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PubMed1988

[Antagonism of caerulein, a CCK-8 receptor agonist, to the behavioral effects of ketamine in mice and rats].

It has been established in experiments on male mice and rats that caerulein antagonized the behavioural effects of ketamine, an agonist of phencyclidine receptors. Caerulein (75-375 micrograms/kg) and haloperidol (0.1-1.5 mg/kg) suppressed the stereotyped behaviour and motor excitation induced by ketamine (30 mg/kg) in mice. Caerulein and haloperidol failed to affect ketamine-induced ataxia. Caerulein (10 micrograms/kg) and the opioid antagonist naloxone (5 mg/kg) completely blocked the amnestic action of ketamine (30 mg/kg) in passive avoidance experiments on rats. It seems likely that the suppression of the behavioural effects of ketamine by caerulein is related to its functional antagonism with dopamine and opioid receptors.

Amnesia↗
PubMed2006

Interaction of the tachykinin NK3 receptor agonist senktide with behavioral effects of cocaine in marmosets (Callithrix penicillata).

Brain neuropeptide transmitters of the tachykinin family are involved in the organization of many behaviors. However, little is known about their contribution to the behavioral effects of drugs of abuse. Recently, antagonism of the tachykinin NK3-receptor (NK3-R), one of the three tachykinin receptors in the brain, was shown to attenuate the acute and chronic behavioral effects of cocaine in rats and the acute effects in non-human primates. In order to expand these findings we investigated the effects of the NK3-R agonist, succinyl-[Asp6, Me-Phe8]SP(6-11) (senktide), on the acute behavioral effects of cocaine in marmoset monkeys (Callithrix penicillata) using a figure-eight maze procedure. Animals were pretreated with senktide (0, 0.1, 0.2, 0.4 mg/kg, s.c.), and received either a treatment with cocaine (10 mg/kg) or saline (i.p.). Cocaine increased locomotor activity and the duration of aerial scanning behavior, but reduced exploratory activity, bodycare activity, the frequency of aerial scanning, and terrestrial glance behavior. Senktide blocked the effects of cocaine on locomotor activity, but enhanced the cocaine effects on exploratory activity, aerial scanning frequency, and terrestrial glance behavior. Senktide alone did not significantly influence monkey behavior in this study. These data expand previous findings suggesting a complex role of the NK3-R in the acute behavioral effects of cocaine in non-human primates.

Animals↗
PubMed1995

Perseveration without hyperlocomotion in a spontaneous alternation task in rats sensitized to the dopamine agonist quinpirole.

Behavioral sensitization induced by intermittent injections of the dopamine agonist quinpirole is characterized by hyperlocomotion and perseveration. This study tested whether in sensitized rats, the expression of perserverative behavior can be independent of hyperlocomotion. Rats received 10 injections of either quinpirole (0.5 mg/kg) or saline in a T-maze apparatus, a procedure that induced locomotor sensitization in the drugged animals. When tested later (under quinpirole) for spontaneous alternation in the same T-maze, in a discrete trial procedure, sensitized rats showed decreased spontaneous alternation, compared either to saline controls or acute quinpirole. The decrease in spontaneous alternation showed a tendency to be lower than chance level of alternation, suggesting perseveration. The possibility is discussed that the sensitization-reduced spontaneous alternation may relate to a diminution in the sense of task completion, and the increased perseveration may model a form of compulsive "checking" shown in obsessive-compulsive disorder.

Animals↗
PubMed1996

Synergistic interaction between an adenosine antagonist and a D1 dopamine agonist on rotational behavior and striatal c-Fos induction in 6-hydroxydopamine-lesioned rats.

