Biomedical subjects

Mohammad-Reza Zarrindast

Publications and source records attributed to Mohammad-Reza Zarrindast.

At least 55 records · Page 3Linked to original sources

PubMed2005

Intracerebroventricular effects of histaminergic agents on morphine-induced anxiolysis in the elevated plus-maze in rats.

Some reports indicate that morphine can induce anxiolytic effects both in animal and in man. It has also been reported that histaminergic system can interfere with some pharmacological effects of morphine. The effects of histaminergic agents on morphine-induced anxiolysis in rats, using elevated plus-maze were investigated in the present study. Intraperitoneal injection of morphine (3, 6 and 9 mg/kg) induced antianxiety effects. Intracerebroventricular administration of histamine at the doses of (5, 10 and 20 microg/rat) also increased anxiety-related behaviours. Intracerebroventricular injection of pyrilamine, a H1 receptor antagonist (25, 50 and 100 microg/rat), increased anxiety whereas injection of ranitidine, a H2 receptor antagonist (5, 10 and 20 microg/rat) at the same site, decreased anxiety. Therefore, it seems that histamine induces anxiogenic response through activation of H2 receptors, while the response of H1 blocker may be due to release of histamine. We also evaluated the interactions between morphine and histaminergic agents. Our data show that histamine (10 microg/rat), pyrilamine (50 microg/rat) and ranitidine (5 microg/rat) did not alter the response induced by different doses of morphine (3, 6 and 9 mg/kg). Similarly, a single dose of morphine did not alter the response induced by different doses of histamine (5, 10 and 20 microg/rat), pyrilamine (25, 50 and 100 microg/rat) or ranitidine (5, 10 and 20 microg/rat). In conclusion, the histaminergic system plays an important role in the modulation of anxiety, although in our experiments, no interaction was found between the effects of histaminergic agents and morphine on anxiety-related indices in the elevated plus-maze. This may imply that morphine-induced anxiolysis probably is independent of the histaminergic system.

Animals↗

PubMed2004

Morphine state-dependent learning: sensitization and interactions with dopamine receptors.

In the present study, the effects of morphine sensitization on impairment of memory formation and the state-dependent learning by morphine have been investigated in mice. Pretraining administration of morphine (0.5, 2.5 and 5 mg/kg) dose dependently decreased the learning of a one-trial passive avoidance task. Pretest administration of morphine (0.5, 2.5 and 5 mg/kg) induced state-dependent retrieval of the memory acquired under pretraining morphine influence. Pretraining or pretest administration of naloxone (0.25, 0.5 and 1 mg/kg) reversed both responses to morphine (5 mg/kg). Amnesia induced by pretraining morphine was significantly reversed in morphine-sensitized mice which had previously received once daily injections of morphine [20 and 30 mg/kg, subcutaneously (s.c.)] for 3 days. Morphine sensitization tended to reverse but did not significantly affect morphine state-dependent memory. The inhibition of morphine-induced amnesia in morphine-sensitized mice was decreased by once daily administration of naloxone (0.5, 1 and 2 mg/kg) 30 min prior to injection of morphine (20 mg/kg/day x 3 days). Three-days administration of 1-phenyl-7,8-dihydroxy-2,3,4,5-tetrahydro-1H-3-benzazepine HCL (SKF 38393; 8, 16 and 32 mg/kg) or SCH 23390; R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine HCL (0.01, 0.05 and 0.1 mg/kg) before morphine (for 3 days) and during morphine-sensitization, decreased and increased, the amnesia induced by pretraining morphine, respectively. Similar administration of quinpirole (0.5, 1 and 2 mg/kg) or sulpiride (25, 50 and 100 mg/kg) before morphine also decreased and increased the amnesia induced by pretraining morphine, respectively. The results suggest that morphine sensitization affects the impairment of memory formation, but not the facilitation of retrieval induced by morphine and thus it is postulated that dopamine receptors may play an important role in this effect.

Animals↗

PubMed2004

GABA(A) receptors in the basolateral amygdala are involved in mediating morphine reward.

