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  • Articles: DFG German National Licenses  (9)
  • Haloperidol  (5)
  • calcium  (4)
  • 1
    Electronic Resource
    Electronic Resource
    The discriminative stimulus properties and detection thresholds of intracranial self-stimulation: Effects of d-amphetamine, morphine, and haloperidol (1985)
    Springer
    Psychopharmacology 85 (1985), S. 289-294 
    Details
    ISSN: 1432-2072
    Keywords: Discriminative stimulus properties ; ICSS detection thresholds ; d-Amphetamine ; Morphine ; Haloperidol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A two-choice discrimination task was used to evaluate the effects of psychoactive drugs on the discriminative stimulus properties of brain self-stimulation in rats. In these experiments, brain stimulation served both as a discriminative stimulus and as a reinforcing stimulus, but the two effects were manipulated separately. Animals were trained to a criterion of 95% correct in choosing between two levers, and when this levels of accuracy was reached, the ability to choose correctly remained stable over an 8-month period. Increasing the current strength of the discriminative stimulus from zero to 100% of the training current produced a graded increase in the number of trials completed on the appropriate lever. The discriminative effects produced by brain stimulation were evaluated pharmacologically by using three prototypical psychoactive drugs in an attempt to change the detection threshold for the discriminative stimulus. Morphine, d-amphetamine, and haloperidol, drugs that reliably alter reinforcement thresholds for brain stimulation, failed to change detection thresholds. These results demonstrated that: (1) brain stimulation produces potent and reliable discriminative effects and (2) the effects of psychoactive drugs on detection thresholds can be dissociated from their effects on reinforcement thresholds for brain stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00428189
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Haloperidol and lithium blocking of the mood response to intravenous methylphenidate (1978)
    Springer
    Psychopharmacology 57 (1978), S. 83-87 
    Details
    ISSN: 1432-2072
    Keywords: Methylphenidate ; Haloperidol ; Lithium ; Euphoria ; Manic-depressive ; Dopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ten euthymic manic-depressive patients with therapeutic plasma lithium levels were each given two i.v. infusions of 30 mg of methylphenidate. The infusions were separated by at least 3 days. Before one infusion each patient was given 5 mg of haloperidol i.v. and before the other infusion each was given an identical volume of saline. A psychiatric observer was blind to the nature of the pretreatment and the order of pretreatment was randomized. Saline pretreated patients showed marked activation and euphoriant responses despite therapeutic lithium levels. Haloperidol pretreatment reduced this response in three patients and eliminated the euphoriant and activating response in the remaining seven patients. These results agree with the existence of a dopaminergic step in the induction of methylphenidate-induced activation and euphoria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00426962
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Serum and CSF levels of haloperidol by radioimmunoassay and radioreceptor assay during high-dose therapy of resistant schizophrenic patients (1981)
    Springer
    Psychopharmacology 73 (1981), S. 197-199 
    Details
    ISSN: 1432-2072
    Keywords: Haloperidol ; Blood levels ; CSF ; Pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serum and cerebrospinal fluid (CSF) levels of haloperidol were measured in 12 chronic neuroleptic-non-responsive schizophrenic patients after 1 month on 60 mg haloperidol daily and then again after 1 month on 120 mg haloperidol daily. Serum haloperidol and CSF haloperidol rose with increasing dose. Serum and CSF levels were significantly correlated. No clinical improvement was achieved despite the high serum and CSF drug levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00429218
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Acute effects of neuroleptics on brain self-stimulation thresholds in rats (1980)
    Springer
    Psychopharmacology 67 (1980), S. 9-15 
    Details
    ISSN: 1432-2072
