Brain 5-hydroxytryptamine and plasma testosterone in L-tryptophan treated rats.
TL;DR: Results suggest that brain 5-HT exerts an inhibitory influence on testicular steroidogenesis by modulating the gonadotropin-releasing-factor (GnRH) release and thence pituitary Gonadotropins.
Abstract: Loading of L-tryptophan for 7 and 21 days increased brain 5-hydroxytryptamine (5-HT) level which was associated with decreased plasma testosterone level. Human chorionic gonadotropin (HCG) administration in L-tryptophan treated rats for 21 days increased the plasma testosterone level in spite of increased brain 5-HT level. These results suggest that brain 5-HT exerts an inhibitory influence on testicular steroidogenesis by modulating the gonadotropin-releasing-factor (GnRH) release and thence pituitary gonadotropins.
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TL;DR: The results may indicate that the analgesia produced by castration and flutamide administration is mediated through functional alteration in spinal cord serotonergic system.
Abstract: The involvement of spinal serotonergic system in testosterone influence on formalin-induced pain was studied in male rats. Four weeks after castration, there was an analgesia in the late phase of formalin test that was reversed by intraperitoneal injection of testosterone enanthate (1 mg/kg) for 3 days. Flutamide (testosterone antagonist) produce analgesia in the late phase on intraperitoneal (10 mg/kg, IP) and intrathecal (60 μg/rat, IT) injections, but not on intracerebroventricular (60 μg/rat, ICV) administration. The antinociceptive effect of castration and IP flutamide (10 mg/kg) was abolished by pretreatment with 5,7-dihydroxytryptamine (5,7-DHT, 100 μg/rat, IT). IT-administered 5-HT (100 μg/rat) produced analgesia in the early and late phase of formalin test. Microdialysis sampling was used to characterize the extracellular concentration of 5-hydroxytryptamine (5-HT, serotonin) in the dorsal horn of the lumbar spinal cord. This technique demonstrated that levels of 5-HT were increased in 4-week castrated and IP flutamide (10 mg/kg) injected rats. The results may indicate that the analgesia produced by castration and flutamide administration is mediated through functional alteration in spinal cord serotonergic system.
35 citations
TL;DR: The results suggest that both serotonin and NPY could be involved in the inhibition induced by PFOS on the reproductive axis activity in adult male rats.
26 citations
Cites background from "Brain 5-hydroxytryptamine and plasm..."
..., 2014) so it also regulates LH and testosterone release (Biswas et al., 1985; Vitale et al., 1986)....
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...Serotonin modulates GnRH secretion (Bhattarai et al., 2014) so it also regulates LH and testosterone release (Biswas et al., 1985; Vitale et al., 1986)....
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TL;DR: The brain 5‐HT levels elevated after Trp administration in different intensities, dependent of the brain region evaluated and the time of administration, are reviewed.
11 citations
TL;DR: It was found a typical for the overtraining syndrome decrease in the concentration of testosterone and the ratio of testosterone/cortisol in T3, which correlates with the hormonal changes.
Abstract: Abstract The diet is essential to the recovery process in athletes, especially those undergoing intensive training. The continuous imbalance between loading and recovery leads to development of overtraining syndrome. The purpose of this study was to establish the changes in the nutritional status of short-term overtrained athletes. Twelve boxers from the team of National Spoils Academy Sofia, Bulgaria during their preparation for the National Championship 2016 were studied. The measurements were conducted three times.in the beginning of preparation (T1), 22 days later (2) and 10 days after (32 days after first measurement), in the beginning of the recovery period, one week prior the competition (T3).The measurements included basic anthropometric data, overtraining questionnaire RESTO-Sport and nutrition questionnaire, plasma concentration of testosterone and cortisol.On the data of dietary survey the percent proportion and the amount of daily consumed proteins, fats and carbohydrates were defined and the energy intake of the tested athletes was calculated. According to the RESTO-Sport a significant decrease in the ratio stress/recovery was observed in the period with the heaviest training load T2, and an increase was estimated in the precompetition recovery period T3. It was found a typical for the overtraining syndrome decrease in the concentration of testosterone and the ratio of testosterone/cortisol in T3. In some respondents a reduction in carbohydrates and proteins intake was observed in T2 and especially in T3, which correlates with the hormonal changes. In this work the diet changes was discussed as a possible consequence and/or a cause of the overtraining syndrome.