The interaction between adenosine and D1 dopamine systems in regulating motor behavior and striatal c-Fos expression was examined in rats with unilateral 6-hydroxydopamine (6-OHDA) lesions. These results were compared to the synergistic interaction between D1 and D2 dopamine systems in 6-OHDA rats. Coadministration of the adenosine antagonist 3,7-dimethyl-1-propargylxanthine (DMPX: 10 mg/kg) and the D1 dopamine agonist SKF38393 (0.5 mg/kg) to 6-OHDA-lesioned rats produced significant contralateral rotation and c-Fos expression in the ipsilateral striatum compared to 6-OHDA rats treated with either drug alone. However, the regional pattern of striatal c-Fos activation following treatment of 6-OHDA rats with SKF38393 and DMPX was different from the dorsolateral pattern of striatal c-Fos induction observed after coadministration of D1 and D2 dopamine agonists (SKF38393: 0.5 mg/kg + quinpirole: 0.05 mg/kg). These data are consistent with a functional interaction between D1 dopamine and adenosine systems in the striatum, but suggest that activation of different subsets of striatal neurons underlie the behavioral synergy observed following combined adenosine antagonist-D1 dopamine agonist and combined D1 dopamine agonist-D2 dopamine agonist treatment.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2006

Suppression of methamphetamine-seeking behavior by nicotinic agonists.

To understand the mechanism of methamphetamine (MAP) craving from the viewpoint of nicotinic acetylcholinergic transmission, we examined the responsible site of the brain for anticraving effects produced by nicotinic agonists by using a MAP self-administration paradigm in rats. Systemic nicotine and an acetylcholinesterase inhibitor, donepezil, attenuated the reinstatement of MAP-seeking behavior by means of the activation of nicotinic acetylcholinergic receptors, but not muscarinic acetylcholinergic receptors, in the nucleus accumbens core, prelimbic cortex, amygdala, and hippocampus. Among these regions, with the exception of the hippocampus, we also found functional differences in this reinstatement. The nicotinic antagonist mecamylamine alone did not reinstate MAP-seeking behavior. These results suggest that the inactivation of nicotinic acetylcholinergic transmission may be an essential factor in the appearance of MAP-seeking behavior, and, thus, the normalization of the inactivated state may result in the suppression of the reinstatement. Our findings also indicate that there are functional differences in the responsible brain subregions. Extending this view to the treatment of MAP dependence, our results suggest that activators of nicotinic acetylcholinergic transmission are possible anticraving agents.

Acetylcholinesterase↗
PubMed1994

Effects of monoamine oxidase inhibitors and dopamine agonists on the behavior of mammal- and frog-eating snakes.

Skin mucus of the frog, Xenopus laevis, induces climbing and attenuates tongue flicking in Nerodia sipedon; these effects are induced alone and are potentiated by L-deprenyl, a monoamine oxidase type B inhibitor (MAO-Bi), but not by clorgyline, an MAO type A inhibitor (MAO-Ai). Both MAO-A and MAO-B metabolize dopamine, with MAO-B having the higher affinity; MAO-A selectively metabolizes serotonin and norepinephrine and MAO-B is selective for phenylethylamine. It was hypothesized that clorgyline and L-deprenyl would differentially modulate tongue flicking and climbing in frog-eating (Nerodia erythrogaster) and mammaphagous (Elaphe o. obsoleta) snakes, based on physiological differences between the species. L-Deprenyl caused a decrease in tongue flicking and climbing by Elaphe and an increase in climbing by Nerodia, whereas clorgyline did not alter tongue flicking, climbing, or locomotor activity in either species. To further assess the role of dopamine, hybrid black/gray rat snakes, E. o. spiloides, were administered the D1 and D2 dopamine receptor agonists SKF 77434 (SKF 38393, N-allyl) and quinpirole, respectively. SKF 77434 and quinpirole attenuated climbing, but only SKF 77434 attenuated tongue flicking in Experiment 3; neither drug affected locomotor activity. Results suggest that dopaminergic stimulation by MAO-Bi and dopamine agonists modulates tongue flicking and climbing behaviors in snakes, and that the contrasting climbing reactions induced by MAO-Bi between Elaphe and Nerodia may be linked to quantitative differences in endogenous catecholamine levels and/or to the numbers and sensitivity of receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2005

Interaction between the antidepressant-like behavioral effects of beta adrenergic agonists and the cyclic AMP PDE inhibitor rolipram in rats.

