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PubMed1988

The possible role of dopamine autoreceptors in neuroleptic atypicality.

Different brain pathways have been shown to subserve the therapeutic effects of neuroleptics and their extrapyramidal side effects. Agents which can discriminate between these pathways, therefore, might be able to produce 'atypical' clinical effects. Molindone, a novel neuroleptic of the indoleamine class, has been shown in basic paradigms to discriminate between brain dopaminergic systems by virtue of its ability to preferentially inhibit dopamine autoreceptors (DARs). Clinical studies suggest that molindone may be less likely than traditional neuroleptics to induce tardive dyskinesia and that molindone may preferentially ameliorate some negative schizophrenic symptoms. We suggest that the distinct clinical effects of molindone result from its ability to block DARs.

Animals↗
PubMed1983

Comparison of the effects of antipsychotic drugs on the schedule-controlled behavior of squirrel monkeys and pigeons.

Lever pressing by squirrel monkeys and key pecking by pigeons were maintained under a multiple 3-min fixed-interval (FI), 30-response fixed-ratio (FR) schedule by the presentation of food. These responses, which differed under the two schedules, but were similar for both species, were used to compare the effects of antipsychotic compounds from different pharmacological classes. Except for differences in potency levels, the effects of intermediate doses of haloperidol and molindone were similar in monkeys and pigeons; these compounds decreased responding under the fixed-interval schedule at doses that did not affect fixed-ratio responding. Similar effects also occurred with chlorpromazine, promazine and thiothixene in pigeons. With monkeys, however, intermediate doses of promazine decreased fixed-ratio responding more than responding maintained under the fixed-interval schedule, while chlorpromazine and thiothixene produced similar effects on responding under both schedules. The effects of novel antipsychotic, clozapine, differed from those of the other agents in both monkeys and pigeons. With both species clozapine increased fixed interval responding at doses that did not affect responding under the fixed-ratio schedule. Doses required to reduce responding at least 50% were approximately 5 to 160 times greater for pigeons than for monkeys for all drugs except clozapine which was equipotent in both species. In monkeys the order of potency was haloperidol greater than molindone = thiothixene greater than chlorpromazine greater than clozapine greater than promazine, whereas in pigeons the order was haloperidol greater than thiothixene greater than clozapine greater than molindone greater than promazine greater than chlorpromazine.

Animals↗
PubMed1988

D-1 and D-2 receptor blockade have additive cataleptic effects in mice, but receptor effects may interact in opposite ways.

The dopaminergic role of D-1 and D-2 receptors in catalepsy was evaluated using drugs with preferential receptor affinities. The D-1 antagonist, SCH 23390, caused distinct catalepsy in mice at 1, 2, and 10 mg/kg, IP, but not at two lower doses. The selective D-1 blocker, molindone, also caused catalepsy at 5 and 10 mg/kg; and blockade of both receptor types produced additive cataleptogenic effects. Apomorphine (4 mg/kg), which is an agonist for both receptors, potentiated SCH 23390-induced catalepsy much more than it did the catalepsy induced by molindone; the potentiation was produced by higher, not lower, doses of apomorphine. To determine if the apomorphine potentiation was mediated by D-1 or D-2 receptors, we tested selective agonists in mice that were concurrently injected with selective blockers. SCH 23390-induced catalepsy was potentiated by a large dose of the D-2 agonist, bromocriptine. The catalepsy of D-2 blockade with molindone was not potentiated by the D-1 agonist, SKF 38393, which slightly disrupted the catalepsy of D-2 blockade. We conclude that catalepsy is not a simple D-2 blockade phenomenon and that preferential antagonism of either receptor type can cause catalepsy. Catalepsy is most profound when both receptor types are blocked. Dopamine agonists, in large concentrations, are known to promote movements, and thus it is not surprising that they tend to disrupt catalepsy.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1997

The incorporation of butyrophenones and related compounds into a pharmacophore for dopamine D2 antagonists.

