ergoline and lergotrile

Topics: Amantadine; Antiparkinson Agents; Atrophy; Brain; Bromocriptine; Cognition; Dementia; Dreams; Drug Interactions; Ergolines; Humans; Levodopa; Libido; Memory; Parasympatholytics; Parkinson Disease; Receptors, Dopamine; Sexual Behavior; Substance-Related Disorders; Visual Perception

Topics: Adenoma; Adrenocorticotropic Hormone; Bromocriptine; Dihydroergotoxine; Dopamine; Drug Administration Schedule; Ergolines; Growth Hormone; Levodopa; Lisuride; Metergoline; Methysergide; Pergolide; Pituitary Neoplasms; Prolactin; Tomography, X-Ray Computed

Topics: Adult; Aged; Drug Therapy, Combination; Ergolines; Humans; Levodopa; Middle Aged; Parkinson Disease; Pergolide; Retrospective Studies

The present study was undertaken to compare the abilities of the dopaminergic agonists apomorphine, bromocriptine, and lergotrile to inhibit the synthesis of dopamine (DA) in terminals of nigrostriatal and mesolimbic DA neurons. The in vivo synthesis of DA was estimated by measuring the rate of accumulation of dihydroxyphenylalanine (DOPA) in terminals of nigrostriatal (striatum) and mesolimbic (nucleus accumbens, olfactory tubercle) neurons 30 min after the administration of NSD 1015, a decarboxylase inhibitor. The activation of DA autoreceptors in these regions was evaluated by measuring the abilities of the DA agonists to inhibit DA synthesis in brain regions of rats pretreated with gamma-butyrolactone (GBL). Apomorphine (0.03-1.0 mg/kg for 45 min) and bromocriptine (0.1-10 mg/kg for 90 min) produced dose-dependent decreases in the rate of DA synthesis in all three brain regions of both vehicle- and GBL-treated rats. A time course of the effects of the highest dose of bromocriptine (10 mg/kg), however, demonstrated dramatic regional differences in the ability of this drug to inhibit DA synthesis in saline-versus GBL-pretreated rats. Bromocriptine inhibited the GBL-induced increase in DA synthesis for 6 hours in all regions examined. In the striatum of saline-treated rats the decrease in DA synthesis was evident only at 1.5 hours after bromocriptine administration, while in the nucleus accumbens and olfactory tubercle DA synthesis remained inhibited for 6 hours. By contrast, lergotrile reduced DA synthesis to a similar extent in all three regions for at least 6 hours in both vehicle- and GBL-treated rats. These results suggest that there is no regional difference in the ability of bromocriptine to inhibit DA synthesis via DA autoreceptor mechanisms, but there appear to be differences in postsynaptic DA receptor-mediated mechanisms which regulate nigrostriatal versus mesolimbic DA neurons.

Topics: 4-Butyrolactone; Animals; Apomorphine; Bromocriptine; Corpus Striatum; Dihydroxyphenylalanine; Dopamine; Ergolines; Limbic System; Male; Nucleus Accumbens; Olfactory Bulb; Prolactin; Rats; Time Factors

Topics: Animals; Drug Evaluation; Drug Evaluation, Preclinical; Ergolines; Fluoxetine; Humans; Models, Biological; Pergolide; Pharmacology, Clinical; Rats

Experiments in rats revealed that the parkinsonian drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) given in multiple daily doses either per os (p.o.) or subcutaneously (s.c.) induced in a dose-dependent manner solitary or double ("kissing") duodenal ulcers in the rat. MPTP also diminished cerebral concentrations of DOPAC and the duodenal ulcers were prevented by pretreatment with dopamine agonists (e.g., bromocriptine, lergotrile) or monoamine oxidase inhibitors (e.g., pargyline, 1-deprenyl). High doses of MPTP also caused gastric erosions and motility changes resembling parkinsonism (e.g., akinesia, rigidity, forward bending of trunk). This chemical decreased gastric secretion of acid and pepsin, as well as pancreatic bicarbonate, trypsin and amylase. Thus, MPTP causes duodenal ulcers that are possibly associated with impaired defense in the duodenal bulb (e.g., decreased availability of duodenal and pancreatic bicarbonate).

Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Amylases; Animals; Bicarbonates; Bromocriptine; Dose-Response Relationship, Drug; Duodenal Ulcer; Duodenum; Ergolines; Female; Gastric Acid; Gastric Emptying; Gastrointestinal Motility; Monoamine Oxidase Inhibitors; Pancreas; Pyridines; Rats; Rats, Inbred Strains; Trypsin

Ergot derivatives, such as bromocriptine, lergotrile and pergolide, are potent dopaminergic agonists in various biological systems. In topical doses ranging from 0.001 to 1% applied unilaterally, each agent produced dose-related ocular hypotension in normal rabbits. Utilizing an intraocular pressure (IOP) recovery rate method (aqueous formation index), each agent was observed to suppress the recovery rate of IOP in normal rabbits. Pretreatment with a prejunctional dopamine receptor antagonist (domperidone) inhibited the ocular hypotensive effect of bromocriptine and pergolide more than that of lergotrile. In rabbits with unilateral superior cervical ganglionectomies, IOP was lowered appreciably less by these compounds in the denervated eyes. These studies indicate that: a) lowering of IOP by these ergot derivatives is dependent, in part, on suppression of sympathetic neuronal activity; b) the most probable sites of action are DA2 receptors on sympathetic nerve endings or in sympathetic ganglia; c) ocular hypotension is produced, in part, by suppressing aqueous humor formation.

Topics: Administration, Topical; Animals; Bromocriptine; Domperidone; Ergolines; Eye; Ganglia, Sympathetic; Intraocular Pressure; Male; Pergolide; Rabbits; Sympathectomy

The following synthetic, structural analogs of dopamine (DA) were examined for their ability to produce hyperglycemia in conscious unrestrained rats: APO (apomorphine), RDS-127 (2-di-n-propylamino-4,7-dimethoxyindane), di-n-propyldopamine, 2-di-n-propylamino-5,6-dihydroxytetralin, 2-dimethylamino-6,7-dihydroxytetralin, lergotrile, pergolide, bromocriptine and d-amphetamine. All the compounds demonstrated dose- and time-dependent hyperglycemic actions. The most potent DA analog to induce hyperglycemia was 2-di-n-propylamino-5,6-dihydroxytetralin (0.18 mumol/kg) and, at the doses used, 2-dimethylamino-6,7-dihydroxytetralin produced the greatest elevation in blood glucose (227% control). APO and RDS-127 were used in experiments designed to provide additional mechanistic information concerning their hyperglycemic action. The hyperglycemia produced by APO or RDS-127 was blocked by adrenalectomy, adrenodemedullation or prior administration of pimozide, a DA receptor antagonist. Phentolamine, an alpha adrenergic receptor antagonist had no effect on the hyperglycemia induced by APO or RDS-127. Oral glucose tolerance tests indicated that APO and RDS-127 caused abnormal glucose tolerance and inhibited the compensatory increase in serum immunoreactive insulin. These effects were prevented by pimozide or phentolamine pretreatment. The potencies of the compounds to produce increases in serum glucose concentrations (SG), inhibit the accumulation of DOPA using the in vivo gamma-butyrolactone procedure (DOPA) and inhibit food intake (FI) were subjected to correlation analysis. Positive correlations were found for FI vs. DOPA, r = 0.96; SG vs. decreases DOPA, r = 0.98 and SG vs. FI, r = 0.98.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenal Medulla; Animals; Apomorphine; Blood Glucose; Bromocriptine; Dextroamphetamine; Dihydroxyphenylalanine; Dopamine; Ergolines; Indans; Insulin; Islets of Langerhans; Male; Pergolide; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha; Receptors, Dopamine; Tetrahydronaphthalenes