    Keywords: Brain self-stimulation ; Thresholds ; Neuroleptics ; Haloperidol ; Loxapine ; Chlorpromazine ; Pimozide ; Clozapine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The acute effects of 5 neuroleptic drugs were tested in rats implanted with stimulating electrodes in the medial forebrain bundle and trained in a brain selfstimulation threshold procedure. Haloperidol (0.01–0.10 mg/kg) and loxapine (0.03–0.56 mg/kg) produced increases in reinforcement thresholds accompanied by reductions in response rates. Chlorpromazine (0.10–3.0 mg/kg) did not significantly alter reinforcement thresholds, but did produce dose-dependent reductions in response rates. Pimozide (0.1–1.75 mg/kg) was similar to chlorpromazine and significantly increased the reinforcement threshold only at the highest dose, although a graded decrease in response rates occurred over a wide dose-range. Clozapine (0.1–1.75 mg/kg) increased reinforcement thresholds without producing any significant changes in response rates, but when 3.0 mg/kg was administered, a marked disruption of behavior occurred. The results suggested that a distinction can be made between the effects of neuroleptics on motor behavior and on central reinforcement thresholds, and this may help in the interpretation of the relation between the chemical and clinical potency of antipsychotic drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427589
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    The effect of haloperidol on epinephrine-stimulated adenylate cyclase in humans (1976)
    Springer
    Psychopharmacology 49 (1976), S. 215-217 
    Details
    ISSN: 1432-2072
    Keywords: Lithium ; Haloperidol ; Epinephrine ; Adenylate cyclase ; Mania
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Administration of epinephrine in man has been shown previously to lead to a rise in plasma cyclic AMP levels by activation of the β-adrenergic-stimulated adenylate cyclase. Therapeutic doses of lithium in humans block the epinephrine-induced rise in plasma cyclic AMP levels, suggesting that lithium inhibits β-adrenergic adenylate cyclase. In contrast, ten subjects receiving haloperidol, a drug also effective in the treatment of mania, show a mean rise in plasma cyclic AMP levels after epinephrine administration and the magnitude of the response is the same as for non-drug treated individuals. These findings are discussed in relation to the possible pharmacological mechanisms of action of lithium and haloperidol in the control of mania.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427293
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Role of calcium and calmodulin in the regulation of the rabbit ileal brush-border membrane Na+/H+ antiporter (1989)
    Springer
    The journal of membrane biology 108 (1989), S. 207-215 
    Details
    ISSN: 1432-1424
    Keywords: calcium ; calmodulin ; absorption ; ileum ; brush-border vesicle ; phosphorylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary In rabbit ileum, Ca2+/calmodulin (CaM) appears to be involved in physiologically inhibiting the linked NaCl absorptive process, since inhibitors of Ca2+/CaM stimulate linked Na+ and Cl− absorption. The role of Ca2+/CaM-dependent phosphorylation in regulation of the brush-border Na+/H+ antiporter, which is believed to be part of the neutral linked NaCl absorptive process, was studied using purified brush-border membrane vesicles, which contain both the Na+/H+ antiporter and Ca2+/CaM-dependent protein kinase(s) and its phosphoprotein substrates. Rabbit ileal villus cell brush-border membrane vesicles were prepared by Mg precipitation and depleted of ATP. Using a freezethaw technique, the ATP-depleted vesicles were loaded with Ca2+, CaM, ATP and an ATP-regenerating system consisting of creatine kinase and creatine phosphate. The combination of Ca2+/CaM and ATP inhibited Na+/H+ exchange by 45±13%. This effect was specific since Ca2+/CaM and ATP did not alter diffusive Na+ uptake, Na+-dependent glucose entry, or Na+ or glucose equilibrium volumes. The inhibition of the Na+/H+ exchanger by Ca2+/CaM/ATP was due to an effect on theV max and not on theK m for Na+. In the presence of CaM and ATP, Ca2+ caused a concentration-dependent inhibition of Na+ uptake, with an effect 50% of maximum occurring at 120nm. This Ca2+ concentration dependence was similar to the Ca2+ concentration dependence of Ca2+/CaM-dependent phosphorylation of specific proteins in the vesicles. The Ca2+/CaM/ATP-inhibition of Na+/H+ exchange was reversed by W13, a Ca2+/CaM antagonist, but not by a hydrophobic control, W12, or by H-7, a protein kinase C antagonist. we conclude that Ca2+, acting through CaM, regulates ileal brush-border Na+/H+ exchange, and that this may be involved in the regulation of neutral linked NaCl absorption.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871735
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  • 7
    Electronic Resource
    Electronic Resource
    Release of norepinephrine and dopamine from brain vesicular preparations: Effects of adenosine analogues (1982)
    Springer
    Cellular and molecular neurobiology 2 (1982), S. 193-204 
    Details
    ISSN: 1573-6830