This study is an attempt to incorporate the butyrophenones, an important class of nontricyclic antipsychotic drugs, into a previously proposed pharmacophore model of tricyclic dopamine D2 receptor antagonist ligands. Conformational energy calculations were performed using the MM3-92 program on spiperone, as a representative butyrophenone, and milenperone and R48455, as related compounds with more limited conformational freedom. Twenty seven conformers were evaluated for spiperone with MM3-92 calculations and nine of these were within 1.1 kcal/mole of the global minima indicating the flexibility of the compound. A conformational analysis of twenty crystal structures of butyrophenones was also performed and six distinct conformers were represented. All of the energy minimized conformers of spiperone were superimposed in a least squares sense onto loxapine as a relatively rigid, typical D2 antagonist and a pair of mirror image conformers, which are observed in one crystal structure of spiperone, were found to be the best fit. However, it was not possible to discriminate between these two conformers since they fit the pharmacophore model equally well. The para-fluoro and carbonyl group of the butyrophenones were found to correspond best to the oxygen and chlorine atoms of loxapine, respectively. The conformations of milenperone and R48455 were also consistent with the two putative biologically active forms of spiperone and the pharmacophore model. Conformational energy calculations were also performed on molindone, an antipsychotic drug in clinical use, which can be related to the butyrophenones since both have a carbonyl group adjacent to an aromatic ring. A putative biologically active form was proposed for molindone and this was related to the structure of piquindone, a rigid analog of molindone. All of the compounds were found to be entirely consistent with the pharmacophore model. However, as previously found, there is great variability in the distance between the ammonium nitrogen and the center of the relevant aromatic ring with the most extreme case in the present study being R48455 where the distance is 7.2 A. The results of the present study should also be relevant to the structures of novel, atypical antipsychotic drugs such as risperidone which appear to be analogs of the butyrophenones.

Antipsychotic Agents↗
PubMed1987

Cytotoxic effects of neuroleptic drugs.

Agranulocytosis and the release of transaminase enzymes from liver cells are known consequences of neuroleptic drug use. These effects are most common with low potency neuroleptic drugs. It has been hypothesized that these effects are due to the direct toxic action of these drugs on blood and liver cells. The purpose of this study is to compare the cytotoxic effects of eight neuroleptic drugs in five different biological test systems. In all of the test systems, thioridazine, chlorpromazine, trifluoperazine, fluphenazine and thiothixene (group one drugs) were the most toxic drugs and molindone was the least toxic. Thioridazine was between 25 and 84 times more toxic than molindone. Loxapine was significantly more toxic than molindone, but less toxic than the group one drugs. Haloperidol was intermediate in toxicity between the group one drugs and loxapine. We conclude that the difference in cytotoxicity of the neuroleptic drugs observed in these experiments accounts in part for the increase in agranulocytosis and hepatotoxicity with thioridazine and chlorpromazine and for the lower incidence of these side effects with less toxic drugs. The possibility that tardive dyskinesia may be due to the cytotoxic effects of neuroleptic drugs is discussed and an experiment to test this hypothesis is suggested.

Animals↗
PubMed1984

Antagonism by neuroleptics of neurotransmitter receptors of normal human brain in vitro.

Using radioligand binding techniques, we determined the equilibrium dissociation constants (KD's) for a series of neuroleptics at the dopamine (D-2), muscarinic, histamine H1, alpha 1- and alpha 2-adrenergic receptors of normal human brain tissue obtained at autopsy. Seventeen different compounds were studied at the D-2 receptor and 15 compounds at the remaining receptors. At the D-2 receptor of caudate nucleus, spiperone was the most potent compound (KD = 0.16 nM); clozapine the least potent (KD = 180 nM). The KD's for six compounds at the D-2 receptor of nucleus accumbens were not significantly different from their respective KD's in the caudate nucleus. The most potent and least potent compounds at the other receptors were clozapine and molindone at the muscarinic receptor, mesoridazine and molindone at the H1 receptor, spiperone and molindone at the alpha 1-receptor, and clozapine and haloperidol at the alpha 2-receptor, respectively.

Adolescent↗
PubMed1988

Effects of clozapine on fixed-consecutive-number responding in rats: a comparison to other neuroleptic drugs.

