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PubMed1994

Tardive dyskinesia: behavioral effects of repeated intracerebroventricular haloperidol injections in rats do not confirm the kindling hypothesis.

The development of tardive dyskinesia (TD) has been claimed to be the result of a kindling-like mechanism. This hypothesis is based on studies suggesting that intermittent neuroleptic treatment may increase the risk of irreversible TD in humans and persistent vacuous chewing movements (VCM) in rats. We investigated the effect of daily intracerebroventricular (ICV) injections of haloperidol 37.5 micrograms/kg for 12 weeks in rats. Behavior was recorded immediately after the first injection, with 2 weeks intervals during treatment, and 3 weeks after drug withdrawal. In a separate experiment, rats received one injection of haloperidol IP. The acute effect of haloperidol ICV was an immediate increase in VCM and a reduction in motor activity that lasted for approximately 2 h. The behavioral response to haloperidol IP was similar, but of much longer duration. No significant behavioral changes were observed either 24 h after the ICV injections during haloperidol treatment or 3 weeks after drug withdrawal. The results did not support the hypothesis that kindling is important for the development of TD.

Animals↗
PubMed1989

Long-term haloperidol treatment decreases somatostatin binding in rat brain.

The effects of short and long-term haloperidol treatment on somatostatin concentration and specific binding in rat cerebral cortex and hippocampus were examined using the binding ligand 125I-Tyr1-somatostatin. Haloperidol treatment did not affect the concentration of somatostatin-like immunoreactivity in the two brain areas. Nevertheless, long-term, and not short-term, haloperidol treatment decreased the number of somatostatin receptors in the cerebral cortex and hippocampus. No significant differences in the apparent binding affinity values were seen after haloperidol treatment. When added at the time of the binding assay haloperidol 34.2 microM produced a 42% and 27% decrease in cerebrocortical and hippocampal membrane somatostatin receptors respectively.

Animals↗
PubMed1983

Lithium prevents adaptation of brain dopamine systems to haloperidol in schizophrenic patients.

To evaluate the effect of lithium treatment on haloperidol-induced changes of brain dopamine systems, cerebrospinal fluid homovanillic acid (HVA) was assessed in nine patients during a sequential treatment protocol with placebo, lithium, lithium plus acute haloperidol, and lithium plus chronic haloperidol. None of the patients developed tolerance to the rise in HVA during treatment with haloperidol and lithium. Concurrent treatment with lithium appears to prevent the development of tolerance in dopamine metabolism during chronic haloperidol treatment. These data provide the first evidence in man that lithium may prevent neuroleptic-induced functional supersensitivity of brain dopamine systems.

Adult↗
PubMed1984

Haloperidol concentrations elevated in Chinese patients.

After 6 weeks of fixed dose oral haloperidol treatment. Chinese schizophrenic patients (in the People's Republic of China) had 52% higher plasma haloperidol concentrations than U.S. non-Asian schizophrenic patients. Chinese and U.S. patients were matched for sex and body weight. The difference in plasma drug concentrations may explain why Asians are reported to require smaller dosages of neuroleptic drugs than non-Asians, and why they may be more sensitive to neuroleptic-induced side effects. When prescribing haloperidol to persons of Asian ancestry, physicians should consider that higher than expected plasma haloperidol concentrations and an increased sensitivity to haloperidol may occur.

Adult↗
PubMed1989

Effects of intravenous cocaine are partially attenuated by haloperidol.

We examined the effect of the dopaminergic blocking agent, haloperidol, on the subjective and physiologic response to cocaine in cocaine-using volunteers. Five subjects received cocaine (40 mg) or placebo administered intravenously 20 min following pretreatment with haloperidol (8 mg) or placebo intramuscularly in a randomized double-blind study design. Haloperidol pretreatment attenuated cocaine-induced increases in systolic and diastolic blood pressure but not heart rate. Pretreatment with haloperidol reduced subject ratings of pleasant sensations but had no effect on drug "rush." Haloperidol (8 mg) has a small and limited effect on the subjective response to cocaine when given 20 min before cocaine.

Adult↗
PubMed1988

Antibodies against haloperidol specific to the butyrophenone moiety.

