PubMed Health⌕ Search

Biomedical subjects

M R Zarrindast

Publications and source records attributed to M R Zarrindast.

At least 109 records · Page 6Linked to original sources
PubMed1991

Methylxanthine-induced attenuation of pecking in chickens.

1. Apomorphine induced dose-dependent pecking in chickens. 2. The response was decreased by theophylline or caffeine in a dose-dependent manner. 3. Administration of theophylline or caffeine alone did not exert any effect on pecking behaviour. 4. Dipyridamole administration neither induced pecking nor altered the pecking induced by apomorphine. 5. Administration of 5-N-ethylcarboxamide-adenosine to animals caused variable effects on pecking induced by apomorphine. The drug did not induce pecking by itself. 6. It is concluded that the inhibitory response to methylxanthines may be mediated through blockade of adenosine receptors. However, to prove this, more experiments are needed.

Adenosine↗
PubMed1990

Bromocriptine induces climbing behaviour: possible D-1 or D-2 dopamine receptor involvement.

The ability of bromocriptine (BRC), a dopamine D-2 receptor agonist, to induce climbing behaviour was studied in mice. BRC (2-32 mg/kg IP) evoked climbing behaviour. The maximum effect was obtained with 8 mg/kg, while higher doses of BRC (16 and 32 mg/kg) were less effective. Climbing began about 2 h after injection and was most marked 5 h after bromocriptine administration. Pretreatment of animals with the dopamine antagonist pimozide (0.5 mg/kg IP) decreased BRC-induced climbing. Sulpiride (0.25-1.25 mg/kg IP), a potent D-2 antagonist and/or SCH 23390 (0.025 and 0.05 mg/kg SC), a D-1 receptor antagonist, also decreased the response. Furthermore, the climbing behaviour induced by BRC was abolished by pretreatment with reserpine plus alpha-methyl-p-tyrosine (AMPT). Concomitant administration of apomorphine (APO) and BRC potentiated the effect of APO on climbing. Concomitant injection of BRC and SKF 38393 (SKF, D-1 agonist) reduced the effect of SKF on climbing, while administration of BRC 4 h before SKF potentiated the effect of both drugs. It is suggested that BRC induces climbing through D-1 and/or D-2 dopamine receptors.

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

Food intake suppressant effect of baclofen in rats.

1. Baclofen given intraperitoneally (i.p.) to rats caused a dose-dependent decrease in food intake. 2. Bicuculline or picrotoxin (GABAA-antagonist) and methergoline (5-HT antagonist) decreased the anorectic effect of baclofen. 3. Pimozide (dopamine receptor blocker), phenoxybenzamine and propranolol (alpha and beta adrenergic blockers) did not diminish the baclofen effect, but even increased the anorexia induced by the drug. 4. It can be postulated that, at least partially, GABAA receptor mechanism, GABA-5HT receptor complex and/or 5-HT mechanism may be involved in baclofen induced anorexia.

Animals↗
PubMed1989

Involvement of GABAA receptor sites in diazepam hypothermia.

1. Intraperitoneal (i.p.) injection of diazepam (1.5-6 mg/kg) decreased the core body temperature (BT) of the rats. The effect was dose-dependent. 2. The hypothermia produced by diazepam (6 mg/kg, i.p.) was decreased in animals pretreated with high doses of bicuculline (BIC, 3 mg/kg, i.p.), while low doses of BIC (1.5 mg/kg, i.p.) potentiated the hypothermia. 3. Picrotoxin (PIC, 1 and 2 mg/kg, i.p.) pretreatment also decreased the hypothermic effect of diazepam. 4. Pretreatment of animals with atropine (AT, 10 mg/kg, i.p.) or propranolol (PRO, 10 mg/kg, i.p.) potentiated the hypothermic response of diazepam. Phenoxybenzamine (PHEN, 0.5 mg/kg, i.p.), methergoline (METH, 0.5 mg/kg, i.p.) or pimozide (PIM, 0.5 mg/kg, i.p.) did not change the diazepam hypothermia. 5. Single administration of BIC, PIC, PRO, PIM or METH also induced hypothermia. 6. One can postulate that diazepam hypothermia may be induced through GABAA receptor sites. However, further studies will clarify this hypothesis.

Adrenergic alpha-Antagonists↗
PubMed1989

Interactions of drugs acting on central dopamine receptors and cholinoceptors on yawning responses in the rat induced by apomorphine, bromocriptine or physostigmine.