The effects of clozapine and several other neuroleptic drugs were examined in rats responding under fixed-consecutive-number (FCN) schedules with minimum response requirements of 4 and 8. Under these schedules, rats were trained to respond either 8 or more times or 4 or more times on one lever, and then respond once on a second lever. In one component of these schedules, an external discriminative stimulus was presented following the completion of the response requirement on the first lever, whereas no stimulus change was programmed under the other. Under the FCN 8 schedule without the external discriminative stimulus, clozapine produced large dose-dependent decreases in accuracy (percent of reinforced response runs), whereas molindone produced small decreases in accuracy. Neither clozapine or molindone, however, altered accuracy under the FCN 4 without the external discriminative stimulus. Under these same schedules, loxapine, chlorpromazine, haloperidol and thioridazine produced small increases in accuracy at intermediate doses without affecting accuracy at the low and high doses. None of the neuroleptics evaluated produced accuracy-altering effects under the FCN schedules with the external discriminative stimulus. In general, all of these drugs decreased response rates in a dose-dependent fashion. The order of potency for the rate-decreasing effects of these drugs was loxapine greater than haloperidol greater than molindone greater than clozapine = chlorpromazine greater than thioridazine. Thus, the effects of clozapine on accuracy under the FCN schedules without the external discriminative stimulus differed qualitatively from those of other neuroleptic agents.

Animals↗
PubMed1993

Thioridazine improves affective symptoms in schizophrenic patients.

Consenting schizophrenic patients ranging in age from 18 to 63 years were withdrawn from antipsychotics for at least 1 week and randomly assigned to receive identical capsules of thioridazine (n = 13), molindone (n = 10), or haloperidol (n = 12) for a minimum of 6 weeks. Compared with the molindone- and haloperidol-treated patients, the thioridazine-treated patients were significantly improved over time as measured by Brief Psychiatric Rating Scale (BPRS) and Hamilton Rating Scale for Depression (HAM-D) total scores. Improvement in BPRS scores was due largely to improvement in symptoms of anxiety and depression. Subjects did not differ significantly on other measures, with the important exception of weight. On average, molindone patients lost 5 pounds over the 6 weeks of treatment, whereas thioridazine patients gained 6 pounds. Haloperidol-treated patients had no significant weight changes.

Adolescent↗
PubMed1982

Neuroleptic-induced seizures. An in vitro technique for assessing relative risk.

To estimate the relative risk of various neuroleptic medications for patients with epilepsy or likely to have neuroleptic-induced seizures, their action on spike activity in perfused guinea pig hippocampal slices was studied. Within the range of concentrations studied, molindone hydrochloride, butaclamol hydrochloride, pimozide, and fluphenazine dihydrochloride produced the least increase in excitability. There were also differences in the dose-response curves. Chlorpromazine, thioridazine, and pimozide produced an inverted U-shaped curve. For haloperidol and fluphenazine, excitability tended to increase and them plateau. Molindone and butaclamol produced no increase in excitability. Combinations of neuroleptics had synergistic effects, while the anticonvulsant diazepam inhibited neuroleptic-induced excitability. This article discusses the clinical implications of these findings and their effect on theories of which neuroleptics might produce the fewest seizures.

Animals↗
PubMed1984

Drug interactions on spontaneous locomotor activity in rats. Neuroleptics and amphetamine-induced hyperactivity.

The locomotor activity of female rats was recorded during 10-min sessions in a circular open-field apparatus after the administration of vehicle or drug. Dose-response curves were obtained for seven neuroleptic drugs both alone (spontaneous activity) and in combination with 1.0 mg/kg of d-amphetamine. Haloperidol, pimozide, loxapine, thiothixene, molindone and chlorpromazine all produced graded decreases in spontaneous locomotor activity. Haloperidol, pimozide, loxapine, thiothixene and molindone also produced graded reversals of the hyperactivity produced by d-amphetamine, while chlorpromazine did not. Clozapine neither altered spontaneous activity nor reversed the hyperactivity produced by d-amphetamine. The data indicate that measures of locomotor activity provide important additional information about the actions of neuroleptics and do not necessarily mirror the actions of these drugs on other measures of performance such as lever-pressing for brain stimulation.

Animals↗
PubMed1987

Quantitative determination of the effects of catecholaminergic agonists and antagonists on the rewarding efficacy of brain stimulation.