RATIONALE: Type 4 phosphodiesterase (PDE4) is critical for hydrolysis of cAMP formed by stimulation of beta adrenergic receptors. However, it is not known if PDE4 is associated with beta adrenergic receptors in the mediation of antidepressant-like effects. OBJECTIVE: The aim of the study is to determine the relationship between PDE4 and beta adrenergic receptor-mediated cAMP signaling in mediating antidepressant-like effects. METHODS: The effects of the PDE4 inhibitor rolipram, alone or combined with dobutamine or clenbuterol, selective beta-1 and beta-2 adrenergic agonists, respectively, on behavior were examined in rats under a differential reinforcement of low rate (DRL) schedule and rats trained to discriminate rolipram from vehicle. Their effects on cAMP in primary cultures of rat cerebral cortical neurons also were determined. RESULTS: Rolipram (0.01-0.3 mg/kg), dobutamine (1-30 mg/kg), and clenbuterol (0.03-0.3 mg/kg) dose-dependently produced antidepressant-like effects on DRL behavior, decreasing response rate and increasing reinforcement rate. The effects of beta adrenergic agonists were potentiated by rolipram. Isobolographic analysis revealed that rolipram enhanced the antidepressant-like effect of dobutamine additively and that of clenbuterol synergistically. Consistently, a combination of ineffective doses of rolipram (0.03 mg/kg) and dobutamine (3 mg/kg) or clenbuterol (0.03 mg/kg) completely substituted for the rolipram discrimination stimulus. Further, incubation with an ineffective concentration of clenbuterol, but not dobutamine, in the presence of a subeffective concentration of rolipram, significantly increased cAMP in cultured cortical neurons. CONCLUSIONS: PDE4 plays an important role in regulating cAMP signaling by either beta-1 or beta-2 adrenergic receptors that mediate antidepressant-like actions; beta-2 adrenergic receptor-mediated cAMP signaling appears more responsive than beta-1 cAMP signaling to PDE4 inhibition.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1993

[Differences in the action of serotonin 1A-receptor agonists on rotating behavior or rats with unilaterally raphe-lesioned rats].

The differences between buspirone and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT)-induced turning behaviour has been investigated in rats with unilateral lesions of the dorsal and/or medial raphe nuclei (DR, MR). 5-MeODMT caused a most intensive contralateral turning in rats with MR lesions and least intensive ones in rats with both MR and DR lesions. Effect of buspirone depended on specific raphe nuclei lesions. Rats with unilateral lesions of both raphe nuclei caused a high locomotor activity in stress situation--free run wheels, the lowest ones--rats with DR lesions.

Animals↗
PubMed2005

Chronic treatment with a serotonin(2) receptor (5-HT(2)R) agonist modulates the behavioral and cellular response to (+)-3,4-methylenedioxymethamphetamine [(+)-MDMA].

3,4-Methylenedioxymethamphetamine [MDMA; ecstasy] evokes a multifaceted subjective experience in human users which includes stimulation, feelings of well-being, mood elevation, empathy towards others as well as distortions in time, sensation and perception. Aspects of this unique psychopharmacology of MDMA are thought to be related to its potent actions to release serotonin (5-HT) and indirectly stimulate the 5-HT(2A) receptor (5-HT(2A)R). In the present studies, we examined the interrelationship between down-regulation of 5-HT(2A)R expression and the behaviorally stimulatory effects generated by acute administration of (+)-MDMA, the most potent enantiomer of (+/-)-MDMA. Male Sprague-Dawley rats were chronically treated with the preferential 5-HT(2A)R agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) which has been shown to down-regulate expression of the 5-HT(2A)R, but not the closely related 5-HT(2C)R. While chronic DOI treatment did not alter the functional sensitivity of either the 5-HT(2A)R or 5-HT(2C)R, this regimen enhanced (+)-MDMA-evoked hyperactivity. Subsequent analysis of c-Fos and 5-HT(2A)R immunoreactivity in brain sections demonstrated that DOI treatment decreased the number of (+)-MDMA-induced c-Fos immunopositive nuclei and 5-HT(2A)R immunostaining in select cortical and striatal areas. These results indicate that chronic DOI exposure results in an enhanced behavioral response to (+)-MDMA and in a pattern of neuronal activation which resembles that seen in psychostimulant sensitization. These data also suggest that expression of the 5-HT(2A)R in the NAc and PFC may play a role in the sensitivity to the locomotor-stimulating effects of (+)-MDMA and in the processes of neural regulation upon repeated psychostimulant administration.