A pharmacologic test is described for assessing selective dopamine (DA) autoreceptor activation using locomotor activity (LMA) of the mouse as the dependent variable. In this test, three criteria must be satisfied to indicate selectivity for the DA autoreceptor. First, a dose-related fall in LMA, taken as a measure of DA autoreceptor activation, should be produced by the putative autoreceptor agonist. Second, to demonstrate a DA system is involved, the reduction in LMA should be blocked by a DA receptor antagonist. Finally, the test compound should produce no LMA-stimulating (i.e., postsynaptic DA receptor agonist) effects over prolonged periods of observation. Using these criteria, 15 DA agonists were evaluated for DA autoreceptor selectivity. Four agents satisfied all criteria as selective DA autoreceptor agonists: CF 25-397, N-n-3-propyl-3- hydroxyphenylpiperidine , 6,7-dihydroxy-2- dimethylaminotetralin (TL-99) and 2-amino-6,7- dibenzoyloxy -1,2,3,4- tetrahydronapthalene . Seven DA agonists produced U-shaped dose-response curves indicative of activity at both the autoreceptor and postsynaptic DA receptor. These agents were: apomorphine, n-propylnorapomorphine, pergolide, RU 24213, RU 24926, (-)-6-ethyl-9-oxaergoline and lisuride. SKF 38393 failed to exert any significant effect on the LMA of the mouse. Both lergotrile and bromocriptine produced dose-related falls in LMA, but both caused a rebound increase in LMA before their durations of action were terminated. Although 3,4-dihydroxyphenylamino-2-imidazoline did produce a dose-related fall in LMA, the inhibition produced by 3,4-dihydroxyphenylamino-2-imidazoline was not reduced by sulpiride, suggesting a nondopaminergic action for 3,4-dihydroxyphenylamino-2-imidazoline.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; Animals; Apomorphine; Benzazepines; Bromocriptine; Ergolines; Female; Methods; Mice; Motor Activity; Receptors, Dopamine; Sulpiride

Although withdrawn from clinical trials because of liver toxicity, the ergot derivative lergotrile has been useful in the treatment of disorders involving dopaminergic systems (e.g., parkinsonism). In various biochemical and behavioral assays, this compound acts most potently as a dopamine (DA) agonist but also has DA antagonist as well as serotonin (5-HT) agonist properties. To elucidate further its effects in vivo, rats were trained to discriminate 0.5 mg/kg of lergotrile from saline in a two-lever water-reinforced task. In tests for similarities to other ergolines, dose-related substitutions were observed with lisuride (0.003-0.04 mg/kg) and d-lysergic acid diethylamide (0.01-0.08 mg/kg); partial substitution occurred with ergonovine (0.063-0.5 mg/kg). The DA agonist apomorphine (0.016-0.5 mg/kg) also substituted for lergotrile whereas the 5-HT agonist quipazine (0.25-2.0 mg/kg) elicited primarily saline-appropriate responding. Tests involving drug combinations indicated that the DA antagonist haloperidol (0.016-0.5 mg/kg) attenuated responding on the drug-appropriate lever; however, neither the DA (D2) antagonist sulpiride (2.0-16.0 mg/kg) nor the 5-HT antagonist BC-105 (1.0-4.0 mg/kg) had an effect upon the lergotrile cue. These results indicate that DA neuronal systems are probably more important than 5-HT neuronal systems in mediating the discriminative stimulus properties of lergotrile; however, the contribution of other neurotransmitter systems (e.g., norepinephrine) to these effects still must be evaluated.

Topics: Animals; Apomorphine; Discrimination Learning; Dose-Response Relationship, Drug; Ergolines; Ergonovine; Haloperidol; Lisuride; Lysergic Acid Diethylamide; Male; Piperidines; Pizotyline; Quipazine; Rats; Rats, Inbred Strains; Sulpiride