The effects of amphetamine, clonidine, molindone, pimozide and yohimbine on the rewarding efficacy of electrical stimulation of the medial forebrain bundle in the rat were determined from the effects of these drugs on the rate-frequency function, which is the plot of the rat's rate of pressing a lever against the frequency of the pulses in a rewarding train of fixed duration. These catecholaminergic agonists and antagonists produced dose-dependent alterations in the measurable rewarding efficacy, but only up to a factor of about 2, even though the method is capable of measuring 25-30-fold changes. At elevated doses, the effects on rewarding efficacy became unmeasurable, because the animals would not consistently self-stimulate at any parameters of stimulation. Amphetamine (0.5-3 mg/kg) enhanced rewarding efficacy. Clonidine (0.05-0.4 mg/kg), molindone (0.25-1 mg/kg) and pimozide (0.1-0.6 mg/kg) attenuated it. Pimozide and clonidine were equipotent despite their radically different receptor affinities. The effects of pimozide, clonidine and amphetamine were approximately additive (amphetamine cancelled the effects of pimozide and clonidine, while clonidine augmented the effect of pimozide). The alpha 2 antagonist yohimbine (0.05-10 mg/kg) had the same effect as the alpha 2 agonist clonidine (attenuation of rewarding efficacy), but these effects did not combine additively: yohimbine neither cancelled nor augmented the effect of clonidine. It is suggested that catecholaminergic agonists and antagonists do not alter the magnitude of the rewarding signal by acting on postsynaptic receptors in the reward pathway; rather, they may drive beyond functional limits a variable that is crucial to the proper recording of the magnitude of the rewarding signal.

Amphetamine↗
PubMed1983

Effects of various antipsychotic drugs upon the striatal concentrations of para-hydroxyphenylacetic acid and meta-hydroxyphenylacetic acid in the mouse.

The endogenous concentrations of p- and m-hydroxyphenylacetic acid in the mouse caudate nucleus were determined by a gas chromatographic or a gas chromatographic-mass spectrometric technique and the concentrations were about 30 and 11 ng g-1 respectively. The subcutaneous administration of (+)-butaclamol (1 mg kg-1), haloperidol (5 mg kg-1), molindone (100 mg kg-1), sulpiride (50 mg kg-1) or chlorpromazine (20 mg kg-1) increased the concentration of mouse striatal p- and m-hydroxyphenylacetic acid; the effects were observed at 2 h after drug administration. Lower doses of chlorpromazine (2 mg kg-1), haloperidol (0.2 mg kg-1) and molindone (2 mg kg-1) did not affect p- or m-hydroxyphenylacetic acid concentrations. The time course for the concentration changes produced by chlorpromazine (20 mg kg-1) revealed that the formation of the metabolites occurred within 30 min after its administration and that their efflux from the caudate nucleus took at least 4 h for p-hydroxyphenylacetic acid and more than 8 h for m-hydroxyphenylacetic acid. Promethazine and (-)-butaclamol which have chemical structures related to chlorpromazine or (+)-butaclamol respectively but which lack antipsychotic activity, produced no effect on striatal p- or m-hydroxyphenylacetic acid concentrations. The results suggest that antipsychotic drugs increase the utilization of mouse striatal p- and m-tyramine and that after use the amines are metabolized by monoamine oxidase to form p- or m-hydroxyphenylacetic acid. The synthesis of the acid metabolites occurs within 30 min after chlorpromazine administration and their efflux from the caudate nucleus takes from 4-8 h.

Animals↗
PubMed1987

The paw test: a behavioural paradigm for differentiating between classical and atypical neuroleptic drugs.