In the present study, the effects of intra-basolateral amygdala (BLA) injection of GABA(A) receptor agonist and antagonist on morphine-induced conditioned place preference (CPP) in male Wistar rats have been investigated. Subcutaneous (s.c.) administration of different doses of morphine sulfate (1-9 mg/kg) produced a dose-dependent CPP. Using a 3-day schedule of conditioning, it was found that the GABA(A) receptor agonist, muscimol (0.125, 0.25 and 0.5 microg/rat) or the GABA(A) receptor antagonist, bicuculline (0.125, 0.25 and 0.5 microg/rat), did not produce a significant place preference or place aversion. Intra-BLA administration of muscimol (0.25 and 0.5 microg/rat) decreased the acquisition of CPP induced by morphine (6 mg/kg). On the other hand, intra-BLA injection of bicuculline (0.25 and 0.5 microg/rat) in combination with an ineffective dose of morphine (1 mg/kg) elicited a significant CPP. The response of different doses of muscimol was attenuated by bicuculline (0.125 and 0.25 microg/rat). Furthermore, intra-BLA administration of bicuculline but not muscimol before testing significantly decreased the expression of morphine (6 mg/kg)-induced place preference. The administration of the higher doses of bicuculline (0.25 and 0.5 microg/rat) during acquisition and the higher dose of muscimol (2 microg/rat) on the test day decreased the locomotor activity of the animals on the testing phase. It can be concluded that GABA(A) receptors in the amygdala are involved in morphine reward.

Amygdala↗

PubMed2004

The effect of electroconvulsive shock seizures on behaviour induced by dopaminergic agonists and on immobility in the Porsolt test.

Male, Wistar rats were given a course of eight electroconvulsive shock seizures (ECS group) or matched handling (control group). They were then tested for locomotion and rearing (7 days post-ECS), for grooming and yawning (9 days post-ECS), and for immobility in the Porsolt test (7, 14 and 21 days post-ECS). Seven days post-seizure, the ECS group showed significantly more locomotion following intraperitoneal administration of apomorphine (0.2 mg/kg), but not following injections of amphetamine (1 mg/kg). Drug-induced rearing was not different in the ECS and control animals. Nine days post-seizure, the ECS group showed significantly more grooming induced by the D-1 dopamine receptor agonist, SKF 38393 (1 mg/kg), but no difference in the yawning induced by the D-2 dopamine receptor agonist, quinpirole (0.05 mg/kg). In the Porsolt test, immobility was decreased in the ECS animals at 7 and 14, but not at 21 days post-ECS. It is concluded that ECS increases activity in the dopaminergic systems of the rat brain for at least 1-2 weeks post-seizure. The beneficial effects of electroconvulsive therapy (ECT) may relate to these dopaminergic alterations.

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

PubMed2004

The role of alpha-adrenoceptor mechanism(s) in morphine-induced conditioned place preference in female mice.

It has been shown that the alpha-adrenergic system is involved in some effects of opioids, including analgesia and reward. Gender differences also exist between males and females in response to alpha-adrenergic agents. This study was designed to determine the effects of alpha-adrenoceptor agonists and antagonists on the acquisition or expression of morphine-induced conditioned place preference (CPP) in female mice. The experiments showed that subcutaneous injections of morphine (0.5-8 mg/kg) induced CPP in a dose-dependent manner in mice. Intrapritoneal administration of the alpha-1-adrenoceptor agonist, phenylephrine (0.03, 0.1 and 0.3 mg/kg), and alpha-2 adrenoceptor agonist, clonidine (0.0001, 0.0005 and 0.001 mg/kg), as well as alpha-1-adrenoceptor antagonist, prazosin (0.01, 0.05 and 0.1 mg/kg) or alpha-2 adrenoceptor antagonist, yohimbine (0.005, 0.01 and 0.05 mg/kg) did not induce motivational effects and also did not alter locomotor activity in the animals. In the second set of experiments, the drugs were used before testing on Day 5, to test their effects on the expression of morphine-induced CPP. Intrapritoneal administration of phenylephrine and clonidine decreased the expression of morphine-induced CPP. In contrast, after application of prazosin or yohimbine, the expression of morphine-induced CPP was increased. Administration of lower (0.03 mg/kg) and higher doses of phenylephrine (0.1 and 0.3 mg/kg) during acquisition of morphine CPP decreased and increased the morphine CPP, respectively. Similarly, the administration of prazosin and clonidine decreased while yohimbine increased the morphine CPP. It may be concluded that alpha-adrenoceptor mechanism(s) influence morphine-induced CPP in female mice.

Animals↗

PubMed2004

Potentiation of imipramine-induced antinociception by nicotine in the formalin test.