Various synthetic dopamine (DA) analogues have been shown to produce glucose intolerance and inhibit the compensatory increase in serum insulin during an oral glucose tolerance test (OGTT). To investigate the possibility that there is a direct action of dopamine analogues to inhibit glucose-stimulated insulin release from the endocrine pancreas, the following compounds were compared with the effects of epinephrine (EPI) on isolated rat pancreatic islets: apomorphine (APO), pergolide, lergotrile, TL-99 (2-dimethylamino-6,7-dihydroxytetralin), and RDS-127 (2-di-n-propyl-amino-4,7-dimethoxyindane). EPI, TL-99, and pergolide inhibited insulin release in a concentration-dependent fashion (10(-7)-10(-5) M), whereas lergotrile inhibited at 10(-5) M but not at 10(-6) M. RDS-127 and APO were ineffective at 10(-5) M, but produced a greater than 50% inhibition at 2 X 10(-4) M. The potencies of the DA analogues fell into two groups: compounds that are approximately as active as EPI (e.g., TL-99 and pergolide) or compounds that are relatively inactive (e.g., APO, lergotrile, and RDS-127). The inhibitory actions of EPI, TL-99, and pergolide were blocked by the alpha 2-adrenergic receptor antagonist yohimbine, whereas the DA receptor antagonist, sulpiride, had no effect, suggesting an action initiated at alpha 2-adrenergic receptors. Drugs from both groups produced marked glucose intolerance and inhibited the compensatory increase in insulin during an OGTT. Adrenodemedullation blocked the glucose intolerance and inhibition of insulin release caused by RDS-127, whereas these effects of TL-99 were not attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenal Medulla; Animals; Apomorphine; Cells, Cultured; Dopamine; Epinephrine; Ergolines; Glucose; Indans; Insulin; Insulin Antagonists; Insulin Secretion; Islets of Langerhans; Male; Pergolide; Rats; Rats, Inbred Strains; Tetrahydronaphthalenes; Yohimbine

The dopaminergic stimulants apomorphine and lergotrile both evoked hypothermia and stereotyped behaviour in rats. These drug effects were sensitive to antagonism by haloperidol, a dopaminergic receptor blocker. In rats pretreated with 5-hydroxytryptaminergic receptor blockers, cinanserin reduced apomorphine-induced hypothermia but cyproheptadine did not. Both cinanserin and cyproheptadine significantly potentiated lergotrile-induced hypothermia. Similarly, the stereotypic effects of apomorphine were partly reduced by cyproheptadine, although higher doses of cyproheptadine did potentiate lergotrile-induced stereotyped behaviour. These findings of different influences of 5-HT antagonists upon the effects of apomorphine and lergotrile indicate that these two dopaminergic stimulants may not work in identical manner to produce outwardly similar drug effects.

Topics: 5-Hydroxytryptophan; Animals; Apomorphine; Body Temperature; Cinanserin; Cyproheptadine; Ergolines; Haloperidol; Humans; Male; Rats; Rats, Inbred Strains; Stereotyped Behavior

A solid basis for the M4-approach has been developed over the past 10 years. Recent examples of the production of difficult-to-synthesize mammalian metabolites through microbial transformations attest to the utility of the methodology. There is, however, much more to be done. Model studies should be conducted to test parallels between microbial and mammalian S- and N-oxidations, O-glucuronidations, and ester and amide hydrolyses. Subsequently, even greater applications of M4- work can be envisioned. We have been pleased to see our colleagues in industry and academia adopt the M4- approach to solve difficult pharmacological and toxicological problems. In large measure, this has been our greatest reward for efforts initially presented before the membership of the American Society of Pharmacognosy in 1973.

Topics: Acronine; Animals; Apomorphine; Biotransformation; Dealkylation; Ellipticines; Ergolines; Guinea Pigs; Humans; Hydroxylation; Imipramine; Mammals; Models, Biological; Papaverine; Pharmaceutical Preparations

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.

Topics: Animals; Behavior, Animal; Bromocriptine; Ergolines; Male; Mice; Mice, Inbred Strains; Motor Activity; Pergolide

The role of endogenous somatostatin in the pathogenesis of duodenal was investigated in the present study by using the cysteamine animal model of the disease. Our previous studies showed a rapid and multiorgan depletion of somatostatin immunoreactivity (SIR) in rats given a single dose of duodenal ulcerogen cysteamine. We now determined whether acetylcholinergic and dopaminergic modulation (both known to influence the development of duodenal ulcer) are accompanied by modification of cysteamine-induced SIR depletion in rat organs. Vagotomy performed either 1 or 18 h before cysteamine administration did not interfere with the chemically induced SIR decrease in pancreas, gastric and duodenal mucosa. Vagal denervation alone had no marked influence on SIR levels but if combined with cysteamine, the SIR depletion in the stomach was significantly more pronounced than after the duodenal ulcerogen alone. Pretreatment with the dopamine agonists bromocriptine or lergotrile (known to prevent the chemically induced duodenal ulcers) did not influence the SIR depletion by cysteamine. Thus cysteamine depletes endogenous somatostatin in peripheral organs (e.g., stomach, duodenum, pancreas) by mechanisms independent of both vagus nerve and dopamine agonists. A role of central somatostatin depletion leading to disinhibition of vagus is also considered in the pathogenesis of experimental duodenal ulcer.

