Effect of midbrain raphe lesion or 5,7-dihydroxytryptamine treatment on the prolactin-releasing action of quipazine andd-fenfluramine in rats

Quattrone, Aldo; Schettini, Gennaro; Renzo, Gianfranco Di; Tedeschi, G; Preziosi, P

doi:10.1016/0006-8993(79)90804-7

Cited by 47 publications

(17 citation statements)

References 21 publications

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“…Quipazine has been shown previously to stimulate prolactin secretion [9,32]. Unlike our results though, Quattrone et al [34] reported that intraventricular injection of the serotonin neurotoxin 5,7-DHT and lesions of the median raphe nucleus prevented the stimulatory ef fect of quipazine on prolactin secretion. This observation, however, is not consistent with the postsynaptic receptor in teraction of quipazine.…”

Section: Discussioncontrasting

confidence: 56%

Pharmacological Evidence that Serotonergic Stimulation of Prolactin Secretion is Mediated via the Dorsal Raphe Nucleus

Kar

Bethea²

1982

Neuroendocrinology

112

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Administration of the serotonin-releasing drug DL-p-chloroamphetamine (PCA) to rats caused a dose-dependent increase in plasma prolactin levels. The effect was maximal 2 h after administration. The effect of PCA was prevented by prior administration of the serotonin synthesis inhibitor p-chlorophenylalanine-methyl ester (PCPA). PCPA pre-treatment did not prevent the increase in plasma prolactin levels after administration of the serotonin agonist quipazine which is consistent with a postsynaptic receptor interaction of quipazine. To determine which serotonergic neurons are involved, the prolactin responses to PCA were determined in rats sustaining lesions of the dorsal or median raphe nuclei. The lesions were produced in desmethylimipramine-pretreated rats by local injections of 5,7-dihydroxytryptamine (5,7-DHT) 2 weeks prior to the PCA challenge. In rats with dorsal raphe lesions, the effect of PCA on prolactin secretion was significantly attenuated. In contrast, median raphe lesions did not prevent the effect of PCA on plasma prolactin levels. In summary, these data support the hypothesis that release of serotonin increases prolactin secretion. In addition, these data suggest that serotonergic neurons in the dorsal raphe nucleus are part of a neural pathway which can mediate increases in prolactin secretion.

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Section: Discussioncontrasting

confidence: 56%

Pharmacological Evidence that Serotonergic Stimulation of Prolactin Secretion is Mediated via the Dorsal Raphe Nucleus

Kar

Bethea²

1982

Neuroendocrinology

112

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“…The observation of a robust PRL response to FEN in these subjects indicates that the dose of FEN (60 mg p.o.) used was sufficient to stimulate a 5-HT-mediated neuroendocrine response as reported in previous an imal and clinical studies [1,28,29,34,36].…”

Section: Discussionmentioning

confidence: 71%

“…FEN is a centrally active 5-HT-releasing and 5-HT reuptake inhibiting agent [6. 12, 13], Its stimulatory effects on the central 5-HT system -vis-à-vis changes in cerebro spinal fluid 5-hydroxyindoleacetic acid and plasma prolac tin (PRL) -after acute administration have been demon strated in animal [28,29] and clinical studies [1,34,36], Un like 5-HTP or zimelidine, however, FEN has little demon strable effect on the release of central catecholamines [1,4,12], The results of this study suggest that central 5-HT may not play a significant stimulatory or inhibitory role in the release of pituitary TSH in euthyroid men. …”

mentioning

confidence: 99%

Central Serotoninergic Stimulation by Fenfluramine Challenge Does Not Affect Plasma Thyrotropin-Stimulating Hormone Levels in Man

et al. 1988

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Thyrotropin-stimulating hormone (TSH) and prolactin (PRL) responses to an acute oral challenge of fenfluramine (60 mg), a central serotoninergic (5-hydroxytryptamine) releasing/uptake inhibiting agent, were examined in 8 healthy males in order to assess the role of central serotoninergic stimulation in the release of TSH. Plasma PRL, but not TSH, was significantly elevated by fenfluramine. These data suggest that central serotoninergic activity does not play an important role in the physiologic release of plasma TSH in man. Further, thyrotropin-releasing hormone is unlikely to be the PRL-releasing factor involved in the fenfluramine-induced stimulation of PRL.

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“…This is supposed to reflect the central serotonin activity [38][39][40][41][42][43][44][45][46][47]. The protocol of the 30-mg d-fenfluramine challenge test dictates an overnight fasting and the oral administration of 30 mg of the substance.…”

Section: Biological Markersmentioning

confidence: 99%

Neurobiological and Psychological Correlates of Suicidal Attempts and Thoughts of Death in Patients with Major Depression

Fountoulakis¹,

Iacovides²,

Fotiou

et al. 2004

Neuropsychobiology

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Suicide is a major problem for psychiatry. Depression is the most common mental disorder related to suicidal behavior. The present study aimed at investigating the relationship between the symptomatology related to death, dying, and suicide and neurobiological factors in depressed patients. Fifty patients aged 21–60 years suffering from major depression were investigated. Schedules for Clinical Assessment in Neuropsychiatry version 2.0 and the International Personality Disorder Examination were used to assist the clinical diagnosis. The psychometric assessment included the Hamilton Depression Rating Scale, the Hamilton Anxiety Scale, the 1965 and 1971 Newcastle Depression Diagnostic Scales, the Diagnostic Melancholia Scale, the General Assessment of Functioning Scale, and the Personality Deviance Scale. Psychophysiological methods included electro-oculogram, flash electroretinogram under photopic and scotopic conditions, and pattern-reversal visual evoked potentials. Biological markers included the 1-mg dexamethasone suppression test, the 30-mg dexfenfluramine challenge test, and brain ^99mTc-HMPAO SPECT. Statistical analysis included one-, two-, and three-way Manova and Mancova and the Scheffé test as post hoc test. Patients without thoughts of death had higher self-confidence levels and less overdependency on others and intropunitiveness. The suicidal patients had a significantly prolonged pattern-reversal visual evoked potential latency in comparison with the other patients. The findings of this were related to the status of the patient at the time of the interview but not to his/her history. They also provide neurobiological data to support the need for a combined presence of self-directed aggression and a higher arousal level or disinhibition of self-directed aggressive thoughts in order for a patient to become suicidal. Further study is needed to test whether psychophysiological methods, which are noninvasive and easy to perform, are of value in the therapeutic planning and monitoring of responses.

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Effect of midbrain raphe lesion or 5,7-dihydroxytryptamine treatment on the prolactin-releasing action of quipazine andd-fenfluramine in rats

Cited by 47 publications

References 21 publications

Pharmacological Evidence that Serotonergic Stimulation of Prolactin Secretion is Mediated via the Dorsal Raphe Nucleus

Pharmacological Evidence that Serotonergic Stimulation of Prolactin Secretion is Mediated via the Dorsal Raphe Nucleus

Central Serotoninergic Stimulation by Fenfluramine Challenge Does Not Affect Plasma Thyrotropin-Stimulating Hormone Levels in Man

Neurobiological and Psychological Correlates of Suicidal Attempts and Thoughts of Death in Patients with Major Depression

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