In this study, the effect of cholinergic agents on imipramine antinociception in mice, in the formalin test, has been investigated. Intraperitoneal (i.p.) administration of different doses of imipramine (2.5, 5, 10, 20 and 30 mg/kg) or nicotine (0.25, 0.5, 0.75 and 1 mg/kg) induced a dose dependent antinociception in both the first and second phases of the formalin test in mice. The combination of imipramine with doses of 0.5 and 0.75 mg/kg of nicotine showed a potentiated response, in both phases of the test. However, neither hexamethonium (5 and 10 mg/kg), atropine (0.25 mg/kg) or mecamylamine (0.25 mg/kg) altered the antinociception induced by imipramine. It is concluded that nicotinic receptor activation but not the cholinergic muscarinic mechanism is involved in the imipramine-induced antinociception.

Analgesics↗

PubMed2004

Nitric oxide agents and apomorphine-induced rat behaviors.

BACKGROUND: Nitric oxide (NO) may alter dopamine release in the brain. Activation of D2-dopamine receptors may suppress NO synthase, and inhibition of NO synthase prevents behaviors induced by psychostimulants. We have investigated the modulatory actions of the precursor of NO synthesis (L-arginine) and the broad-spectrum NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on apomorphine-induced behaviors in the rat. METHODS: Apomorphine was injected subcutaneously, and behaviors induced by the drug were examined in the presence or absence of intracerebroventricular administration of L-arginine and L-NAME. RESULTS: Our data indicate that L-arginine or L-NAME treatment decreased licking and yawning, but not penile erection induced by apomorphine. CONCLUSION: Apomorphine-induced behaviors may be modulated by NO levels.

Animals↗

PubMed2003

Role of nitric oxide in the acquisition and expression of apomorphine- or morphine-induced locomotor sensitization.

In the present study, the effects of L-arginine, a nitric oxide (NO) precursor, and N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, on apomorphine- or morphine-induced locomotor sensitization in male albino mice were investigated. Our data showed that subcutaneous (s.c.) injection of apomorphine (2-10 mg/kg) or morphine sulphate (5-50 mg/kg) significantly increased locomotor behaviour in a dose-dependent manner. Intraperitoneal (i.p.) administration of L-arginine (100 mg/kg) increased locomotor activity, whereas L-NAME (20 mg/kg) decreased it. L-Arginine and L-NAME increased and decreased apomorphine- or morphine-induced locomotions, respectively. The locomotor behavioural response was enhanced in mice pretreated with apomorphine (2 mg/kg, daily x3 days) or morphine (10 mg/kg, daily x3 days) alone, indicating that sensitization had developed. Administration of L-arginine 30 min before each of three daily doses of apomorphine or morphine increased the development of sensitization, while administration of L-NAME 30 min before each of three daily doses of apomorphine or morphine decreased the acquisition of sensitization induced by apomorphine or morphine. Administration of L-arginine significantly increased and L-NAME significantly and dose-dependently decreased the expression of both apomorphine- and morphine-induced sensitization. The results indicate that NO may be involved in the acquisition and expression of apomorphine- or morphine-induced sensitization.

Animals↗

PubMed2003

Effects of imipramine on the expression and development of morphine dependence in mice.

In the present study, the effects of imipramine and/or alpha-adrenoceptor agents on naloxone-induced jumping in morphine-dependent mice were examined. In the first set of experiments, the drugs were used before naloxone injection, to test their effects on the expression of jumping. Administration of imipramine (10-60 mg/kg) 15 min before naloxone increased the number of jumping in mice. Injection of the alpha2-adrenoceptor agonist, clonidine (0.1 mg/kg), or alpha1-adrenoceptor agonist, phenylephrine (4 mg/kg), themselves neither altered naloxone-induced jumping nor influenced the imipramine response. The alpha2-adrenoceptor antagonist, yohimbine (4 mg/kg), itself but not the alpha1-adrenoceptor antagonist, prazosin (1 mg/kg), increased jumping and decreased the imipramine effect. In the second set of experiments, imipramine and/or the alpha-adrenoceptor drugs were injected during the development of morphine dependence. Imipramine (10-40 mg/kg) increased the development of dependence and increased jumping was seen. Clonidine did not influence the imipramine effect. Phenylephrine was lethal in combination with imipramine. Both yohimbine and prazosin decreased the effect of imipramine. Imipramine and phenylephrine but not clonidine, yohimbine or prazosin decreased locomotion. It is concluded an alpha2-adrenoceptor mechanism may be involved in the influence of imipramine on the expression and development of naloxone-induced withdrawal signs in mice.