Topics: Animals; Bromocriptine; Cysteamine; Duodenum; Ergolines; Female; Hypothalamus; Pancreas; Rats; Rats, Inbred Strains; Somatostatin; Stomach; Vagotomy

The concentration of blood glucose was measured in rats after administration of a number of drugs characterized as dopamine agonists. Compounds that cause release of dopamine, or agents that block the reuptake of dopamine, did not elevate blood glucose. Some direct dopamine receptor stimulants (lergotrile, bromocriptine, apomorphine) caused hyperglycemia, but other agonists (e.g. pergolide) did not. Further experiments with lergotrile, the most active hyperglycemic dopamine agonist, revealed that the blood glucose increase was accompanied by a marked elevation in liver glycogen, indicating a gluconeogenic effect of the compound. This hypothesis was supported by using inhibitors of gluconeogenesis (L-tryptophan or 3-mercaptopicolinic acid) to block lergotrile's hyperglycemic action. Structure-activity relationships among close analogues of lergotrile suggest that the cyano moiety in the lergotrile molecule may be of importance in the hyperglycemic action of lergotrile. These results indicate that central dopamine stimulation per se does not cause hyperglycemia in rats.

Topics: Animals; Blood Glucose; Dopamine; Ergolines; Glucagon; Glycogen; Insulin; Liver Glycogen; Male; Muscles; Pergolide; Picolinic Acids; Rats; Rats, Inbred Strains; Structure-Activity Relationship; Tryptophan

The possible participation of D1 versus D2 dopamine receptors in mediating dopaminergic neurotransmission of self-stimulation (SS) in the medial prefrontal cortex (MPC) of the rat was studied neuropharmacologically. Intracerebral as well as intraperitoneal injections of agonists and antagonists of dopamine receptors were used in this study. In all experiments performed with systemic injections, spontaneous motor activity (SM) was measured parallel to self-stimulation behavior as control for non specific effects of the drugs. Intracranial injections were done unilaterally serving SS of the contralateral side (not injected or injected with 0.9% NaCl) as control in the same animals. Spiroperidol and pimozide were used as D1-D2 dopamine antagonists, while sulpiride was used as a specific D2 antagonist. Apomorphine was used as D1-D2 agonist, while bromocriptine and lergotrile were used at doses in which these ergot drugs are considered predominantly D2 agonists. Sulpiride, intraperitoneally or intracerebrally injected at the same locus at which the stimulating electrode was located produced no effect on SS. On the contrary, the D1-D2 antagonists, spiroperidol and pimozide intraperitoneally or intracerebrally injected produced a dose-dependent decrease on SS. On the basis of these data it is suggested, that the dopamine neurotransmission involved in SS of the MPC is mediated via D1 dopamine receptors. This suggestion is further emphasized by the results obtained with the agonists, apomorphine, bromocriptine and lergotrile. Apomorphine produced a dose-related decrease on SS and a decrease at lower doses and an increase at higher doses on SM. Bromocriptine and lergotrile had, on the contrary, no effect on SS and a dose-related decrease on SM.

Topics: Animals; Apomorphine; Bromocriptine; Cerebral Cortex; Dose-Response Relationship, Drug; Ergolines; Functional Laterality; Male; Pimozide; Rats; Rats, Inbred Strains; Receptors, Dopamine; Self Stimulation; Spiperone; Sulpiride; Synaptic Transmission

The effect of three dopamine agonists, apomorphine, bromocriptine and lergotrile, was tested on the release of gamma-aminobutyric acid, (GABA) and acetylcholine (ACh) from tissue slices of rat nucleus accumbens and striatum. All three agents in vitro caused a dose dependent depression of the K+-evoked release of [14C]-GABA in corpus striatum. This effect was also obtained following in vivo drug application and when endogenous GABA release was determined. A similar depression of GABA release was obtained in the nucleus accumbens. Both dopamine and dibutyryl adenosine-3':5'-cyclic monophosphoric acid inhibited the K+-evoked release of [14C]-GABA in corpus striatum. This inhibitory effect was not reversed by sulpiride. Bromocriptine and lergotrile also depressed the K+-evoked release of [3H]-acetylcholine from tissue slices of corpus striatum but not nucleus accumbens, as has previously been demonstrated for dopamine and apomorphine. In contrast, sulpiride enhanced the release of [3H]-acetylcholine and molindone reversed the apomorphine inhibition of [3H]-acetylcholine release. These results indicate that dopaminergic agents may influence the release of both GABA and ACh in the corpus striatum but only GABA in the nucleus accumbens.

