Biomedical subjects

M R Zarrindast

Publications and source records attributed to M R Zarrindast.

At least 91 records · Page 5Linked to original sources

PubMed1994

Caerulein changes morphine-induced antinociception depending on pretreatment times.

1. In the present study, the effect of caerulein (CLN) on morphine analgesia has been tested. 2. Different doses of morphine produced antinociception in a dose dependent manner. When animals were pretreated with CLN 5 min before morphine administration, the morphine response was decreased. However, when CLN was injected 30 or 60 min prior to morphine, the drug effect was increased. 3. Naloxone, sulpiride, metergoline or proglumide decreased the potentiation of morphine response caused by CLN. CLN, proglumide, sulpiride, metergoline and naloxone alone did not exert any effect on tail-flick latency. 4. It is concluded that, depending on pretreatment times of CLN administration the response of morphine was decreased or increased and D-2 dopamine, serotonin and/or CCK receptors may be involved in the potentiation of morphine response induced by CLN.

Analgesics↗

PubMed1994

Morphine inhibits dopaminergic and cholinergic induced ejaculation in rats.

1. Subcutaneous injection (s.c.) of apomorphine (0.1-0.5 mg/kg) and intraperitoneal administration (i.p.) of quinpirole (0.01-0.25 mg/kg), physostigmine (0.05-0.2 mg/kg) and pilocarpine (0.75-3 mg/kg, i.p.) but not neostigmine (0.1-1 mg/kg) induced ejaculation in rats. 2. The responses of drugs were reduced by morphine (1-6 mg/kg, s.c.) pretreatment. 3. The inhibitory effect of morphine was reversed by naloxone (1.5 mg/kg, s.c.). 4. Naloxone (0.75-3 mg/kg, s.c.) alone induced slight but significant ejaculation. 5. Ejaculatory responses induced by apomorphine and quinpirole but not those by physostigmine and pilocarpine were reduced by sulpiride (100 mg/kg, i.p.) pretreatment. 6. Domperidone (1-30 mg/kg, i.p.) did not change the response induced by apomorphine. 7. Pretreatment of animals with the cholinergic antagonist atropine (10 mg/kg, i.p.) decreased the frequency of ejaculation induced by apomorphine, quinpirole, physostigmine or pilocarpine. 8. It may be concluded that D-2 activation induces ejaculation through influence on cholinergic mechanisms and morphine inhibits the ejaculation induced by activation of both cholinergic and dopaminergic systems via opiate receptor sites.

Animals↗

PubMed1993

Influences of different adenosine receptor subtypes on catalepsy in mice.

The effects of adenosine A1 and A2 receptors on catalepsy were studied in mice. The adenosine agonists 5-N'-ethylcarboxamide-adenosine (NECA), N6-phenylisopropyladenosine (PIA) and N6-cyclohexyladenosine (CHA) induced dose dependent catalepsy. The A1 adenosine antagonist 8-phenyltheophylline (8-PT) potentiated catalepsy induced by NECA, R-PIA and CHA. However, theophylline did not potentiate but inhibited the responses induced by NECA, R-PIA and CHA. Neither 8-PT nor theophylline alone has any effect on catalepsy in mice. It is concluded that catalepsy induced by the adenosine agonists may be due to A2 receptor stimulation and that the A1 antagonism may potentiate the response.

Adenosine↗

PubMed1993

Bombesin-induced anorexia requires central bombesin receptor activation: independence from interaction with central catecholaminergic systems.

Intraperitoneal (IP) administration of bombesin (BBS; 2.5-20 micrograms/kg) induced a dose-dependent inhibition of food intake. The effect was decreased by intraventricular (ICV) administration of bombesin receptor antagonist [Leu14-psi (CH2NH)-Leu13] (3 micrograms/rat) but not by the D1 antagonist SCH 23390, the D2 antagonists sulpiride and pimozide, the dopamine antagonist cis-flupentixol, adrenoceptor blockers phenoxybenzamine or propranolol and serotonergic antagonist methergoline. It is concluded that BBS-induced suppression of feeding may be mediated through central BBS receptors, and is independent of interaction with brain catecholaminergic system.

Adrenergic alpha-Antagonists↗

PubMed1993

Involvement of dopaminergic receptor subtypes in straub tail behaviour in mice.

1. Administration of apomorphine to mice induced straub tail behaviour dose-dependently. The response was decreased by the D1 antagonist SCH 23390, the D2 antagonist sulpiride. Reserpine plus alpha-methyl-p-tyrosine (AMPT), caused a marked increase in the response of the drug. 2. The D1 agonist SKF 38393 induced the straub tail behaviour in a dose-dependent manner, which was decreased by SCH 23390, sulpiride or reserpine + AMPT. 3. When animals were administered the D2 agonist quinpirole, a dose-dependent response was produced. This effect was decreased by sulpiride and reserpine + AMPT, but not by SCH 23390. 4. In animals pretreated with reserpine + AMPT, the combination of SKF 38393 with quinpirole produced a significant straub tail behaviour. 5. It is concluded that the concurrent D1/D2 dopamine receptor stimulation is necessary to produce straub tail behaviour in mice.

