Variability of prolactin response to intravenous and intramuscular haloperidol in normal adult men

Rubín, Robert T.; Hays, Sally E.

doi:10.1007/bf00426804

Cited by 39 publications

(12 citation statements)

References 29 publications

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“…PRL findings are graphed in Figure 1. This plot indicates that significant inhibitory effects of bromocriptine and facilitatory effects of haloperidol on PRL secretion appeared approximately 1-2 hours postingestion, a time course that is typical of both bromocriptine's and haloperidol's postsynaptic D2 receptor effects (Hays & Rubin, 1981;Markey et al, 1979;Mehta & Tolis, 1979;Rubin & Hays, 1979;Pizzolato, Soncrant, & Rapoport, 1985).…”

Section: Exclusionsmentioning

confidence: 94%

“…Because of the tonic inhibitory influence of DA on PRL secretion, neuroleptic blockade of DA activity results in a dosedependent increase in serum prolactin secretion, beginning about 20 min postinjection (Kolakowska et al, 1981;Rubin & Hays, 1979), presumably due to haloperidol's blockage of DA receptors on the pituitary lactotrophs (Carlsson, 1978). Peak PRL responses to a single acute dose of haloperidol in normal subjects occur 40-180 min postinjection (Hays & Rubin, 1981; Keks et al, 1987; Kolakowska et al, 1981;McClelland, Cooper, & Pilgrim, 1990;Rubin & Hays, 1979) with no correlation observed between baseline PRL levels and PRL response to haloperidol challenge (Hays & Rubin, 1981).…”

Section: Halo Peridolmentioning

confidence: 98%

“…Because antipsychotic agents are known to stimulate prolactin secretion in both psychiatric patients (Copolov et al, 1990;Gruen et al, 1978;Keks, Copolov, & Singh, 1987;Markianos, Sakellariou, & Bistolaki, 1991) and normal controls (Hays & Rubin, 1981;Rubin & Hays, 1979;Rubin et al, 1976), prolactin response to haloperidol has been used to test the neuroendocrine responses to both acute (Copolov et al, 1990) and chronic (Kolakowska et al, 1991;Markianos et al, 1991) neuroleptic treatment. Because of the tonic inhibitory influence of DA on PRL secretion, neuroleptic blockade of DA activity results in a dosedependent increase in serum prolactin secretion, beginning about 20 min postinjection (Kolakowska et al, 1981;Rubin & Hays, 1979), presumably due to haloperidol's blockage of DA receptors on the pituitary lactotrophs (Carlsson, 1978).…”

Section: Halo Peridolmentioning

confidence: 98%

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Dopaminergic Modulation of Working Memory for Spatial but Not Object Cues in Normal Humans

Luciana

Collins²

1997

Journal of Cognitive Neuroscience

161

131

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It appears that functionally segregated visual pathways exist in the primate brain for the processing of visuospatial versus nonspatial information. Functional segregation has been demonstrated for the early associative processing of sensory information but may also exist at higher levels of cognitive analysis. Namely, connections between the dorsal visual system and dorsolateral prefrontal cortex (PFC) appear to mediate spatial working memory, which is modulated by dopamine receptor fields in the principal sulcal region of the PFC. It is speculated that nonspatial working memory may be modulated within connections between ventral visual processing regions and the inferior convexity of the PFC. Whether dopamine facilitates nonspatial memory through connections between the ventral visual system and ventral PFC has not been examined. In this study, normal humans completed spatial and nonspatial working memory tasks under pharmacological challenges with a dopamine receptor agonist (bromocriptine) and antagonist (haloperidol) in a double-blind placebcxontrolled repeated measures design. Findings indicated facilitation of spatial delayed working memory functions by bromocriptine and impairment of spatial working memory functions by haloperidol. Neither drug was effective in manipulating nonspatial memory performance. Control tasks were included to measure drug effects on basic sensorimotor and attentional processes. Findings suggest that separate processing mechanisms for remembering "What" versus "Where" an object is may exist at structural, but also neurochemical, levels in the human brain.