1. Yawning was induced by subcutaneous (s.c.) injection of low doses of apomorphine to rats. This effect decreased with increasing doses of the drug. 2. Intraperitoneal (i.p.) pretreatment of animals with sulpiride (D2-receptor blocker) reduced the frequency of the yawns induced by apomorphine, while SCH 23390 (D1-receptor blocker, s.c.) pretreatment increased the small number of yawns which was induced by higher doses of apomorphine. Administration of SCH 23390 alone to rats also produced a low degree of yawning. 3. Apomorphine-induced yawning was decreased in animals treated with SK&F 38393 (D1-agonist, i.p.), atropine (i.p.) or theophylline (i.p.). 4. Intraperitoneal injection of bromocriptine (D2-agonist) in rats also induced dose-dependent yawning. The effect was decreased in animals pretreated with sulpiride, while SCH 23390 pretreatment did not change bromocriptine-induced yawning significantly. Pretreatment of animals with SK&F 38393, atropine or theophylline reduced the number of yawns induced by bromocriptine. 5. Physostigmine (i.p.) but not neostigmine (i.p.) also induced yawning. The effect was antagonized by atropine or theophylline but not by sulpiride. Administration of SK&F 38393 decreased yawning induced by physostigmine. This inhibitory influence of SK&F 38393 was reduced by SCH 23390 in pretreated animals. Treatment of animals with SCH 23390 or bromocriptine increased the frequency of yawns induced by physostigmine. 6. It is concluded that D2-receptor activation elicits yawning through influence on cholinergic mechanisms, whereas D1-receptor stimulation decreases yawning behaviour by a negative influence on the cholinergic system.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Anorectic and behavioural effects of bupropion.

1. Bupropion (12.5-75 mg kg-1) was given intraperitoneally to rats and was found to decrease the food consumption of the animals dose-dependently. While phenoxybenzamine, propranolol and methergoline failed to antagonize the anorectic effect of the drug; pimozide a dopamine receptor blocker decreased anorexia induced by bupropion. 2. Bupropion (12.5-50 mg kg-1) also caused a marked increase in locomotor activity of the rats. The increase in locomotion produced by bupropion was completely antagonized by pretreatment of the animals with pimozide and reserpine plus a-methyl-p-tyrosine, but not by pretreatment with phenoxybenzamine, propranolol or methergoline. 3. Taking into considerations the evidences of dopaminergic properties of bupropion shown by the others, it could be suggested that the anorexia and hyperactivity produced by bupropion may be induced through the indirect dopaminergic mechanism.

Animals↗
PubMed1988

GABAA and GABAB receptor sites involvement in rat thermoregulation.

1. Intraperitoneal (i.p.) injection of muscimol (MUS, 2-8 mg kg-1) decreased the core body temperature (BT) of the rats dose-dependently. 2. Intracerebroventricular (i.c.v.) injection of MUS (1 microgram/microliter/rat) also caused a fall in BT. 3. The hypothermia induced by MUS was inhibited by pretreatment of the animals with either bicuculline (BIC) or picrotoxin (PIC). 4. i.p. Injection of baclofen (BAC, 2.5-10 mg kg-1) induced hypothermia. Higher dose of the drug (20 mg kg-1) caused an initial fall followed by a marked increase in BT. 5. i.c.v. Injection of BAC produced a rise in BT. 6. The hypothermic effect of BAC was antagonized in animals pretreated with either BIC or PIC, while hyperthermic effect of the drug was potentiated with PIC pretreatment. 7. i.c.v. Injection of isoguvacine (ISO) induced hypothermia, which was attenuated in rats pretreated with either BIC or PIC. 8. It can be concluded that: activation of GABAA or GABAB receptor sites respectively may induce hypothermia or hyperthermia in rats.

Animals↗
PubMed1988

GABAA-antagonists and baclofen analgesia.

1. Intraperitoneal (i.p.) injection of different doses of baclofen (5, 7.5 and 10 mg/kg) induced analgesia in tail-flick test. The effect was dose-dependent. 2. The antinociception induced by baclofen (10 mg/kg, i.p.) was decreased in animals pretreated with bicuculline (1.5 mg/kg, i.p., 30 min), but not with naloxone (1.5 mg/kg, i.p., 30 min). 3. In picrotoxin (1 mg/kg, i.p., 15 min) pretreated mice, baclofen (5 mg/kg, i.p.) showed a significant analgesic effect. 4. Morphine (6 mg/kg, s.c.) induced analgesia which was antagonized by naloxone pretreatment (1.5 mg/kg, i.p.), while bicuculline or picrotoxin did not alter the morphine response. 5. These data suggest that a part of analgesic effect of baclofen may be mediated through GABAA receptor sites, and differs from that of morphine.

Analgesia↗
PubMed1987

Anorectic effect of ephedrine.

1. Different doses of ephedrine (3.1-50 mg kg-1) were given intraperitoneally to rats and found to decrease food intake dose-dependently. 2. The anorectic effect of ephedrine was decreased by animal pretreatment with pimozide, but phenoxybenzamine, propranolol and methergoline did not decrease the response. 3. The results show that the anorexia produced by ephedrine may be due to indirect dopaminergic mechanism of the drug.

Animals↗
PubMed1984

Brain stem tonic inhibition of thermoregulation in the rat.