Adrenergic Uptake Inhibitors↗

PubMed2003

Effects of histamine and cholinergic systems on memory retention of passive avoidance learning in rats.

In the present study, the effects of the histamine and cholinergic systems on memory retention in adult male rats were investigated. Post-training intracerebroventricular injections were carried out in all the experiments. Cholinoceptor agonist, acetylcholine (1-10 microg/rat) or nicotine (1-10 microg/rat), increased, while a cholinoceptor antagonist, scopolamine (5-20 microg/rat), decreased memory retention. The response to acetylcholine was attenuated by scopolamine. Administration of histamine (5-20 microg/rat) reduced, but the histamine H(1) receptor antagonist, pyrilamine (10-50 microg/rat), and the histamine H(2) receptor antagonist, cimetidine (1-50 microg/rat), increased memory retention in rats. The histamine receptor antagonists attenuated the response to histamine. Histamine reduced the acetylcholine- or nicotine-induced enhancement. The histamine receptor antagonists enhanced the nicotine- or acetylcholine-induced response. Histamine potentiated the inhibitory effect induced by scopolamine. It is concluded that histaminergic and cholinergic systems have opposing effects on memory retention. Also, the histaminergic system elicits an interaction with the cholinergic system in memory retention.

Acetylcholine↗

PubMed2003

Adenosine receptor agonists or antagonists alter antinociception, but did not show an interaction with imipramine-induced antinociception in the formalin test in mice.

In this study, the antinociceptive effect of imipramine and adenosine agents, and interactions between imipramine with adenosine drugs in mice in the formalin test, have been investigated. Intraperitoneal administration of different doses of imipramine (10, 20, 30 and 40 mg/kg) induced a dose dependent antinociception in mice, in both the first and second phases of the formalin test. The adenosine A(1) receptor agonists, R-(N(6)-phenylisopropyl)-adenosine (0.015, 0.03 and 0.1 mg/kg) and 5'-N-ethylcarboxamide adenosine (0.001, 0.005, 0.01 mg/kg), but not 2-chloroadenosine (0.1 and 0.5 mg/kg), and the adenosine receptor antagonist, 8-phenyltheophylline (0.1, 0.5 and 1 mg/kg), but not 1,3-dipropyl-7-methyl-xanthine (0.5 and 5 mg/kg), also produced an antinociceptive response. Lower dose of the adenosine receptor antagonist theophylline induced antinociception, while a higher dose of the drug caused hyperalgesia. Theophylline reduced the response induced by imipramine. It is concluded that adenosine systems are not involved in imipramine responses in the formalin test.

2-Chloroadenosine↗

PubMed2003

Effect of acute and chronic lead exposure on apomorpine-induced sniffing in rats.

Sniffing is a behaviour which can be induced by dopamine D1/D2 receptor agonists. In order to test the effect of chronic lead exposure on dopamine receptor subtypes, we studied the effects of acute and chronic lead exposure on sniffing induced by apomorphine, a dopamine receptor agonist. Intraperitoneal injection of the dopaminergic receptor agonist, apomorphine (0.25-1 mg/kg), induced dose-dependent the sniffing behaviour in rats. Acute administration of lead acetate (50, 100 and 200 mg/kg) deceased the apomorphine-induced sniffing. Chronic lead (0.25%) exposure also decreased the apomophine response Dopamine D1 or D2 receptor antagonists reduced the apomorphine effect. Lead exposure could not potentiate the blockade induced by the dopamine receptor antagonists. It is concluded that the response of lead is not mediated by alteration of dopamine receptors.

Analysis of Variance↗

PubMed2003

Influence of alpha-adrenoceptor agonists and antagonists on imipramine-induced hypothermia in mice.