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

PubMed1992

Involvement of dopamine receptor subtypes in mouse thermoregulation.

The effects of dopamine agonists on core body temperature (BT) were tested in mice. Apomorphine (APO) reduced BT of the mice dose dependently. The response was inhibited by the D-2 antagonist sulpiride, but not by the D-1 antagonist SCH 23390. The D-2 agonist quinpirole also decreased BT and this was prevented by sulpiride pretreatment. Administration of the D-1 agonist SKF 38393 increased BT. This hyperthermia was decreased by SCH 23390 pretreatment. In reserpinized animals, APO caused a dose-related increase in BT. The hyperthermic response of the drug was abolished in animals pretreated with a combination of sulpiride with SCH 23390, but not by single administration of sulpiride or SCH 23390. Quinpirole and SKF 38393 caused hyperthermia in reserpinized mice. The response was decreased in animals pretreated with sulpiride or SCH 23390, respectively. BT of the intact mice was decreased, while that of reserpinized animals was increased by SCH 23390 but not by sulpiride pretreatment. It is concluded that the presynaptic dopamine neurons are involved in hypothermia, while both postsynaptic D-1 and D-2 dopamine receptors may mediated the hyperthermia induced by dopaminergic agents.

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

PubMed1992

Role of D-1 and D-2 receptors in apomorphine-induced pecking in chicks.

The possible involvement of subtypes of dopamine (DA) receptors in pecking induced by apomorphine (APO) in chicks was studied. D-1/D-2 agonist APO dose-dependently induced pecking in chicks. The APO response was decreased in animals pretreated with either the D-2 receptor antagonist sulpiride or the D-1 receptor antagonist SCH 23390. The inhibitory effects of both antagonists were also dose dependent. The pecking induced by APO was completely inhibited in animals pretreated with a combination of SCH 23390 and sulpiride and was potentiated with reserpine. Single administration of D-2 agonist quinpirole or D-1 agonist SKF 38393 did not induced pecking, although quinpirole, but not SKF 38393 caused considerable response in reserpine or reserpine + alpha-methyl-p-tyrosine (AMPT)-treated animals. When quinpirole was administered with SKF 38393, a slight pecking response was shown. This was also potentiated in reserpine or reserpine + AMPT-treated chicks. The results may indicate that both D-1 and D-2 DA receptors are involved in pecking induced by APO, and reserpine treatment caused the sensitization of the D-2 receptors for the induction of pecking in chicks.

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

PubMed1992

Effects of bupropion on core body temperature of mice.

The effects of bupropion on core body temperature of intact or reserpinized mice were studied. Intraperitoneal (IP) administration of bupropion to mice induced a dose-dependent hypothermia. The response of bupropion was decreased by the D-2 antagonist sulpiride or pimozide, but not by the D-1 antagonist SCH 23390, antimuscarinic drug atropine, alpha-adrenergic blocker phenoxybenzimine, beta-adrenergic antagonist propranolol or antiserotonergic methergoline. Reserpine induced hypothermia, which was reversed by bupropion administration. The reversal response of bupropion was reduced by propranolol, but not sulpiride, SCH 23390, phenoxybenzamine, atropine or methergoline. It is concluded that bupropion-induced hypothermia may be mediated through D-2 receptor activation, while the reversal of reserpine-induced hypothermia by bupropion may be exerted through beta-adrenergic stimulation.

Adrenergic alpha-Antagonists↗

PubMed1992

Characterization of dopamine receptors involved in apomorphine-induced pecking in pigeons.

1. The possible involvement of subtypes of dopamine-receptors in apomorphine induced pecking was studied in pigeons. Different doses of apomorphine induced pecking in pigeons which was dose-dependent. 2. The response was decreased by SCH 23390 (D-1 antagonist) or high doses of sulpiride (D-2 antagonist) pretreatment, but increased by lower doses of sulpiride. 3. Combination of SCH 23390 with sulpiride completely antagonized the apomorphine effect. 4. Single dose administration of SKF 38393 (D-1 agonist) or bromocriptine (D-2 agonist) and combination of these drugs did not induce pecking, although either SK 23390 or bromocriptine increased the apomorphine-induced pecking which was decreased by SCH 23390 or sulpiride pretreatment. 5. It may be concluded that pecking, induced by apomorphine in pigeons, is elicited through activation of both D-1 and D-2 dopamine-receptors.

Animals↗

PubMed1992

Opposite influences of dopaminergic receptor subtypes on penile erection.