It was shown, by selective levels of decerebration, that a drop in body temperature occurred in a midpontine rat due to impairment in thermoregulatory responses. Lowering the level of decerebration to the lower pons restored a coordinated thermoregulatory response. The response was inadequate to raise the core temperature to normal level, but it was nevertheless an integrated response of vasoconstriction, piloerection, and shivering and was appropriately turned off by warming the skin or core. In intact unanesthetized rats, microinjection of a local anesthetic in the pontine tegmentum resulted in thermoregulatory responses, such as curling of the body, piloerection, tremor in facial muscles, and shivering. Similar injections in the pontine tegmentum of the midpontine decerebrate rat also restored some heat gain responses, including shivering. These experiments suggest that in rats the heat gain responses are powerfully regulated by a tonic inhibitory mechanism located in the midbrain and upper pons that exerts a complete inhibitory effect on the thermoregulatory areas caudal to the midbrain in decerebrate rats and a partial inhibitory effect in intact animals. These experiments also confirm the previous observation in the cat of the presence of a facilitatory area(s) in lower levels of the central nervous system which is responsible for coordinated heat gain responses observed in low-level decerebrate animals. In addition, these experiments suggest that the brain stem thermoregulatory mechanisms are in fact functioning in intact unanesthetized animals.

Animals↗
PubMed1984

Sympathomimetic activity of mazindol on rat anococcygeus muscle and vas deferens.

Mazindol contracted the isolated anococcygeus muscle of the rat. This effect was prevented by pretreatment with reserpine and antagonized by phentolamine but not by atropine, cocaine, hexamethonium, methysergide or promethazine. The drug potentiated the contractile response of the rat anococcygeus to noradrenaline and field stimulation and released tritium from the rat vas deferens and anococcygeus preloaded with [3H]-noradrenaline. The release of radioactivity was unaffected by incubation of the tissue in calcium free or high potassium (60 mM) solution.

Animals↗
PubMed1981

Dopamine-like properties of ephedrine in rat brain.

1 Ephedrine (3.1-50 mg/kg) was given intraperitoneally to rats and was found to cause a marked increase in spontaneous locomotor activity. 2 In rats with a unilateral lesion in the substantia nigra made by stereotaxic injections of 6-hydroxydopamine, ephedrine (12.5-150 mg/kg i.p.) caused a dose-dependent turning towards the lesioned side. 3 Turning behaviour and increase in locomotion produced by ephedrine were antagonized by pretreatment of the animals with pimozide, amino-oxyacetic acid or reserpine plus alpha-methyl-p-tyrosine, but not by pretreatment with phenoxybenzamine, propranolol or methergoline. 4 In in vitro studies with synaptosomes prepared from rat brain, ephedrine blocked the uptake and caused the release of [3H]-dopamine. 5 Similar results with regard to locomotion and turning behaviour were obtained with (+)-amphetamine. 6 It is concluded that the increase in locomotion and turning behaviour produced by ephedrine is mediated through an indirect dopaminergic mechanism.

Animals↗
PubMed1980

Pharmacological study of the anococcygeus muscle of the dog.

1 The response of the dog anococcygeus muscle to field stimulation and to some drugs has been studied. The results are compared with those reported previously in the rat, cat and rabbit. 2 Field stimulation produced frequency-dependent contractions which were inhibited by guanethidine and phentolamine. When the tonus of the muscle was increased with guanethidine, field stimulation always produced frequency-dependent relaxation. The relaxation was not prevented by propranolol. 3 The muscle was contracted by noradrenaline, tyramine, acetylcholine, histamine (H1), 5-hydroxy-tryptamine, prostaglandin E2 and vasopressin. Phentolamine, atropine, promethazine (but not cimetidine) and methysergide inhibited the effect of the respective agonists. 4 After increasing the tonus of the muscle, it was relaxed by low concentrations of isoprenaline. The relaxation was antagonized by propranolol. 5 The response to adenosine triphosphate (ATP) was variable. In some preparations, it relaxed the muscle, in others it contracted the muscle prior to relaxation, in others still it only contracted the muscle. Indomethacin did not prevent ATP-induced contraction. 6 It is concluded that the anococcygeus of the dog, like that of rat, cat and rabbit, has an adrenergic motor innervation and an inhibitory innervation, the transmitter of which is not identified.

Anal Canal↗
PubMed1978

Tachyphylaxis to ethacrynic acid in the isolated atrium of guinea-pig and its relation to noradrenaline stores.

1 The isolated electrically-paced atrium of the guinea-pig developed a dose-dependent increase in the force of contraction in response to ethacrynic acid (12-100 microgram/ml) which was blocked by pretreatment of the animals with reserpine but was unaffected by desipramine or colchicine added to the bathing medium. 2 There was a rapidly developing tachyphylaxis to repeated doses of ethacrynic acid which was not reversed by rest or incubation of the tissue with noradrenaline. 3 There was no cross tachyphylaxis between ethacrynic acid and tyramine, amphetamine or nicotine. 4 Ethacrynic acid (200 microgram/ml) decreased the noradrenaline content of the atria by 32%. 5 It is concluded that ethacrynic acid exerts its effects indirectly through the release of endogenous noradrenaline and that the mechanism of release seems to be different from that of other known indirect sympathomimetic drugs.

Animals↗