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Section: Exclusionsmentioning

confidence: 94%

Section: Halo Peridolmentioning

confidence: 98%

Section: Halo Peridolmentioning

confidence: 98%

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Dopaminergic Modulation of Working Memory for Spatial but Not Object Cues in Normal Humans

Luciana

Collins²

1997

Journal of Cognitive Neuroscience

161

131

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“…In contrast to the very large stimulation of prolactin release which characterizes dopamine D2 receptor antagonists (Rubin and Hays 1979;Wiesel et al 1982), the buspirone-and umespirone-stimulated release was comparatively modest (an increase of 4-5 fold over 6 h).…”

Section: Discussionmentioning

confidence: 97%

Single dose human pharmacology of umespirone

Holland¹,

Wesnes²,

Dietrich

1994

Eur J Clin Pharmacol

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We have compared the cognitive, EEG, and neuroendocrine effects of single doses of umespirone (20 mg and 80 mg) with those of buspirone (30 mg) and placebo in double-blind, cross-over studies in 44 healthy men. The pattern and time-course of the cognitive effects with umespirone and buspirone were dissimilar. Peak effects of buspirone were seen shortly after dosing and then receded, whilst the effects of umespirone persisted for up to 23 h. Although both drugs objectively impaired attention, buspirone reduced subjective alertness, calmness, and contentedness, whilst umespirone increased subjective alertness and contentedness and showed potential to improve secondary verbal memory. The EEG effects of umespirone were different from those seen with buspirone; they included a decrease of power in the alpha 1 band and the beta bands in the frontocentral area and an increase in the delta and theta bands in the occipitotemporal area. Umespirone had a later onset of action than buspirone but its effects lasted longer. Similar transient increases in serum prolactin and growth hormone concentrations were seen with buspirone and 80 mg umespirone; umespirone 20 mg had no effect. Plasma concentrations of ACTH and adrenaline and serum concentrations of cortisol were unaffected by either dose of umespirone. There was some evidence that buspirone increased ACTH and cortisol concentrations in some cases, and that umespirone increased noradrenaline concentrations. The frequency of adverse events was higher with buspirone than with 80 mg of umespirone. At the lower dose of umespirone, the frequency was similar to that with placebo.

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“…A clear elevation of serum prolactin levels has been observed after dopaminergic blockade with antipsychotics, in the range of 5-10 times baseline levels [Rubin and Hays, 1979], The doses necessary for such a maximal prolactin response, typically 0.04 mg/kg of haloperidol in humans [Gruen, 1978], are much smaller than those needed for antipsychotic effect [Donlon et al, 1979], The possibility has been raised that endorphins partic ipate in the kindling of seizures [Henriksen et al, 1977;Snead and Bearden, 1980], This present investigation incidentally involves a test of the converse aspect -is normal endorphinergic activity necessary for seizures to occur without plainly visible alterations? Method 36 white male Sprague-Dawley rats, weighing between 180 and 320 g each, were restrained within 5 s and immediately administered a single dose of either 150 V 60 Hz AC for 1 s (28 rats) or 5 V (8 controls) for 2-3 s across the ears (through alligator clips and EKG sol).…”

mentioning

confidence: 97%

Postictal Prolactin Elevations in Rats

Swartz

Dunbar²

1983

Neuropsychobiology

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Electrically induced seizures were followed by temporary elevations in serum prolactin over baseline in rats, while electrical irritation made no change. Naloxone 4 mg/kg i.p. pretreatment preserved this pattern but attenuated all levels including baseline by about 50%. While atropine 0.1 mg/kg s.c. did not change baseline levels, the prolactin levels after electrical irritation without seizure were about the same as those following a genuine seizure; atropine apparently facilitated stress-induced prolactin release. Seizures did not raise post-haloperidol prolactin levels above their high baseline levels.

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Variability of prolactin response to intravenous and intramuscular haloperidol in normal adult men

Cited by 39 publications

References 29 publications

Dopaminergic Modulation of Working Memory for Spatial but Not Object Cues in Normal Humans

Dopaminergic Modulation of Working Memory for Spatial but Not Object Cues in Normal Humans

Single dose human pharmacology of umespirone

Postictal Prolactin Elevations in Rats

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