1. Mixed D-1/D-2 dopamine agonist apomorphine induced a penile erection (PE) in rats in a biphasic manner. 2. The response was decreased with increasing doses of the drug. 3. The maximum effect was obtained by 0.1 mg/kg of apomorphine. 4. In animals pretreated with D-1 antagonist SCH 23390, high doses of apomorphine showed higher PE response, while D-2 antagonist sulpiride pretreatment decreased the response of the low doses of the drug. 5. The inhibitory effect of sulpiride was dose-dependent. 6. The D-2 agonists bromocriptine or quinpirole induced a dose-dependent PE. 7. The effects of both drugs were decreased by sulpiride or SKF 38393 pretreatment. 8. Cholinergic drugs physostigmine and neostigmine did not induce PE, but antimuscarinic agent atropine decreased the effects of apomorphine, bromocriptine or quinpirole. 9. It is concluded that D-2 dopamine receptor stimulation may induce PE, while D-1 activation elicit an opposite effect. 10. However, cholinergic stimulation is not able to induce PE, cholinergic inhibition may decrease the PE induced by dopaminergic agents.

Animals↗

PubMed1992

Influences of dopamine receptors on chewing behaviour in rats.

1. Intraperitoneal (i.p.) injection of different doses of pilocarpine induced purposeless chewing in rats. Physostigmine (i.p.), but not neostigmine (i.p.) also induced chewing behaviour. 2. Subcutaneous (s.c.) pretreatment of animals with the D-1 receptor blocker SCH 23390 decreased the number of chews induced by pilocarpine. 3. The D-2 dopamine antagonist sulpiride (i.p.) and anticholinergic atropine (i.p.) pretreatment also decreased the frequency of chews induced by the drug. 4. The response induced by pilocarpine (1 mg/kg i.p.) also was dose-dependently decreased in animals pretreated with apomorphine (0.25-1 mg/kg s.c.). 5. Administration of low doses of apomorphine (s.c.) also induced chewing, which was decreased with increasing the doses of the drug. 6. Chewing-induced by apomorphine was decreased by sulpiride or atropine and increased by SCH 23390 pretreatment. 7. Single administration of D-2 dopamine agonist bromocriptine also showed a slight but significant purposeless chewing, which was decreased by sulpiride pretreatment. 8. Single administration of D-2 agonist quinpirole, D-1 agonist SKF 38393 or D-1 antagonist SCH 23390, but not sulpiride caused a slight chewing. 9. It may be concluded that D-1 or D-2 activation exert opposite influences on chewing behaviour in rats, although to prove this effect more elucidation is needed.

Animals↗

PubMed1992

Morphine stimulates locomotor activity by an indirect dopaminergic mechanism: possible D-1 and D-2 receptor involvement.

1. The effect of morphine on locomotor activity in mice and the mechanism involved were evaluated. 2. Subcutaneous (s.c.) injection of different doses of morphine (10, 20 and 40 mg kg-1) into mice induced a dose-dependent locomotor activity. 3. The response to morphine was decreased in animals pretreated by the D-1 antagonist SCH 23390, the D-2 antagonist sulpiride or the opiate receptor antagonist naloxone, but not by atropine, phenoxybenzamine, propranolol and methergoline. 4. The inhibitory effects of SCH 23390, sulpiride or naloxone were dose-dependent. 5. Pretreatment with reserpine prevented the effect of morphine. SKF 38393 (D-1 agonist) or quinpirole (D-2 agonist) also induced locomotor activity in mice. Also this effect was decreased by reserpine pretreatment. 6. Combination of SKF 38393 with quinpirole but not of morphine with SKF 38393 or quinpirole induced a high degree of locomotor activity in intact and reserpinized animals. 7. It is concluded that locomotor activity induced by morphine is mediated by opiate receptor through an indirect dopaminergic mechanism.

Animals↗

PubMed1992

Ephedrine and amphetamine induced pecking in chickens: possible indirect D-1/D-2 dopaminergic mechanism.

The involvement of dopaminergic mechanism in pecking behaviour has been suggested. In the present work, the involvement of D-1/D-2 dopamine receptors in pecking induced by ephedrine and amphetamine in chickens has been studied. Both ephedrine and amphetamine induced pecking in a dose-dependent manner. Pretreatment of animals with D-1 antagonist SCH 23390, D-2 antagonist sulpiride or reserpine decreased the pecking response induced by both drugs. Phenoxybenzamine or propranolol (alpha- or beta-adrenergic blockers, respectively) and the antimuscarinic drug atropine did not decrease the response of these drugs. The results may indicate that the pecking induced by these drugs in chickens are mediated indirectly through D-1/D-2 dopaminergic mechanisms.

Amphetamine↗

PubMed1992

Inhibitory effect of morphine on yawning induced by cholinoceptor and dopamine D2 receptor activation in rats.