Amphetamines↗
PubMed1993

Adenosine receptor antagonists potentiate dopamine receptor agonist-induced rotational behavior in 6-hydroxydopamine-lesioned rats.

Adenosine receptor antagonists, DMPX, PACPX and theophylline, produce contralateral rotations in unilateral 6-hydroxydopamine-lesioned rats. DMPX and theophylline markedly increase rotations produced by bromocriptine (a dopamine D2 receptor agonist) and/or SKF38393A (a dopamine D1 receptor agonist). All of these effects are inhibited by CGS21680C (an adenosine A2 receptor agonist). These findings suggest synergistic interactions among D1, D2 and A2 receptors that may be relevant to the treatment of Parkinson's disease.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2006

Nalfurafine, a kappa opioid receptor agonist, inhibits scratching behavior secondary to cholestasis induced by chronic ethynylestradiol injections in rats.

Scratching is the behavioral manifestation of pruritus. The pruritus of cholestasis can be severe, intractable and affect the quality of life. We investigated if ethynylestradiol (EE)-induced cholestasis is associated with scratching in rats and if nalfurafine, a kappa opioid receptor agonist with antipruritic effects in human uremic pruritus, would antagonize such scratching. Chronic injection of EE (2 mg/kg, s.c., for 14 days) induced cholestasis as documented by increased serum concentrations of bile acids and caused a higher incidence of body scratching compared to vehicle, thus providing an animal model to study scratching behavior secondary to cholestasis. Pretreating the rats with nalfurafine (0.005-0.04 mg/kg, s.c.) inhibited EE-induced scratching dose-dependently with an A(50) value of 0.013 (0.009-0.021) mg/kg. Serum levels of dynorphin A and nitric oxide were decreased in rats with cholestasis compared to control animals. Our data suggest that (a) nalfurafine has the potential to relieve cholestatic pruritus and (b) both kappa opioid and nitric oxide systems are involved, at least in part, in mediating the pruritus of cholestasis.

Animals↗
PubMed1995

The effects of dopamine agonists on rotational behavior in non-tolerant and caffeine-tolerant rats.

Tolerance develops to caffeine-induced stimulation of both locomotor activity and rotational behavior. The role of dopamine in tolerance to the locomotor stimulant effects of caffeine has been documented. However, the role of dopamine in caffeine-induced turning behavior remains to be elucidated. Therefore, the present study determined the role of dopamine receptors in tolerance to caffeine-induced rotational behavior. Rats with a unilateral lesion of the nigrostriatal tract, induced by 6-hydroxydopamine (6-OHDA), were treated chronically with either caffeine (1.0mg/ml) or with drug-free tap water, by a method of scheduled access. Agonists with and without selectivity for dopamine receptor sub-types were tested in both groups of rats (nonselective: apomorphine, d-amphetamine; D1 selective: SKF-38393, SKF-77434; D2 selective: R(-)-propylnorapomorphine (NPA), quinpirole). All drugs produced dose-dependent increases in turning that, with the exception of quinpirole, were comparable in both groups. Quinpirole produced a smaller effect in rats treated with caffeine than in control rats. Thus, there was significant cross-tolerance only to the effects of quinpirole. The concurrent administration of SKF-38393 with NPA produced a synergistic interaction on rotational behavior in control rats, to which cross-tolerance did not develop in caffeine-treated rats. In contrast to what occurs with locomotor activity, in control rats the selective D1 dopamine receptor antagonist SCH 23390 completely blocked SKF-38393-induced turning behavior and the selective D2 dopamine receptor antagonist eticlopride partially attenuated this effect. NPA-induced turning behavior was blocked only by eticlopride; SCH 23390 was without effect. Both SCH 23390 and eticlopride blocked d-amphetamine-induced rotational behavior. The results of this study suggest that D1 dopamine receptors are not involved in tolerance to caffeine-induced rotational behavior. The role of D2 dopamine receptors in this effect is unresolved. Results obtained from rotational behavior studies generally do not parallel those obtained from locomotor activity studies, suggesting that different mechanisms underlie the effects of caffeine on these two behaviors.