Polyclonal and monoclonal antibodies to the D2-dopamine receptor antagonist haloperidol were produced by immunization with haloperidol conjugated to bovine serum albumin either through the tertiary hydroxy group of the piperidine ring (halo(OH)-BSA), or through the keto group of the butyrophenone (halo(CO)-BSA). Polyclonal rabbit antisera raised against halo(OH)-BSA exhibited high affinity for [3H]haloperidol. A fraction of these antibodies also bound [3H]spiperone with high affinity. Inhibition of the [3H]spiperone binding by various butyrophenone derivatives displayed a specificity similar to that observed for the inhibition of [3H]spiperone binding to the D2-dopamine receptor. Both monoclonal antibodies raised against halo(CO)-BSA(AG-58) and against halo(OH)-BSA(AC-91) exhibited high binding affinities to haloperidol. Monoclonal antibody AG-58 cross-reacted primarily with butyrophenone derivatives that are closely related to haloperidol in their substitutions on the piperidine ring. On the other hand, monoclonal antibody AC-91 cross-reacted with a wide range of butyrophenones with binding specificities resembling those of the dopamine receptor.

Animals↗
PubMed1996

The differential haloperidol effect on the immobility response elicited by clamping, grasping, bandaging and inversion in guinea pig, hamster and rat.

The induction and modification by haloperidol of inhibitory responses, by 4 inducing stimuli (inversion, clamping, bandaging and grasping) were studied and compared in guinea pig, hamster and rat. When undrugged, all 4 stimuli induced immobility responses in guinea pig; only clamping, bandaging and grasping, but not inversion, induced immobility responses (IR) in hamsters; only clamping and grasping, but not inversion and bandaging induced IR in rats. Haloperidol significantly potentiated the occurrence and duration of the IR by clamping, grasping and bandaging in rats. In hamsters haloperidol only potentiated the IR induced by bandaging, and in guinea pigs, haloperidol had no effect on IR produced by any of the stimuli. These findings suggest an inverse relationship between susceptibility to IR and the potentiation of IR by haloperidol.

Animals↗
PubMed1996

Differential effects of clozapine and haloperidol on dopamine receptor mRNA expression in rat striatum and cortex.

The regulation of the dopamine (DA) receptors is of considerable interest, in part because treatment with antipsychotic drugs is known to upregulate striatal D2-like receptors. While previous studies have focused on the regulation of striatal DA receptors, less is known about the pharmacological regulation of cortical DA receptors. The purpose of this study was to examine the regulation of DA mRNA receptor expression in the cortex compared to the striatum following treatment with antipsychotic agents. Adult male Sprague-Dawley rats were injected daily with haloperidol (2 mg/kg/day), clozapine (20 mg/kg/day) or a control vehicle for a period of 14 days. Following treatment, brains were subjected to in situ hybridization for the mRNAs encoding the five dopamine receptors; only D1, D2, and D3 receptor mRNAs were detected in these regions. Haloperidol tended to either modestly upregulate or have no effect on dopamine receptor mRNAs detected in striatal structures, while clozapine generally downregulated these mRNAs. On the other hand, in the cortex, both drugs had striking effects on D1 and D2 mRNA levels. Cortical D1 mRNA was upregulated by haloperidol, but this effect was primarily restricted to cingulate cortex; clozapine also upregulated D1 mRNA, but primarily in parietal regions. Haloperidol downregulated D2 mRNA in the majority of cortical regions, but most dramatically in frontal and cingulate regions; clozapine typically upregulated this mRNA, but primarily in regions other than frontal and cingulate cortex. These results indicate that clozapine and haloperidol each have regionally-specific effects, and differentially regulate dopamine receptor mRNA expression in striatal and cortical regions of the rat brain.

Animals↗
PubMed1984

Monitoring of haloperidol serum levels and it's clinical significance.

Haloperidol serum levels were determined by the recently developed radioimmunoassay technique to elucidate the relationship between serum levels and clinical effects and that between serum levels and adverse effects. The serum levels of haloperidol in divided daily doses schedule reached to the steady state more rapidly (within 7 days) than in single dose schedule. The single daily dose schedule showed significantly wider diurnal variation than the divided daily doses schedule. No remarkable differences in serum concentration was noted between different types of oral haloperidol preparation (liquid, granule, tablet). No definite relationship was established between the serum concentration of haloperidol and incidence of tardive dyskinesia. No definite positive relationship between clinical effects and serum concentration of haloperidol could obtained.

Administration, Oral↗
PubMed1989

Doubleblind evaluation of the antimanic properties of carbamazepine as a comedication to haloperidol.