1. Bromocriptine (2, 4 and 8 mg kg-1, i.p.), physostigmine (0.05, 0.1 and 0.2 mg kg-1, i.p.) and pilocarpine (1, 3 and 5 mg kg-1, i.p.) induced dose-dependent yawning in rats. 2. These responses were reduced in a dose-dependent manner by pretreatment with morphine. 3. The inhibitory effect of morphine was reversed by naloxone. 4. Naloxone alone induced slight but significant yawning. 5. The present results suggest that morphine inhibits yawning in rats at an opiate receptor downstream from the sites at which cholinoceptor and dopamine D2 activation induce yawning. The anatomical location of these sites remains to be established.

Animals↗

PubMed1991

Evaluation of dopamine receptor involvement in rat feeding behaviour.

1. The anorectic effect of dopamine agonists and antagonists were studied in rats. 2. Dopamine agonists bromocriptine, quinpirole or SKF 38393 treatment induced, a dose-dependent anorexia in rats. 3. Anorectic effect of bromocriptine was decreased in animals pretreated with pimozide (D-2 antagonist), but not by sulpiride (D-2 antagonist) or SCH 23390 (D-1 antagonist) pretreatment. 4. Anorexia induced by quinpirole was decreased by sulpiride or pimozide, but not by SCH 23390 administration. 5. While sulpiride and SCH 23390 failed to antagonize the anorectic response of SKF 38393, methergoline (5-HT antagonist) decreased anorexia induced by the drug. 6. A combination of quinpirole with SKF 38393 did not elicit potentiated anorectic response. 7. Decrease in food intake induced by bromocriptine, quinpirole or SKF 38393 was potentiated in reserpinized animals, although single administration of reserpine also induced a marked decrease in feeding. 8. Single administration of sulpiride, pimozide or methergoline did not change the feeding behaviour of rats, but SCH 23390 induced anorexia. 9. It is concluded that D-2 activation may induce inhibition of feeding and anorexia induced by SKF 38393 may be mediated through serotonergic mechanism(s).

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

PubMed1991

Different effects of direct and indirect dopamine receptor agonists on immobility time in reserpine-treated mice.

1. The effects of dopamine agonists on the immobility time in mice were examined. 2. Apomorphine (APO), bupropion (BUP), bromocriptine (BRC) and quinpirole but not SKF 38393 elicited anti-immobility effect. The effect of the agonists was decreased by the D-2 antagonist sulpiride but not by the D-1 antagonist SCH 23390. 3. In animals pretreated with reserpine, the anti-immobility effects of APO and quinpirole were potentiated, while the response of BPU was decreased and that of BRC was not changed. 4. It is concluded that D-2 dopamine receptors are involved in the anti-immobility effects of dopaminergic agents, D-2 dopamine receptors may become hypersensitive by reserpine and BUP exerts its response through indirect dopaminergic if mechanism.

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

PubMed1991

Blockade of both D-1 and D-2 dopamine receptors may induce catalepsy in mice.

1. The catalepsy induced by dopamine antagonists has been tested and the possible dopamine subtypes involved in catalepsy was determined. 2. Dopamine antagonist fluphenazine, D-1 antagonist SCH 23390 or D-2 antagonist sulpiride induced catalepsy. The effect of fluphenazine and sulpiride was dose-dependent. Combination of SCH 23390 with sulpiride did not induce catalepsy potentiation. 3. D-1 agonist SKF 38393 or D-2 agonist quinpirole decreased the catalepsy induced by fluphenazine, SCH 23390 or sulpiride. 4. Combination of SKF 38393 with quinpirole did not cause potentiated inhibitory effect on catalepsy induced by dopamine antagonists. 5. The data may indicate that although D-2 receptor blockade is involved in catalepsy, the D-1 receptor may plan a role.

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

PubMed1991

Differential effects of dopamine agonists on locomotion in intact and reserpine-treated mice.

1. Apomorphine and bromocriptine induced a dose-dependent locomotion in mice. The responses of both drugs were decreased by SCH 23390 or sulpiride pretreatment. 2. Locomotor activity induced by apomorphine was increased and that of bromocriptine was decreased by reserpine. 3. SKF 38393 or quinpirole also induced locomotion. The response of SKF 38393 was decreased by reserpine. 4. Combination of SKF 38393 with bromocriptine induced a significant locomotor activity different from that of SKF 38393 or bromocriptine in reserpinized animals. 5. Combination of quinpirole with bromocriptine even decreased the response of bromocriptine in intact animals. 6. In conclusion, bromocriptine needs intact dopaminergic neurons and activation of D-1 receptor for expression of locomotion. High doses of quinpirole may induce locomotor activity possibly through D-1/D-2 receptor activation and quinpirole may potentiate the effect of bromocriptine on autoreceptor for inducing sedation.

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