An often used animal model based on the effects of neuroleptics on spontaneous behaviour is the catalepsy test. However, this test seems to be particularly insensitive to the atypical neuroleptics thioridazine and, especially, clozapine. We have therefore developed an alternative test, the paw test, which measures the ability of drugs to prevent the spontaneous withdrawal of fore- and hindlimbs in rats, and have compared this with the classical catalepsy test. The results show that: 1) the classical neuroleptic drugs haloperidol and chlorpromazine, the atypical neuroleptic drugs clozapine and thioridazine, the potential atypical neuroleptic drugs molindone and SCH 23390, and the potential classical neuroleptic drug metoclopramide are potent in increasing the hindlimb retraction time; 2) the paw test discriminates between classical neuroleptics which are equipotent in prolonging both the forelimb (FRT) and hindlimb retraction time (HRT) an atypical neuroleptics which are much more potent in prolonging HRT than in prolonging FRT; 3) the non-neuroleptic drugs desipramine, diazepam and morphine do not influence the variables measured in the paw test, although morphine does produce catalepsy; 4) Molindone as well as SCH 23390 behave like atypical neuroleptic drugs in the paw test. In comparison with the classical wood block catalepsy test, the paw test is shown to be superior for predicting the profile of the neuroleptics tested. Although more neuroleptics and non-neuroleptics have to be tested to determine whether false positives and false negatives do occur, we feel that the paw test might be an interesting animal model, because the increase in hindlimb retraction time was associated with the antipsychotic potential, whereas the increase in forelimb retraction time was associated with the potential to induce so-called extrapyramidal side effects.

Animals↗
PubMed1984

Neuroleptic-induced striatal dopamine receptor supersensitivity in mice: relationship to dose and drug.

Clozapine and molindone administered to mice for 21 days did not elevate the density of striatal 3H-spiperone binding sites at doses clinically equivalent to 1.5 mg/kg haloperidol, which elevated binding by 29%. Thioridazine (25 mg/kg) elevated binding by 25%. It appears that clinically equivalent doses of clozapine and molindone have reduced ability to induce striatal D-2 dopamine receptor supersensitivity. These data are discussed in relationship to in vitro potencies and toxicity. The dose-response relationship of chronic haloperidol treatment and specific striatal 3H-spiperone binding was complex, i.e., binding was elevated at all doses, but the dose-response curve was concave upward. These data suggest that supersensitization is a complex interactive phenomenon comprised of elevation of striatal D-2 dopamine receptor density and other compensatory mechanisms.

Animals↗
PubMed1984

[3H]Ro 22-1319 (piquindone) binds to the D2 dopaminergic receptor subtype in a sodium-dependent manner.

Ro 22-1319, a novel pyrroloisoquinoline compound, is a potent antipsychotic agent with low potential for extrapyramidal effects and tardive dyskinesia. In this study, the specific binding of [3H]Ro 22-1319 to the rat striatal homogenates has been examined. The binding of [3H]Ro 22-1319 was found to be critically dependent on the presence of sodium in the incubation medium. There appeared to be a single saturable binding component for [3H]Ro 22-1319 with a high affinity. The binding sites showed a stereochemical specificity for (-)Ro 22-1319, (+)butaclamol, and (alpha)flupenthixol. Ro 22-1319 and three D2 antagonistic antipsychotics (sulpiride, metoclopramide, and molindone) exerted a more potent inhibition of [3H]Ro 22-1319 binding than of [3H]spiroperidol binding, whereas other classical antipsychotics were almost equipotent at both binding sites. The requirement for sodium to detect Ro 22-1319 binding was also verified by the use of [3H] spiroperidol binding. The competition curves of Ro 22-1319, sulpiride, metoclopramide, and molindone for [3H]spiroperidol binding were shifted to the right by the omission of sodium in the incubation medium, whereas spiroperidol, chlorpromazine, and domperidone were equiactive under both conditions. These results suggest that Ro 22-1319 has a sulpiride-like property and binds to a D2 dopaminergic receptor subtype in a sodium-dependent manner. Nineteen pyrroloisoquinoline derivatives were also tested for their inhibitory effects on [3H]Ro 22-1319 and [3H] spiroperidol binding. An interesting finding was that small changes in chemical structure modulated the potency at D2 dopaminergic receptor subtypes. Thus, the compounds having a nonlipophilic functional group on the basic nitrogen (Ro 22-1319, Ro 22-3822, etc.) showed a stronger potency at [3H]Ro 22-1319 receptors whereas the compounds having a lipophilic group (Ro 22-6600, etc.) were nonselective antagonists at both [3H]Ro 22-1319- and [3H]spiroperidol-binding sites. However, all pyrroloisoquinoline derivatives including Ro 22-6600 showed a sodium dependency for [3H]spiroperidol-binding sites, indicating that the functional moiety which displays a sodium dependency may be the pyrroloisoquinoline moiety itself.