Journal Article↗
PubMed1990

Effects of serotonin agonists on operant behavior in the squirrel monkey: quipazine, MK-212, trifluoromethylphenylpiperazine, and chlorophenylpiperazine.

The behavior of squirrel monkeys was studied under fixed-interval (FI) schedules with responding maintained either by food presentation or by termination of stimuli correlated with impending electric shock delivery (stimulus-shock termination). The 5-HT agonists m-trifluoromethylphenylpiperazine (TFMPP), m-chlorophenylpiperazine (mCPP), and 6-chloro-2(l-piperazinyl)pyrazine (MK-212) decreased responding under both the food and shock schedules (0.3-5.6 mg/kg). These decreases in responding were blocked by the nonselective 5-HT antagonists methysergide and mianserin (0.3, 1.0 mg/kg), but not by the selective 5-HT2 antagonists ketanserin (0.3-1.7 mg/kg) or pirenperone (0.001-0.1 mg/kg). Quipazine (0.3-5.6 mg/kg) decreased responding under the food schedule, and this effect was blocked by both the nonselective and selective 5-HT2 antagonists. This pattern of antagonism suggests that the decreases in responding produced by quipazine involve significant actions at 5-HT2 sites, whereas those produced by TFMPP, mCPP, and MK-212 do not. In contrast to the decreases in responding seen with the food schedules, quipazine produced moderate increases in responding under the shock schedules. Moreover, these increases in responding were not blocked by methysergide or mianserin, but instead were enhanced. The results with antagonists suggest that certain behavioral effects of quipazine are probably due to actions at 5-HT2 sites, whereas similar effects of TFMPP, mCPP, and MK-212 are more related to actions at other 5-HT receptor subtypes.

Animals↗
PubMedDate not supplied

[The development of pathological forms of behavior in submissive male C57BL/6J mice during agonistic zoosocial interactions. A possible model of depression?].

It is shown that a long experience of defeats in daily zoosocial collisions (ZC) elicits changes in the structure of submissive behaviour. Male mice of C57BL/6J line after 20 defeats demonstrated poses of passive subordination instead of active defence and run away which they manifested in the first ZC. Moreover, new immobile poses appeared which were rare in the first ZC. Submissive animals (CA) demonstrated a decrease of travels in the open field test and an increase of immobility time in the Porsolt test. Chronic administration of imipramine (10 mg/kg, i.p., twice a day during two weeks against the background of repeated ZC) prevented an increase of depressivity, estimated in Porsolt test. Changes were noted in the content of serotonin and 5-HIAA in some brain structures of subordinated mice in comparison to control animals (five days of isolation). The data are discussed from a position of the development of depression in SA of C57BL/6J line as a result of a long nonavoided zoosocial stress.

Aggression↗
PubMed1993

Behavioral sensitization and tolerance to the D2 agonist RU 24213: dissociation between several behavior patterns in mice.

Previous studies have shown that different components of behavioral effects of indirect agonists given chronically to laboratory rodents can follow different courses during treatment. Whether repeated injections of a D2 agonist can lead to the same phenomenon was investigated in mice using the D2 agonist N-n-propyl-N-phenylethyl-p-(3-hydroxy-phenyl)-ethylamine (RU 24213). Five mutually exclusive behaviors were examined over seven intermittent administrations (every other day over 13 daily injections) of RU 24213 (2.5 mg/kg SC) in mice. Rapid tolerance to the clearest initial effect of RU 24213, stillness, was found. Suppression of grooming also showed tolerance later in the treatment regimen (from the fourth test). From the third test, parallel time courses of sensitization were obtained for ambulation and rearing. Sleeping position was strongly depressed throughout the chronic treatment. These results show that the development in time of the behavioral effects of RU 24213 injected chronically strongly depend upon the behavioral measure. This supports the use of multiple measures in the same animal in the behavioral analysis of chronically injected dopaminergic drugs.

