Responses of prolactin and growth hormone to L-tryptophan infusion: Effects in normal subjects and schizophrenic patients receiving neuroleptics

Cowen, Philip J.; Gadhvi, H; Gosden, Barbara; Kołakowska, T

doi:10.1007/bf00431703

Cited by 74 publications

(34 citation statements)

References 35 publications

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“…Two studies reported an increased prolactin response and a blunted GH release (Cowen et al, 1985;Kolakowska et al, 1987). One study found decreased prolactin responses and decreased GH response only in long-term haloperidol-treated patients, whereas short-term treated patients did not differ from controls in both measures (Hoshino et al, 1985).…”

Section: Serotonergic Challenge Studiesmentioning

confidence: 99%

Serotonin and Schizophrenia

Quednow

Geyer

Halberstadt

2010

Handbook of Behavioral Neuroscience

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Although the serotonin hypothesis of schizophrenia is one of the oldest neurochemical hypotheses on the pathogenesis of this disease, it is still highly topical. The concept of how the serotonin system is involved in the origin and progress of schizophrenia has considerably changed over the past decades. Therefore, the present work will give an overview about the development and the current directions of the serotonin hypothesis of schizophrenia. In this regard, we will discuss the phenomenology of hallucinogenic drug action, model psychosis and translational research, post-mortem studies on receptors and transporters, imaging studies, antipsychotic drug action, neuroendocrine challenge studies, platelet and cerebrospinal fluid data, genetic association studies, developmental aspects, and the cross-talk between the glutamate and the serotonin system. In sum, there are several lines of evidence suggesting that the serotonin system plays a major role in the pathogenesis of at least a subpopulation of schizophrenia patients. Further studies are needed to better characterize patients whose psychotic symptoms are suspected to have a serotonergic origin. Serotonin and Schizophrenia AbstractAlthough the serotonin hypothesis of schizophrenia is one of the oldest neurochemical hypotheses on the pathogenesis of this disease, it is still highly topical. The concept of how the serotonin system is involved in the origin and progress of schizophrenia has considerably changed over the past decades.Therefore, the present work will give an overview about the development and the current directions of the serotonin hypothesis of schizophrenia. In this regard, we will discuss the phenomenology of hallucinogenic drug action, model psychosis and translational research, post-mortem studies on receptors and transporters, imaging studies, antipsychotic drug action, neuroendocrine challenge studies, platelet and cerebrospinal fluid data, genetic association studies, developmental aspects, and the cross-talk between the glutamate and the serotonin system. In sum, there are several lines of evidence suggesting that the serotonin system plays a major role in the pathogenesis of at least a subpopulation of schizophrenia patients. Further studies are needed to better characterize patients whose psychotic symptoms are suspected to have a serotonergic origin.3

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Section: Serotonergic Challenge Studiesmentioning

confidence: 99%

Serotonin and Schizophrenia

Quednow

Geyer

Halberstadt

2010

Handbook of Behavioral Neuroscience

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“…To obtain evidence (independent of rCBF changes) for an effect of buspirone on central monoamine systems, four measurements of plasma prolactin and growth hormone were obtained from blood drawn from an in-dwelling venous cannula (t = -20, 0, 20 and 40 rain post-buspirone). Prolactin and growth hormone were measured by radioimmunoassay as described previously (Cowen et al 1985). Plasma buspirone concentrations were measured at t= -20, 0, 20 and 40 min post-drug using high performance liquid chromatography with coulometric detection (Franklin 1990).…”

Section: Methodsmentioning

confidence: 99%

Effect of the 5-HT1A partial agonist buspirone on regional cerebral blood flow in man

et al. 1992

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Abstract. Repeated measurements of regional cerebral blood flow (rCBF) were made in normal volunteers before, and after, the administration of the 5-HTaA partial agonist, buspirone, or placebo. The difference in rCBF, before and after drug, (buspirone versus placebo) was used to identify brain areas affected by buspirone. Buspirone-induced changes in rCBF were studied under two behavioural conditions (5 word-list learning and 15 word-list learning). Compared to placebo, buspirone increased blood flow in the cuneus during both behavioural states. However, decreases in blood flow, centred in the left dorso-lateral prefrontal cortex and posterior cingulate cortex, were only observed under one of the two behavioural conditions. It is concluded that buspironeinduced alterations in regional cerebral blood flow are better understood, not in relation to the known distribution of monoamine neurotransmitter systems (particularly ascending 5-HT projections), but rather in relation to putative neuronal circuits possibly many synapses "downstream" of buspirone's pharmacological site of action.

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“…CCC 0885-6222/96/020139-05 tophan (LTP) and 5-hydroxytryptophan (SHTP) results in a consistent elevation in plasma growth and prolactin hormone (Handwerger et al, 1975;Lancranfan et al, 1977;Meltzer et al, 1982;Westenberg et al, 1982;Charney et al, 1982;Maschat et al, 1983;Cowen et al, 1985). Increases in PRL, cortisol and GH have been demonstrated following both oral and intravenous administration of m-chlorophenylpiperazine (m-CPP), which binds to SHTla, 5HTlc and 5HTld receptors as well as 5HT2 receptors (Charney et al, 1987;Murphy et al, 1989).…”

Section: Introductionmentioning

confidence: 95%

Sumatriptan mediated growth hormone responses do not alter throughout the menstrual cycle

Lavelle

Williams

Dinan

1996

Hum. Psychopharmacol. Clin. Exp.

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The objective of this study was to determine the effects of oral sumatriptan on growth hormone (GH) release throughout the menstrual cycle in healthy female volunteers. A placebo-controlled cross-over design was employed. Subjects were tested a total of six times over two consecutive menstrual cycles; twice in the early follicular phase, twice in midcycle and twice in the late luteal phase. Oral sumatriptan (100 mg) and placebo were administered on alternate visits. Twelve healthy female volunteers aged between 18-40 years with regular menses and not taking oral contraceptives were recruited. Baseline blood samples at 0 min were taken for GH, oestrogen and progesterone estimation. G H was measured at +60, +90, + 120 and + 180 min following administration of oral sumatriptan 100 mg or matched placebo. GH, progesterone and oestrogen were measured by radioimmunoassay. At each phase of the menstrual cycle serum GH levels peaked at 60-90 min following administration of oral sumatriptan compared to placebo which showed no response. Analysing GH response to sumatriptan and placebo over time for the three phases of the menstrual cycle (three-way ANOVA) demonstrates that the G H response to sumatriptan did not alter.

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Responses of prolactin and growth hormone to L-tryptophan infusion: Effects in normal subjects and schizophrenic patients receiving neuroleptics

Cited by 74 publications

References 35 publications

Serotonin and Schizophrenia

Serotonin and Schizophrenia

Effect of the 5-HT1A partial agonist buspirone on regional cerebral blood flow in man

Sumatriptan mediated growth hormone responses do not alter throughout the menstrual cycle

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