Effects of adrenoceptor agonists and antagonists on imipramine-induced hypothermia in mice were studied. Intraperitoneal injection of imipramine (10-40 mg x kg(-1)), alpha2-adrenoceptor agonist clonidine (0.05-0.1 mg x kg(-1)), alpha1-adrenoceptor agonist phenylephrine (6 mg x kg(-1)) and alpha1-adrenoceptor antagonist prazosin (1-4 mg x kg(-1)) but not alpha2-adrenoceptor antagonist yohimbine (1-4 mg x kg(-1)) induced significant hypothermia. The hypothermic response induced by imipramine (10-30 mg x kg(-1)) was not altered by clonidine (0.05-0.1 mg x kg(-1)) or phenylephrine (2-6 mg x kg(-1)). The response of imipramine (10-30 mg x kg(-1)) was reduced significantly by yohimbine (2 mg x kg(-1)) and was potentiated by prazosin (1 mg x kg(-1)). The hypothermic effect of clonidine (0.1 mg x kg(-1)) and imipramine (20 mg x kg(-1)) were also decreased significantly by different doses of yohimbine (1-4 mg x kg(-1)). The hypothermia induced by different doses of prazosin (1-4 mg x kg(-1)) was not altered by yohimbine (2 mg x kg(-1)) or by low dose of imipramine (10 mg x kg(-1)). It is concluded that alpha2-adrenoceptor mechanism may be involved in the hypothermic effect of imipramine.

Adrenergic alpha-Agonists↗

PubMed2003

Imipramine-induced antinociception in the formalin test. Receptor mechanisms involved and effect of swim stress.

This study concerned the effect of swim stress on imipramine-induced antinociception in mice. The data showed that intraperitoneal (i.p.) administration of different doses of imipramine (10-40 mg/kg) and 0.5-3 min of swim stress (17 degrees C) induced antinociception in the first and second phases of the formalin test. Low period of swim stress (10 s) with low doses of imipramine (2.5, 5 and 10 mg/kg i.p.), which did not have any effect by themselves, in combination showed antinociception in the second phase of the test. Either yohimbine (0.5 mg/kg i.p.) or naloxone (1 mg/kg i.p.) reversed the response induced by the combination of low doses of imipramine plus swim stress. Yohimbine (1 mg/kg i.p.) decreased the response of imipramine (20 mg/kg i.p.) but not that of 30 s swim stress in the second phase. However, naloxone (1 mg/kg i.p.) reduced the antinociception induced by imipramine (20 mg/kg i.p.) or 30 s swim stress in the second phase of the test, the combination of imipramine with swim stress was not altered by yohimbine or naloxone. Prazosin induced antinociception by itself in the first phase of the test and increased swim-stress-induced antinociception with no interaction. It is concluded that antinociception induced by imipramine in the second phase of formalin test may be mediated through alpha(2)-adrenoceptor antagonists. The results indicate that the responses of swim stress and imipramine may be mediated by an opioid mechanism, but the combination of both drugs induced higher antinociceptive effects.

Animals↗

PubMed2003

Involvement of dopamine receptors of the dorsal hippocampus on the acquisition and expression of morphine-induced place preference in rats.

In the present study, the effects of bilateral intrahippocampal CA1 injections of dopamine receptor agonists and antagonists on the acquisition and expression of morphine-induced place preference were examined in male Wistar rats. Subcutaneous administration of different doses of morphine sulphate (0.5-10 mg/kg) produced a conditioned place preference (CPP) dose-dependently. Using a 3-day schedule of conditioning, it was found that dopamine D1 receptor agonist, SKF 38393 (0.01-1 microg/rat), dopamine D1 receptor antagonist, SCH 23390 (0.25-1 microg/rat), dopamine D(2/3) receptor agonist, quinpirole (0.3-3 microg/rat) or dopamine D2 receptor antagonist, sulpiride (0.04-5 microg/rat) did not produce significant place preference. The administration of SKF 38393 (1 microg/rat) significantly potentiated the acquisition of morphine (0.5 and 2.5 mg/kg)-induced place preference. This potentiation was reversed by SCH 23390 (1 microg/rat) pretreatment. Quinpirole injection (0.3 microg/rat) induced CPP in combination with the lower doses of morphine but decreased the response of the higher doses of morphine. These responses of quinpirole were reversed by sulpiride (5 microg/rat) pretreatment. SCH 23390 or sulpiride reduced the acquisition of morphine (7.5 mg/kg)-induced place preference. The administration of sulpiride, but not other drugs, during acquisition showed an increase in the locomotor activity on the testing days. SKF 38393, SCH 23390 or sulpiride, but not quinpirole when used before testing, reduced the expression of morphine-induced place preference. Sulpiride, but not other drugs, increased locomotion when used before testing. It is concluded that dorsal hippocampal dopamine receptors may play an active role in morphine reward.

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

PubMed2002

Effects of alpha-adrenoceptor agonists and antagonists on histamine-induced impairment of memory retention of passive avoidance learning in rats.