    Keywords: adenosine ; catecholamines ; neurotransmission ; calcium ; brain ; striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. Adenosine analogues inhibit calcium-dependent K+-evoked release of [3H]norepinephrine from guinea pig cerebral cortical and hippocampal vesicular preparations. Inhibition requires high concentrations (100µM) of the adenosine analogues and is abolished in the presence of high concentrations (2 mM) of calcium ions. The inhibitory effect of 2-chloroadenosine is blocked by theophylline. The structure activity profile (N 6-d-phenylisopropyladenosine ≥N 6-l-phenylisopropyladenosine ≥ 2-chloroadenosine 〉N 6-cyclohexyladenosine, adenosine 5′-cyclopropylcar-boxamide) is not that expected of either A1 (high-affinity) or A2 (low-affinity) adenosine receptors. 2. Calcium-dependent K+-evoked release of [3H]dopamine from guinea pig striatal vesicular preparations is inhibited by apomorphine. However, only 2-chloroadenoine causes an inhibition of K+-evoked release of [3H]dopamine. Other adenosine analogues such asd- andl-phenylisopropyladenosine and adenosine 5′-cyclopropylcar-boxamide cause a facilitation of K+-evoked release. The facilitation is abolished or reduced in the presence of high concentrations (2 mM) of calcium ions. The sites of action of adenosine analogues do not appear to have structural requirements identical to those expected of A1 (high-affinity) or A2 (low-affinity) adenosine receptors. 3. The results indicate that adenosine analogues can have either inhibitory or facilitory effects on K+-evoked release of catecholamines from central synaptic terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711147
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  • 8
    Electronic Resource
    Electronic Resource
    Release of norepinephrine from brain vesicular preparations: Effects of an adenylate cyclase activator, forskolin, and a phosphodiesterase inhibitor (1982)
    Springer
    Cellular and molecular neurobiology 2 (1982), S. 179-192 
    Details
    ISSN: 1573-6830
    Keywords: adenylate cyclase ; catecholamines ; adrenergic receptors ; cyclic AMP ; phosphodiesterase ; neurotransmission ; calcium ; brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. The calcium-dependent K+-evoked release of [3H]norepinephrine from guinea pig cerebral cortical vesicular preparations is inhibited by norepinephrine, clonidine, and epinephrine. Isoproterenol has no effect and phentolamine prevents the inhibition by norepinephrine. The results indicate that anα-adrenergic receptor mediates an inhibitory input to the calcium-dependent release process. The inhibition by norepinephrine is prevented by high concentrations (3.0 mM) of calcium ions. 2. A cyclic AMP phosphodiesterase inhibitor, ZK 62771, slightly elevates [3H]cyclic AMP levels in the guinea pig cerebral cortical preparation and potentiates the marked elevation of [3H]cyclic AMP elicited by the adenylate cyclase activator, forskolin. 3. Neither ZK 62771 nor forskolin alone has significant effects on K+-evoked release of [3H]norepinephrine from the cerebral cortical vesicular preparation; however, a combination of ZK 62771 and forskolin inhibits K+-evoked release by as much as 60%. The inhibition is reversed by high concentrations (2.0 mM) of calcium ions. The results suggest that a marked accumulation of cyclic AMP elicited via both activation of adenylate cyclase and inhibition of phosphodiesterase can be inhibitory to neurotransmitter release from central synaptic terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711146
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  • 9
    Electronic Resource
    Electronic Resource
    Release of norepinephrine and dopamine from brain vesicular preparations: Effects of calcium antagonists (1982)
    Springer
    Cellular and molecular neurobiology 2 (1982), S. 205-213 
    Details
    ISSN: 1573-6830
    Keywords: calcium ; catecholamines ; neurotransmission ; brain ; striatum ; calcium antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. The calcium antagonists D-600 (1–10µM) and diltiazem (10–25µM) inhibit K+-evoked release of [3H]norepinephrine from guinea pig cerebral cortical vesicular preparations. The inhibition of release is partially reversed by increasing concentrations of calcium to 2 mM. Diltiazem at 100µM has no effect on K+-evoked release of [3H]norepinephrine at 0.15 mM calcium but does inhibit release at 2.0 mM calcium. 2. The calcium antagonist nifedipine and dantrolene, an agent purported to antagonize release of calcium from intracellular storage sites, have no effect on K+-evoked release of [3H]norepinephrine. 3. The calcium antagonists D-600 (1µM) and diltiazem (10µM) inhibit K+-evoked release of [3H]dopamine from guinea pig striatal vesicular preparations. Higher concentrations of drug, namely, 10µM for D-600 and 100µM for diltiazem, cause a potentiation rather than an inhibition of K+-evoked release. The potentiation is reduced in magnitude upon raising the extracellular calcium to 2.0 mM. Indeed, 10µM D-600 then inhibits K+-evoked release of [3H]dopamine. 4. The results indicate that putative calcium antagonists can have both inhibitory and facilitory effects on calcium-dependent K+-evoked release of catecholamines from central synaptic endings. Furthermore, certain peripheral calcium antagonists such as nifedipine and dantrolene may prove ineffective in central systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711148
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    Paper (German National Licenses)
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