Topics: Acetylcholine; Afferent Pathways; Animals; Apomorphine; Bromocriptine; Bucladesine; Corpus Striatum; Culture Techniques; Dose-Response Relationship, Drug; Ergolines; gamma-Aminobutyric Acid; Male; Molindone; Muridae; Nucleus Accumbens; Receptors, Dopamine; Septal Nuclei; Sulpiride; Synaptic Transmission

Cardiovascular effects of the dopamine receptor agonists, bromocriptine and lergotrile, were examined in renal hypertensive rats (RHR), spontaneously hypertensive rats (SHR) and in normotensive rats (NTR). In SHR, bromocriptine at 0.3 and 1.0 mg/kg i.p. and lergotrile at 0.3 mg/kg i.p. produced significant decreases in blood pressure and heart rate and the effects were prevented by haloperidol pretreatment. These results are consistent with the hypothesis that bromocriptine- and lergotrile-induced cardiovascular effects are due to a reduction in sympathetic tone via activation of neuronal dopamine receptors. In contrast to SHR, bromocriptine as well as lergotrile, at doses of 0.3 mg/kg i.p., were ineffective in RHR. Only at the 1 mg/kg i.p. dose, both the agents reduced blood pressure in RHR, but increased heart rate and only the effects of bromocriptine were antagonized by haloperidol. The magnitude and the duration of the hypotensive effect produced by both the agents were smaller in RHR than in SHR. The ganglion blocking agent, chlorisondamine, reduced blood pressure equally in RHR and SHR, but not in NTR, indicating a role for the sympathetic nervous system in the maintenance of high blood pressure in both SHR and RHR. It is further suggested that neuronal dopamine receptors that mediate reduction in resting sympathetic tone are less sensitive in RHR as compared to SHR.

Topics: Animals; Blood Pressure; Bromocriptine; Ergolines; Heart Rate; Hypertension; Hypertension, Renal; Male; Rats; Rats, Inbred Strains

The effects of the dopamine agonists apomorphine, lisuride and lergotrile were evaluated on cat spinal cord monosynaptic transmission by stimulating the dorsal root and recording the ventral root compound action potential. All 3 agonists decreased the area of the monosynaptic response. This effect was prevented by pretreatment with the dopamine antagonists haloperidol and metoclopramide, but not with the alpha-adrenergic antagonist phentolamine. These results suggest the existence of spinal cord dopamine receptors which can modulate motor output.

Topics: Action Potentials; Animals; Apomorphine; Cats; Ergolines; Female; Haloperidol; Lisuride; Male; Metoclopramide; Phentolamine; Receptors, Dopamine; Spinal Cord; Synapses; Synaptic Transmission

In rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal system we compared the behavioral effects of pergolide with those of L-dopa, bromocriptine, and lergotrile. In this animal model of parkinsonism, doses of 0.25 mg per kilogram pergolide (free base) induced vigorous circling for 24 hours. Pergolide was more potent than bromocriptine or lergotrile. Pretreatment with alpha-methylparatyrosine nearly abolished the effects of bromocriptine, markedly diminished the effects of lergotrile, and only partially diminished the effects of pergolide. These findings suggest that pergolide should be more effective than bromocriptine in the treatment of parkinsonism.

Topics: Animals; Behavior, Animal; Brain Diseases; Bromocriptine; Ergolines; Female; Hydroxydopamines; Oxidopamine; Parkinson Disease; Pergolide; Rats; Rats, Inbred Strains

Topics: Adenylyl Cyclases; Aging; Animals; Corpus Striatum; Dextroamphetamine; Ergolines; Female; Male; Motor Activity; Rats; Receptors, Dopamine; Rotation; Sex Factors; Spiperone