Animals↗
PubMed1994

Induction patterns of Fos-like immunoreactivity in the forebrain as predictors of atypical antipsychotic activity.

Clozapine and haloperidol produce different induction patterns of c-fos expression in the forebrain, with haloperidol increasing Fos-like immunoreactivity (FLI) in the striatum, nucleus accumbens, lateral septal nucleus and clozapine producing such effects in the nucleus accumbens, prefrontal cortex and lateral septal nucleus. Accordingly, it was deemed possible that this approach may be useful in characterizing compounds with known or suggested antipsychotic actions. We therefore examined the effects of 17 compounds considered to be either typical, or atypical, antipsychotics on FLI in the prefrontal cortex, medial and dorsolateral striatum, nucleus accumbens and the lateral septal nucleus. Consistent with the hypothesis that the prefrontal cortex may be a target for some antipsychotic actions, FLI was elevated in this structure by clozapine, ICI 204,636, fluperlapine, RMI-81,582, remoxipride, molindone, melperone and tiospirone. Likewise, the ability of all of the compounds, except for risperidone, to enhance FLI in the lateral septal nucleus suggests that this limbic region also may be an important locus of antipsychotic action. All of the compounds examined elevated FLI in the nucleus accumbens and medial striatum, indicating that potential antipsychotic activity is predicted most consistently on this basis. Neuroleptics with a clearly documented liability for producing extrapyramidal side effects (EPS) such as chlorpromazine, fluphenazine, haloperidol, loxapine, metoclopramide and molindone elevated FLI in the dorsolateral striatum. In contrast, compounds unlikely to produce EPS such as clozapine, thioridazine, risperidone, remoxipride, fluperlapine, sulpiride, melperone and RMI-81,582 either failed to increase or produced minor elevations in FLI in the dorsolateral striatum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Differential regulation of D2 and D4 dopamine receptor mRNAs in the primate cerebral cortex vs. neostriatum: effects of chronic treatment with typical and atypical antipsychotic drugs.

The RNase Protection Assay was used to examine the regulation of D2 and D4 dopamine receptor mRNAs in the cerebral cortex and neostriatum of nonhuman primates after chronic treatment with a wide spectrum of antipsychotic medications (chlorpromazine, clozapine, haloperidol, molindone, olanzapine, pimozide, remoxipride and risperidone). Tiapride, a D2 antagonist that lacks antipsychotic activity, was also included. All drugs were administered orally for 6 months at doses recommended for humans. All antipsychotic drug treatments examined in this study caused a statistically significant up-regulation of both the long and short isoforms of the D2 receptor mRNAs in the prefrontal and temporal cortex. Tiapride, in contrast, significantly up-regulated only the level of D2-long mRNA in these areas. The same drug treatments produced less uniform effects in the neostriatum than in the cortex: clozapine and olanzapine failed to significantly elevate either D2-long or D2-short receptor messages in this structure unlike all other drugs, including tiapride. In both the cerebral cortex and striatum, D4 receptor mRNA was upregulated by certain typical (chlorpromazine and haloperidol) and certain atypical (clozapine, olanzapine and risperidone) antipsychotic agents as well as by tiapride. Other drugs of the typical (molindone and pimozide) and atypical (remoxipride) classes had no effect on D4 mRNA levels in either cortical or striatal tissue. The finding that up-regulation of D2 dopamine receptor mRNAs was a consistently observed effect of a wide range of antipsychotic agents in the cerebral cortex but not in the neostriatum, coupled with the fact that the D2-short isoforms in the cortex were not regulated by a nonantipsychotic D2 antagonist, tiapride, draws attention to the importance of the D2 dopamine receptor in the cerebral cortex as a potentially critical, common site of action of antipsychotic medications.

Animals↗
PubMedDate not supplied

Neuroleptic bioequivalency: tablet versus concentrate.

Two forms of the antipsychotic neuroleptic molindone were administered to newly admitted psychotic patients. A coated tablet was administered for ten days, followed by administration of liquid concentrate in equivalent doses for four days. Plasma was analyzed by gas chromatography with electron capture for the parent compound following each dosing phase. Our data suggest that oral doses of the tablet and concentrate forms of this neuroleptic are equivalent in clinical bioavailability.

Antipsychotic Agents↗