1. Today carbamazepine is the most important alternative to neuroleptic drugs for the treatment of manic psychoses. Often carbamazepine is administered as a comedication to a neuroleptic. 2. A doubleblind study with 20 patients suffering from manic or schizomanic psychoses was performed to determine whether carbamazepine and haloperidol in comedication are more effective than haloperidol alone. 3. Under the tested conditions (24 mg haloperidol p.d.) only the smaller amount of additional medication with levomepromazine in the experimental group gave evidence for the antimanic effect of carbamazepine in combination with haloperidol. 4. Especially the patients with pure manic psychoses seem to benefit from carbamazepine as an adjunct to haloperidol.

Adult↗
PubMed1990

Neurochemical effects of chronic haloperidol and lithium assessed by brain microdialysis in rats.

1. Psychotropic drugs ameliorate psychotic symptoms only after repeated administration. 2. To assess the neurochemical effects of chronic haloperidol and lithium administration, microdialysis was performed simultaneously in the prefrontal cortex, the nucleus accumbens, and the striatum after haloperidol, and separately in the lateral hypothalamus and the hippocampus after lithium. 3. Chronic administration of haloperidol decreased dopamine turnover in the prefrontal cortex and the striatum. It did not affect the nucleus accumbens detectably. 4. No tolerance to haloperidol developed in any of the three regions. 5. Lithium enhanced the response of the serotonergic system to amphetamine in the lateral hypothalamus but not in the hippocampus. 6. The antipsychotic effect of haloperidol might be related to dopamine turnover decrease in the prefrontal cortex. 7. The antidepressant effect of lithium might be related to enhancement of serotonin responsiveness in the hypothalamus.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Diltiazem suppresses quinpirole-induced oral stereotypies in haloperidol withdrawn rats.

1. Tardive dyskinesia (TD) is one of the most serious untoward effects of chronic neuroleptic therapy. Dopaminergic receptor sensitization is assumed to be involved in its pathogenesis. 2. Male Wistar rats were administered (b.i.d.) intragastrically haloperidol (2 mg/kg), diltiazem (5 mg/kg), diltiazem plus haloperidol, and water (controls), for 21 days. 3. Forty eight hours after withdrawal the rats were injected ip with 0.3 mg/kg of quinpirole and observed for stereotypic behaviors (rearing, grooming, licking, and tongue protrusions). 4. There was a significant overall between-group difference in the duration of grooming and the number of tongue protrusions. The haloperidol withdrawn rats scored markedly higher than control and diltiazem alone treated rats. 5. Conjoint treatment with diltiazem and haloperidol prevented the increase of tongue protrusion episodes. 6. We conclude that concurrent diltiazem and haloperidol administration can prevent the occurrence of some behavioral manifestations of dopaminergic receptor supersensitivity, including a lingual dyskinesia.

Analysis of Variance↗
PubMed1991

Chronic haloperidol treatment attenuates receptor-mediated phosphoinositide turnover in rat brain slices.

The long-term effects of haloperidol on phosphoinositide turnover in rat brain slices were investigated. Continuous treatment with haloperidol decanoate (21 mg/kg I.M. biweekly for 6 weeks) significantly attenuated carbachol- and norepinephrine (NE)-induced inositol phosphate accumulation in rat frontal cortex and hippocampus. In the striatum, the haloperidol treatment also significantly decreased carbachol-stimulated inositol phosphate level but did not significantly affect NE-sensitive phosphoinositide turnover. These effects were not observed in rats treated with a single dose of haloperidol (1.5 mg/kg). Basel levels of inositol phosphate in these 3 brain regions did not change following continuous or single haloperidol doses.

Animals↗
PubMed1987

Effect of chronic administration of haloperidol on secretory response mediated by cholinergic receptors in rat submandibular glands.

Administration of haloperidol influences peripheral non-dopaminergic receptors. The sialagogue response of the submandibular glands of the rats to methacholine was enhanced by chronic administration of haloperidol. The binding of [3H]QNB to muscarinic receptors in the submandibular glands was not changed by chronic haloperidol. The supersensitivity of postsynaptic cholinergic receptors to drugs in haloperidol treated rats is not related to changes in the number or affinity of such receptors. This paper confirmed the sialagogue supersensitivity to adrenergic drugs related to an increase in alpha 1-adrenoceptors in the submandibular glands of haloperidol injected rats.