3 citations
TL;DR: Quantitative analysis of spermatogenesis at stage VII of the cycle of the seminiferous epithelium, radioimmunoassay of plasma testosterone and spectrofluoro‐metric assay of brain 5‐hydroxytryptamine (5‐HT) levels were performed following administration of L‐trytophan alone and in Carbidopa pretreated Wistar strain rats.
Abstract: Summary: Quantitative analysis of spermatogenesis at stage VII of the cycle of the seminiferous epithelium, radioimmunoassay of plasma testosterone and spectrofluoro-metric assay of brain 5-hydroxytryptamine (5-HT) levels were performed following administration of L-trytophan (LT) alone and in Carbidopa pretreated Wistar strain rats. Carbidopa, an inhibitor of peripheral L-aromatic amino acid decarboxylase, was used to prevent the peripheral conversion of LT to 5-HT. The rats were sacrificed in groups on the day after (8th day) and 13 days after (21st day) the cessation of 7 days of treatment. The time duration of 13 days is approximately equivalent to one cycle of the seminiferous epithelium in Wistar strain rats.
LT enhanced the brain 5-HT level, the increase being much greater in Carbidopa plus LT treated rats. However, reduction of plasma testosterone was similar in both the treated groups. There was no significant change in count of the germ cells on the day after cessation of treatment. However, marked degeneration of step 7 spermatids was observed when the analysis was performed 13 days after cessation of treatment. Human chorionic gonadotropin (HCG) administration along with Carbidopa plus LT treatment partially prevented the step 7 spermatid degeneration. These findings suggest that the inhibition of spermatogenesis and steroidogenesis following LT administration was secondary to decreased pituitary gonadotropin secretion which is in turn under the influence of brain 5-HT neurones. There is a minimum possibility of a direct action of LT, after conversion to 5-HT, on testicular tissue.
Weiterer Beweis fur einen Hemmeffekt von L-Tryptophan auf die Hodenfunktionen der Ratte
Zusammenfassung: Nach Zufuhr von L-Tryptophan (LT) allein und bei Carbidopa-be-handelten Wistar-Ratten wurde eine quantitative Analyse der Spermatogenese (Stadium VII) sowie des Plasma-Testosterons (RIA) und des Hirn-5-Hydroxytryptamin (5-HT) vor-genommen. Carbidopa (ein Inhibitor der peripheren L-aromatischen Aminosauren-De-carboxylase) wurde verwendet, urn die periphere Konversion von LT zu 5-HT zu verhin-dern. Die Ratten wurden bei einer 7tagigen Behandlungsdauer am 8. und 21. Tage geto-tet. Der normale Spermatogenesezyklus der Wistarratte betragt etwa 13 Tage.
LH erhoht den Hirn-5-HT-Wert, und zwar ist der Anstieg sehr viel groser bei Tieren, die Carbidopa plus LT erhielten. Die Reduzierung von Testosteron war jedoch in beiden Gruppen gleich. Es ergab sich keine signifikante Anderung hinsichtlich der Keimzellzah-len am Tage nach Beendigung der Therapie. Es fand sich jedoch eine deutliche Degeneration der Spermatiden (Stufe VII), wenn die Analyse 13 Tage nach Ende der Therapie vor-genommen wurde. Eine HCG-Anwendung wahrend Carbidopa plus LT-Therapie verhin-derte teilweise die Degeneration der Spermatiden (Stadium VII). Diese Ergebnisse legen es nahe, das die Hemmung der Spermatogenese und der Steroidgenese nach LT-Anwen-dung bedingt war durch die verminderte Gonadotropinsekretion der Hypophyse, die un-ter dem Einflus der Hirn-5-HT-Neurone steht. Es besteht eine geringe Moglichkeit direk-ter Aktion von LT nach Konversion zu 5-HT auf das Hodengewebe.
