Psychotropic Drugs and Neuroendocrine Function in Psychopathological Conditions

Gruen, Peter; Sachar, Edward J.; Altman, Norman H.; Langer, Gerhard; Halpern, Frieda S.

doi:10.1016/b978-1-4832-8322-7.50132-1

Cited by 4 publications

(4 citation statements)

References 25 publications

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“…It has a weak D-I dopamine receptor blocking effect, with special affinity to mesolimbic areas, while it also has strong anti-noradrenergic, anti-histaminergic, and anti-cholinergic 46.8 ± 3.4dopamine + haloperidol (5 nM) 74.8 ± 1.4 "-b The cells had been precultured for 3 days. Incubation time 4 h. Mean ± SEM (n= 4 wells per group) -p<0.01 vs control bp<0.01 vs dopamine (500 nM) (11,15,22). Chronic therapy of psychotic patients for 2-4 weeks with 600 mg clozapine per day did not increase the PRL levels of the cerebrospinal fluid (12).…”

Section: Resultsmentioning

confidence: 82%

The effect of clozapine on prolactin secretion at the level of the lactotroph

1990

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Clozapine is an antipsychotic drug which is unusual in that it has no dopamine receptor-blocking activity. Previous studies gave conflicting results whether administration of clozapine induces hyperprolactinemia. In the present study it was shown that a wide concentration range of clozapine does not interfere with dopamine-mediated inhibition of prolactin (PRL) secretion by normal cultured rat pituitary cells. This in contrast to other neuroleptics, like haloperidol and trifluoperazine. Clozapine does also not antagonize norepinephrine-mediated inhibition of PRL secretion. Clozapine exerts at micromolar concentrations a direct inhibitory action on PRL release by cultured normal rat pituitary cells. In cultured rat pituitary tumor cells, these high concentrations of clozapine directly inhibit PRL release as well as the DNA content of the cells, suggesting a direct antimitotic action. In this model clozapine was about 5-10 times less potent than trifluperazine. Clozapine and trifluoperazine exert an additive inhibitory action both on PRL release and on the DNA content of the pituitary tumor cells. It is concluded that clozapine does not interfere at the pituitary level with dopamine-mediated inhibition of PRL release. At micromolar concentrations clozapine may act on lactotrophs as a calmodulin-inhibitor. These observations suggest that the transient PRL-releasing effects which have been observed in both animal and human studies after clozapine administration are mediated via supra-pituitary actions of the drug.

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Section: Resultsmentioning

confidence: 82%

The effect of clozapine on prolactin secretion at the level of the lactotroph

1990

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“…Doses below 0.25 mg of haloperidol (or dose-equivalence of another neuroleptic) did not consistently release PRL and doses above 1.5 mg of haloperidol (or dose-equivalence of another neuroleptic) did not consistently elevate peak PRL responses further. We have also shown that male schizophrenics on high doses of neuroleptic maintenance medication had sustained PRL levels in the range of the peak PRL concentrations which these normal men achieved in response to a single administration of haloperidol 1.5 mg (15).…”

Section: Discussionmentioning

confidence: 95%

The Prolactin Response to Neuroleptic Drugs. A Test of Dopaminergic Blockade: Neuroendocrine Studies in Normal Men

Langer¹,

Sachar²,

Halpern³

et al. 1977

The Journal of Clinical Endocrinology & Metabolism

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The tonic inhibition of prolactin (PRL) secretion, which appears to be sustained mainly by hypothalamic dopaminergic activity, can be reliably disinhibited by neuroleptic, antidopaminergic drugs. The heuristic potential of this PRL response as a neuroendocrine model for studying hypothalamicpituitary regulation in man initiated the present intensive investigation.Nineteen normal young men were studied in a series of weekly experiments; at each session a single drug and dose, out of seven neuroleptic drugs in various doses, was given parenterally (mostly im). Plasma PRL concentrations were then monitored for at least 3 h. 1. Repeated administrations of haloperidol (1 mg im) and prochlorperazine (4 mg iv) demonstrated a high reproducibility of the PRL response within a subject. 2. The PRL-response to four doses of haloperidol, ranging from 0.25 mg to 1.5 mg, showed a sigmoid dose-response curve. A dose as small as 1.5 mg of haloperidol induced maximal PRL response. 3. Dose-PRL response curves of haloperidol, prochlorperazine, and thiothixene, representing three chemical classes of neuroleptic drugs, showed a parallel relationship. This suggests a common pharmacological, very likely antidopaminergic, mechanism of the drugs when releasing PRL. 4. In response to haloperidol (1 mg), chlorpromazine (25 mg), and trifluoperazine (4 mg), plasma PRL concentrations remained elevated for at least 7 h, consistent with reported plasma half-lives of these drugs. 5. Dose equivalencies of seven neuroleptic drugs in inducing PRL secretion in man are given.The presented data indicate that the PRL response to neuroleptic drugs is sensitive and reliable and is probably a valid test of dopaminergic blockade in man. Our findings suggest a model for studying drug and hormonal interactions with neuroleptics in man. (J Clin Endocrinol Metab 45: 996, 1977)

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“…One placebo-controlled study found that alcohol, a GABA agonist, enhances hypnotic suggestibility (Semmens-Wheeler et al, 2013) (see also (Hull, 1933). By contrast, a well-powered study reported that another GABA agonist, diazepam, did not significantly enhance hypnotic suggestibility relative to nicotinic acid, although this was potentially attributed to sample heterogeneity (Gibson et al, 1977); see also (Halpern & Merlis, 1961). Multiple anecdotal findings have also suggested that GABA agonists, such as benzodiazepines, enhance responsiveness to suggestion (for a review, see (Acunzo et al, 2021)).…”

Section: Gabamentioning

confidence: 99%

The neurochemical bases of verbal suggestion and hypnosis

Smith¹,

Acunzo²,

Deeley³

et al. 2023

Preprint

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Characterizing the neurochemical systems involved in responsiveness to hypnotic suggestions has the potential to advance our understanding of the neurocognitive bases of verbal suggestion but also to develop novel interventions for enhancing responsiveness to suggestions in clinical and experimental contexts. In this chapter, we draw on pharmacological, genotyping, neuroimaging, and electrophysiological research to synthesize the available evidence regarding the involvement of different neurochemicals in response to suggestion. We highlight multiple converging lines of evidence that point to potential fruitful targets for future research but we also draw attention to multiple limitations in this body of evidence. We consider the extent to which these results are consistent with different theories of verbal suggestion and hypnosis and outline multiple avenues by which these theories could be discriminated using pharmacological methods. Finally, we conclude by highlighting the clinical implications of this research and how it may help to advance our understanding of the neurocognitive basis of verbal suggestion.

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Psychotropic Drugs and Neuroendocrine Function in Psychopathological Conditions

Cited by 4 publications

References 25 publications

The effect of clozapine on prolactin secretion at the level of the lactotroph

The effect of clozapine on prolactin secretion at the level of the lactotroph

The Prolactin Response to Neuroleptic Drugs. A Test of Dopaminergic Blockade: Neuroendocrine Studies in Normal Men

The neurochemical bases of verbal suggestion and hypnosis

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