Animals↗
PubMed1989

Increase of muscarinic cholinergic receptors in the rat submandibular glands after parasympathectomy and repeated administration of haloperidol.

1. The mechanisms of the supersensitivity to cholinergic drugs after chronic haloperidol was studied in normal and parasympathectomized submandibular glands of the rats. 2. Both parasympathectomy and haloperidol treatment for 7 days (2 mg/kg/day, i.p.) increased the sialogogue response of the glands to methacholine, a cholinomimetic drug. 3. Both denervation and haloperidol administration induce up-regulation of the muscarinic receptors as expressed per gram of the tissue. 4. Haloperidol causes no further increase in sensitivity than denervation alone. 5. These data demonstrate that secretory supersensitivity to cholinergic drugs in the rat submandibular glands, after chronic haloperidol and parasympathectomy is related to an increase in muscarinic cholinergic receptors.

Animals↗
PubMed1985

Effect of haloperidol and sulpiride on dopamine metabolism in nucleus accumbens and olfactory tubercle: a study by in vivo voltammetry.

Differential pulse voltammetry used with electrochemically pretreated carbon fibre microelectrodes enables separation between the two peaks corresponding to the ascorbic acid and catechol oxidation currents. The effects of haloperidol and sulpiride on the 3,4-dihydroxyphenylacetic acid peak recorded in the nucleus accumbens and olfactory tubercle of rats were studied. Chloral hydrate anaesthetized preparations and chronic preparations were used. A microdevice was designed to implant electrodes in freely moving rats. Voltammograms were recorded every minute in each structure in acute preparations and every 2 min in chronic preparations. In acute preparations haloperidol induced a similar dose-dependent increase in the catechol oxidation peak in both structures. Sulpiride at all doses only induced an increase in the olfactory tubercle. In chronic preparations haloperidol and sulpiride had even larger effects on the 3,4-dihydroxyphenylacetic acid peak in both regions. In these preparations sulpiride induced a significant increase in nucleus accumbens. The effects induced by haloperidol in the two regions were greater than those induced by sulpiride. The main conclusions of this study are that the results of voltammetry agree with biochemical results on the effects of haloperidol and sulpiride on dopamine metabolism. An interaction of chloral hydrate with the effects of the two neuroleptics was also observed.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Subchronic administration of clozapine, but not haloperidol or metoclopramide, decreases dopamine D2 receptor messenger RNA levels in the nucleus accumbens and caudate-putamen in rats.

The effects of unique profile antipsychotic drugs on dopamine D2 receptors and D2 receptor messenger RNA were assessed following subchronic administration in rats. Male, Sprague-Dawley rats were administered oral haloperidol, clozapine, metoclopramide or no drug for three weeks via their drinking water. Tissue from the medial nucleus accumbens and dorsolateral caudate-putamen was dissected and analyzed by Northern blot analysis for levels of dopamine D2 receptor messenger RNA and binding assays conducted with [3H]spiperone for dopamine D2 receptors. Haloperidol and metoclopramide, but not clozapine, significantly increased [3H]spiperone in the caudate-putamen, but not the nucleus accumbens. Clozapine significantly decreased D2 messenger RNA levels in the caudate-putamen and the nucleus accumbens, while metoclopramide and haloperidol had no significant effect in either brain region. The finding of decreased D2 receptor messenger RNA levels produced by subchronic clozapine may account for the lack of striatal D2 receptor up-regulation, which was robustly observed after subchronic haloperidol and metoclopramide. Furthermore, since haloperidol and metoclopramide have a high liability for motor side effects, the current results relate favorably to the low motor side effect profile of clozapine.

Actins↗
PubMed1984

Effect of estradiol and haloperidol on hypophysectomized rat brain dopamine receptors.

The effect of chronic haloperidol and estradiol treatments on dopamine receptors independent from the pituitary has been studied in ovariectomized (ovx) and hypophysectomized (hypox) rats. The striatal dopamine receptor density (Bmax) of hypox rats as measured with [3H]spiperone binding was increased after chronic estradiol or haloperidol treatment, while receptor affinity was unchanged. In hypox rats, estradiol given during withdrawal from haloperidol decreased the characteristic increase in dopamine receptor density observed upon withdrawal from this neuroleptic, while the estrogen was ineffective when given concomitantly with haloperidol. These results in hypox rats are similar to those observed in ovx rats, suggesting that haloperidol and estradiol influence striatal dopamine function independently of the pituitary.

Animals↗