Animals↗
PubMed1997

Modulation of dopamine receptor agonist-induced rotational behavior in 6-OHDA-lesioned rats by a peptidomimetic analogue of Pro-Leu-Gly-NH2 (PLG).

The present study was undertaken to determine if the previously reported in vitro interactions of the Pro-Leu-Gly-NH2 (PLG) peptidomimetic analogue 3(R)-[(2(S)-pyrrolidinylcarbonyl)amino]-2-oxo-1-pyrrolidineacet amide (PAOPA) with the dopaminergic system could be exhibited in an in vivo animal model using 6-hydroxydopamine (6-OHDA)-lesioned rats. In this model, PAOPA was found to potentiate the contralateral rotational behavior induced by either apomorphine or L-DOPA. PAOPA was 100-fold more potent than PLG, and produced a fourfold greater response than PLG when administered i.p. PAOPA also potentiated contralateral rotations induced by SKF-38393 and quinpirole. In summary, the results of this study indicate that PAOPA, a conformationally constrained peptidomimetic analogue of PLG, can modulate dopaminergic activity in vivo with higher potency and efficacy than PLG.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

Effects of the opiate antagonists diprenorphine and naloxone and of selected opiate agonists on feeding behavior in guinea pigs.

Opiate-sensitive feeding behavior has now been demonstrated in a number of species. We sought information on which opioid receptors might be involved in the observed feeding behaviors. Guinea pigs are known to have higher concentrations of the opioid kappa receptor than any other laboratory animal, so we compared the feeding suppressive potency of the general opiate antagonist, diprenorphine to that of the relatively more mu-specific antagonist, naloxone in that species. We found that diprenorphine was over twenty times more effective than naloxone in suppressing feeding in guinea pigs, suggesting the importance of receptors other than mu in feeding initiation in the guinea pig. Confirmatory evidence for the role of kappa receptors was sought, but not found, in comparisons of the effectiveness of different types of opiate agonists in promoting feeding in these animals. These agonists suppressed, rather than stimulated feeding. We conclude that no feeding stimulatory effects of opiates can be demonstrated in guinea pigs. This observation may indicate that opioids play little role in the natural regulation of feeding in this species or that opioids result in prolonged sedation during which the animals fail to eat. The greater feeding suppressive potency of diprenorphine, a general opiate antagonist, versus naloxone, a mu-preferential antagonist, indicates that to whatever extent opiates are involved in guinea pig feeding, the opiate effect is probably not a mu receptor effect.

Animals↗
PubMedDate not supplied

Glucocorticoids modulate behavioral effects induced by dopaminergic agonists in rats.

Studies showing the presence of glucocorticoids, and their binding sites in the central nervous system indicate that these hormones may affect central neurotransmission. Both, dopaminergic brain system and glucocorticoids are considered to be involved in certain psychopathological conditions in humans, including depression, addiction or schizophrenia. The present study aimed to investigate the influence of glucocorticoids on dopamine agonists-induced stereotyped behavior and locomotor hyperactivity in rats. The results of the experiment demonstrate that prior to administration of prednisolone (4, 6, 10 or 20 mg/kg) or dexamethasone (4 or 8 mg/kg) intensified and prolonged the stereotypy induced by apomorphine (1 mg/kg sc) or amphetamine (2 mg/kg ip). The effect of dexamethasone was more potent. Amphetamine (0.4 mg/kg)- or amantadine (50 mg/kg)-induced locomotor hyperactivity was significantly reduced in rats pretreated with dexamethasone at a dose of 8 mg/kg or 4 mg/kg. Our observations suggest that exogenous glucocorticoids may enhance the activity of the dopaminergic agonists in the striatum but reduce it in the mesolimbic system of rats.

Animals↗