Evaluating Prolactin Response to Dopamine Agonists in Schizophrenia

Davis, Bonnie M.; Davis, Kenneth L.; Mohs, Richard C.; Mathé, Aleksander A.; Rothpearl, Allen; Johns, Celeste A.; Levy, Michael I.; Horvath, Thomas

doi:10.1001/archpsyc.1985.01790260053006

Cited by 17 publications

(5 citation statements)

References 34 publications

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“…After the second baseline blood drawing, the subject received the chal lenge drug consisting of either placebo or 0.4 mg/kg of bu spirone. There was a 2-hour delay after insertion of the catheter to allow for stabilization of hormone levels (Davis et al 1985). Blood drawing was repeated at 15-minute intervals from 10:45 AM till 1:00 PM.…”

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confidence: 99%

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Moeller

Steinberg

Fulton

et al. 1994

Neuropsychopharmacol

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We administered the serotonin-1a agonist buspirone (0.4 mglkg orally) as a neuroendocrine challenge agent to a group of male patients with DSM-III -R major depressive disorder (MOD) (n = 13) and a group of male healthy controls (n = 10). The primary hypothesis of the study was that the prolactin response to buspirone would be blunted in the depressed patients. The prolactin response was significantly lower in depressed patients than in controls. There was no significant relationship between KEY WORDS: Depressive disorder; Serotonin; Buspirone; Prolactin 655 Avenue of the Americas, New York, NY 10010 placebo corrected-peak prolactin level and severity of depression or suicidality. There was a nonsignificant trend for the melancholic (n = 5) depressed patients to have a lower placebo corrected-peak prolactin level than nonmelancholic depressed patients (n = B).Our findings support a role for the serotonin-1a receptor in the etiology of MOD, specifically at the postsynaptic site. and 5-HT -releasing agents (Siever et al. 1984; Coccaro et al. 1989;Mitchell and Smythe 1990;Lichtenberg et al. 1992;Shapira et al. 1992aShapira et al. , 1992b.There has been a relatively consistent ii.nding of de creased prolactin response to various serotonergic agents in subjects with major depressive disorder (MOD) using nonspecific 5-HT challenge agents; thus, recent research has focused on the role of specific subtypes

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confidence: 99%

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Moeller

Steinberg

Fulton

et al. 1994

Neuropsychopharmacol

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“…Even in the acute phase of psychosis, scores on the mini-TRH test were about two times higher in two populations of acutely psychotic men than in normal men [20]. In schizophrenic exacerbation and in control subjects, no difference was found in dopamine-agonist-induced decrease in serum prolactin [36]. These results suggest that decreased TIDA release could not be fully compensated by increased sensitivity of dopamine receptors [26], suggesting a predominant role for TIDA release in determining the mini-TRH test.…”

Section: Studies In Schizophrenia Disordersmentioning

confidence: 80%

The Mini-TRH Test

Spoov

2022

Pharmacopsychiatry

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Thyrotropin-releasing hormone (TRH), at doses lower than those needed to stimulate prolactin secretion directly, can almost completely antagonize dopamine inhibition of prolactin release. In normal men, prolactin increases 15 min following an i. v. bolus of 12.5 µg TRH (the mini-TRH test), but not the maximal prolactin response to TRH or basal prolactin, positively correlated with prolactin response to haloperidol and negatively with 24-h urinary excretion of homovanillic acid (HVA). These results suggest that the mini-TRH test is a better estimate of dopamine inhibition of prolactin release than the maximal prolactin response or basal prolactin level. A recent neuroimaging study suggested that in schizophrenia, there is a widely distributed defect in extrastriatal dopamine release, but the patients were not in the most acute phase of psychosis. The evidence is reviewed that this defect extends to tuberoinfundibular dopamine (TIDA) and which symptoms are associated with the test. In patients with acute nonaffective psychosis, the mini-TRH test positively correlated with nonparanoid delusions and memory dysfunction, indicating decreased dopamine transmission in association with these symptoms. In patients with acute drug-naïve first-episode schizophrenia, the mini-TRH test negatively correlated with negative disorganization symptoms and with basal prolactin. The latter correlation suggests the contribution of factors related to maximal prolactin stimulation by TRH; therefore, an alternative dose of 6.25 μg TRH could be used for the mini-TRH test in first-episode patients, allowed by increased sensitivity of the present prolactin tests. Future studies are needed to investigate whether the mini-TRH test could help in finding the optimal antipsychotic medication.

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“…A decreased PRL suppression was reported by some investigators [15,24], particularly in chronic SCZs, but the vast majority of studies found no significant difference between SCZs and healthy controls (HCs) or patients with affective disorders [3][4][5][11][12][13][14][21][22][23]31]. The APO-PRL response does not predict clinical response to subsequent classical antipsychotic treatment [12].…”

Section: Prolactin Responsementioning

confidence: 99%

“…A major issue is that the magnitude of PRL suppression following APO is correlated with baseline, meaning that the higher the PRL baseline values, the greater the suppression [24]. This is why PRL suppression (PRLs) is frequently expressed as a percentage of change from baseline [3], rather than an area under the curve; by doing so, PRL values are no longer correlated with PRL baseline values (this also minimizes the gender effect since women often have higher baseline PRL levels [4]).…”

Section: Prolactin Responsementioning

confidence: 99%

Systematic Review of the Apomorphine Challenge Test in the Assessment of Dopaminergic Activity in Schizophrenia

Duval

2023

Healthcare

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So far, neuroendocrine studies conducted in schizophrenic patients have yielded conflicting results. Many of these discrepancies may be explained by the diversity of factors that influence the hormonal levels (at baseline and in response to pharmacological stimuli), the heterogeneity of the populations studied, the absence of standardization of test challenges and the confounding and long-lasting effects of previous treatments. Numerous studies have used apomorphine (APO) in the evaluation of dopaminergic (DA) function in schizophrenic patients. APO, a direct acting DA receptor agonist, decreases prolactin (PRL) and stimulates growth hormone (GH), adrenocorticotropic hormone (ACTH) and cortisol secretion. Therefore, the magnitude of hormonal responses to APO is an indirect assessment of the functionality of DA receptors at the hypothalamic–pituitary level. This review provides an update on the applications of the APO test in schizophrenia in clinical, pathophysiological and therapeutic fields.

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Evaluating Prolactin Response to Dopamine Agonists in Schizophrenia

Cited by 17 publications

References 34 publications

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

The Mini-TRH Test

Systematic Review of the Apomorphine Challenge Test in the Assessment of Dopaminergic Activity in Schizophrenia

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