3 citations
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TL;DR: Brain serotonin cocentrations at 1 p.m. were significantly elevated 1 hour after rats received a dose of L-tryptophan and plasma and brain tryptophan levels were elevated 10 to 60 minutes after the injection, but they never exceeded the concentrationis that occur nocturnally in untreated aninmals as result of their normal 24-hour rhythms.
Abstract: Brain serotonin cocentrations at 1 p.m. were significantly elevated 1 hour after rats received a dose of L-tryptophan (12.5 milligrams per kilogram. intraperitoneally) smaller than one-twentieth of the normal daily dietary intake. Plasma and brain tryptophan levels were elevated 10 to 60 minutes after the injection, but they never exceeded the concentrationis that occur nocturnally in untreated aninmals as result of their normal 24-hour rhythms. These data suggest that physiological changes in plasma tryptophan concentration influenice brain serotonin levels.
980 citations
705 citations
TL;DR: With this method, it is possible to measure serotonin in organs in which endogenous serotonin had not been previously detected and to study the subcellular distribution of this amine in the rat pineal and adrenal glands.
510 citations
TL;DR: Evidence is presented for occurrence of many steps of metabolism starting with tryptophan and proceeding through 5-Hydroxytryptophan to the various 5-hydroxyindole compounds in a number of organisms and tissues.
216 citations
TL;DR: The results support the concept that the effect of L-tryptophan on the secretion of human prolactin is mediated through its conversion to serotonin and are consistent with reported experimental observations that serotonin may participate in the reciprocal regulation of Prolactin and gonadotropins.
Abstract: Previous studies have demonstrated that the secretion of human prolactin is regulated primarily by factors that influence catecholamines of the hypothalamus. In an effort to identify other factors that may regulate prolactin secretion, the amino acid L-tryptophan, a precursor in the synthesis of serotonin, was infused into normal human volunteers. Intravenous infusion of L-tryptophan, 5-10 g over a 20 min period, but not equivalent amounts of 17 other amino acids, induced marked increases in serum prolactin concentrations in eight normal human volunteers. Increases of 20-200 ng/ml above the control level were observed with peak values at 20-45 min after initiation of the infusion. In addition, infusion of L-tryptophan was associated with decreases in serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and thyrotropin in those subjects in whom the base-line serum hormone concentration was above the lower limits of assay detectability. No consistent change was observed in serum concentrations of growth hormone, cortisol, or glucose. Four subjects with juvenile diabetes demonstrated increases in serum prolactin values comparable with those observed in healthy individuals in response to infusions of L-tryptophan. Serum prolactin values in patients with surgically induced hypopituitarism were undetectable or deficient after infusion of 10 g of L-tryptophan. In this respect, infusion of L-tryptophan was equally effective in these subjects as the standard chlorpromazine stimulation test in identifying patients with hypopituitarism, indicating that the infusion of L-tryptophan may serve as a sensitive and reliable clinical test of prolactin secretory reserve. Further studies relating to the possible mechanism of action of L-tryptophan indicated that infusion of 5-hydroxytryptophan represents a much more potent stimulus for the secretion of prolactin and that premedication with the serotonin antagonist, methysergide maleate, serves to blunt the effect of L-tryptophan on prolactin secretion. These results support the concept that the effect of L-tryptophan on the secretion of human prolactin is mediated through its conversion to serotonin and are consistent with reported experimental observations that serotonin may participate in the reciprocal regulation of prolactin and gonadotropins.
186 citations