The effect of alpha-adrenoceptor agents on the impairment induced by histamine was measured for memory retention of passive avoidance learning in rats. Post-training intracerebroventricular (i.c.v.) injection was carried out in all the experiments. Histamine (5, 10 and 20 microg/rat) reduced, while a histamine H(1) receptor antagonist, chlorpheniramine (0.1, 1 and 10 microg/rat), increased memory retention. The histamine H(2) receptor antagonist, ranitidine (0.1, 1, 10 and 20 microg/rat), did not elicit any response in this respect. Different doses of chlorpheniramine but not ranitidine reversed the histamine-induced impairment of memory. Clonidine and prazosin decreased, but yohimbine and phenylephrine increased, memory retention. Yohimbine decreased the inhibitory response to histamine. Phenylephrine, clonidine and prazosin did not alter the histamine effect. It is concluded that a histamine-induced impairment of memory retention through histamine H(1) receptors and an alpha(2)-adrenoceptor mechanism may be involved in the histamine response.

Adrenergic alpha-Agonists↗

PubMed2002

Effects of histamine and opioid systems on memory retention of passive avoidance learning in rats.

The present study investigated the effect of interactions between histamine receptor agents and the opioid peptidergic system on memory retention of passive avoidance learning in rats. Post-training intracerebroventricular (i.c.v.) injections were carried out in all the experiments. Administration of histamine (20 micro g/rat) reduced, but the histamine H(1) receptor antagonist, pyrilamine (20 and 50 micro g/rat), and the histamine H(2) receptor antagonist, cimetidine (10 and 50 micro g/rat), increased memory retention in rats. The histamine receptor antagonists decreased the response induced by histamine. Morphine (1-10 micro g/rat) reduced, while pentazocine (5 and 10 micro g/rat) or the opioid receptor antagonist, naloxone (5 and 15 micro g/rat), increased memory retention. The combination of histamine with morphine showed potentiation. Effects of pyrilamine and cimetidine were attenuated by morphine. The responses to pentazocine and naloxone also were decreased by histamine. It is concluded that the histaminergic system has an interaction with opioidergic system that is involved in the memory retention process.

Animals↗

PubMed2002

The effects of dopamine receptor agents on naloxone-induced jumping behaviour in morphine-dependent mice.

In the present study, the effects of dopamine receptor agonists and antagonists on naloxone-induced jumping in morphine-dependent mice were examined. Mice were rendered dependent as described in the methods section. Naloxone was injected to elicit jumping (as withdrawal sign). The first group received dopamine receptor drugs before naloxone injection to test the effects of the drugs on the expression of jumping. Administration of the dopamine D1/D2 receptor agonist, apomorphine (0.25, 0.5 and 1 mg/kg), decreased jumping, but not diarrhoea, induced by naloxone. The effect of apomorphine on jumping was reduced by the dopamine D2 receptor antagonist, sulpiride. The dopamine D2 receptor agonist, quinpirole (0.1, 0.3 and 0.5 mg/kg), increased jumping, while it decreased diarrhoea in mice. Different doses of sulpiride did not alter jumping, but one dose of the drug (12.5 mg/kg) decreased jumping. Neither the dopamine D1 receptor agonist, SKF38393 (1-phenyl-7,8-dihydroxy-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride; 8 and 16 mg/kg), nor the dopamine D1 receptor antagonist, SCH23390 (R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-benzazepine-7-ol maleate; 5, 10 and 25 mg/kg), altered jumping, but they decreased diarrhoea. The second group of animals received the drugs during the development of dependence. Administration of quinpirole (0.1, 0.3 and 0.5 mg/kg), but not bromocriptine (4, 8 and 16 mg/kg), apomorphine (0.25, 0.5, 1 and 2 mg/kg) or sulpiride (12.5, 25 and 50 mg/kg) decreased naloxone-induced jumping and diarrhoea. A dose of SKF38393 (8 mg/kg) decreased jumping, while both SKF38393 (4 and 16 mg/kg) and SCH23390 (5 and 10 microg/kg) increased diarrhoea. It is concluded that activation of both dopamine D1 and D2 receptors may suppress naloxone-induced jumping in morphine-dependent mice, and that stimulation of dopamine D1 receptors during development of morphine dependence may increase diarrhoea through peripheral mechanism.

Analysis of Variance↗