reinforcement. The fixed-interval schedule maintained relatively low rates of responding that increased up to food presentation. The fixed-ratio schedule maintained relatively constant high rates of responding. Quinpirole increased rates and disrupted the temporal pattern of responding under the fixed-interval schedule at doses (0.1-1.0 mg/kg) that decreased rates of responding under the fixed-ratio schedule. Under the fixed-interval schedule, the D2 antagonists, spiperone (0.003-0.006 mg/kg) and haloperidol (0.003-0.01 mg/kg), and the D1 antagonist, SCH 23390 (0.03 mg/kg), shifted the quinpirole dose-effect curve to the right. The maximal effects of quinpirole were decreased at the highest doses of the antagonists. However, only spiperone antagonized effects of quinpirole on the rates of responding under the fixed-ratio schedule. The D1 agonist, SKF 38393, dose-dependently (1.0-10.0 mg/kg) decreased rates of responding under both schedules. Those effects were not antagonised by any doses studied of either spiperone (0.003 mg/kg) or SCH 23390 (0.003-0.3 mg/kg). Rather, both antagonists enhanced the effects of SKF 38393.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