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1.
J Anim Sci ; 95(5): 2211-2221, 2017 May.
Artículo en Inglés | MEDLINE | ID: mdl-28726984

RESUMEN

Compromised placental function can result in fetal growth restriction which is associated with greater risk of neonatal morbidity and mortality. Large increases in transplacental nutrient and waste exchange, which support the exponential increase in fetal growth during the last half of gestation, are dependent primarily on the rapid growth and vascularization of the uteroplacenta. The amplitude of melatonin secretion has been associated with improved oxidative status and altered cardiovascular function in several mammalian species; however, melatonin mediated alterations of uteroplacental capacity in sheep and cattle are lacking. Therefore, our laboratories are examining uteroplacental blood flow and fetal development during maternal melatonin supplementation. Using a mid- to late-gestation ovine model of intrauterine growth restriction, we examined uteroplacental blood flow and fetal growth during supplementation with 5 mg/d of dietary melatonin. Maternal nutrient restriction decreased uterine arterial blood flow, while melatonin supplementation increased umbilical arterial blood flow compared with non-supplemented controls. Although melatonin treatment did not rescue fetal weight in nutrient restricted ewes; we observed disproportionate fetal size and fetal organ development. Elevated fetal concentrations of melatonin may result in altered blood flow distribution during important time points of development. These melatonin specific responses on umbilical arterial hemodynamics and fetal development may be partially mediated through vascular melatonin receptors. Recently, we examined the effects of supplementing Holstein heifers with 20 mg/d of dietary melatonin during the last third of gestation. Uterine arterial blood flow was increased by 25% and total serum antioxidant capacity was increased by 43% in melatonin supplemented heifers vs. non-supplemented controls. In addition, peripheral concentrations of progesterone were decreased in melatonin supplemented heifers vs. non-supplemented controls. Using an in vitro model, melatonin treatment increased the activity of cytochrome P450 2C, a progesterone inactivating enzyme, which was blocked by treatment with the melatonin receptor antagonist, luzindole. Elucidating the consequences of specific hormonal supplements on the continual plasticity of placental function will allow us to determine important endogenous mediators of offspring growth and development.


Asunto(s)
Bovinos/embriología , Suplementos Dietéticos , Hemodinámica/efectos de los fármacos , Melatonina/administración & dosificación , Ovinos/embriología , Animales , Antioxidantes/metabolismo , Bovinos/fisiología , Dieta/veterinaria , Endocrinología , Femenino , Desarrollo Fetal/efectos de los fármacos , Feto/efectos de los fármacos , Placenta/irrigación sanguínea , Placenta/efectos de los fármacos , Embarazo , Receptores de Melatonina/antagonistas & inhibidores , Ovinos/fisiología , Triptaminas/farmacología , Cordón Umbilical/irrigación sanguínea , Cordón Umbilical/efectos de los fármacos , Útero/irrigación sanguínea , Útero/efectos de los fármacos
2.
Biochem Biophys Res Commun ; 465(4): 719-24, 2015 Oct 02.
Artículo en Inglés | MEDLINE | ID: mdl-26296463

RESUMEN

We have recently discovered that melatonin, given acutely and directly to the isolated heart at the concentration found in wine, confers cardioprotection against ischemia-reperfusion (I/R). However, whether the presence of melatonin in wine contributes to the cardioprotective effect of chronic and moderate consumption of wine and its signalling mechanisms of protection are unknown. We therefore used both in vivo and in vitro models of I/R to investigate whether the presence of melatonin in red wine may contribute to the cardioprotective effect of chronic and moderate consumption of red wine. Wistar rats and C57black6 mice (WT) received drinking water supplemented daily with a moderate amount of red wine or melatonin given at the concentration found in the red wine. Rats were also pretreated with luzindole, a specific inhibitor of melatonin receptors 1 and 2 (2.3 mg/kg/day, intraperitoneally) or prazosin, a specific inhibitor of melatonin receptor type 3 (2.5 mg/kg/day, intraperitoneally). After 14 days, hearts were subjected to I/R in vivo or ex vivo. Red wine reduced the infarct size in both rats and WT mice (p < 0.001). Luzindole did not affect wine-induced cardioprotection, while prazosin reduced the infarct sparing effect of red wine (p < 0.05). Furthermore, red wine or melatonin failed to protect tumor necrosis factor alpha (TNF) receptor 2 knockout or cardiomyocyte specific signal transducer and activator of transcription 3 (STAT3) deficient mice (n.s. vs. control). Our novel findings suggest that the presence of melatonin in red wine contributes to the cardioprotective effect of chronic and moderate consumption of red wine against lethal I/R injuries. This effect is most likely mediated, at least in part, via melatonin receptor 3 and the activation of TNF and STAT3, both key players of the prosurvival and well described SAFE pathway.


Asunto(s)
Cardiotónicos/administración & dosificación , Melatonina/administración & dosificación , Melatonina/metabolismo , Receptores de Melatonina/metabolismo , Factor de Transcripción STAT3/metabolismo , Vino/análisis , Animales , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Infarto del Miocardio/dietoterapia , Infarto del Miocardio/metabolismo , Infarto del Miocardio/patología , Prazosina/farmacología , Ratas , Ratas Wistar , Receptor de Melatonina MT1/antagonistas & inhibidores , Receptor de Melatonina MT1/metabolismo , Receptor de Melatonina MT2/antagonistas & inhibidores , Receptor de Melatonina MT2/metabolismo , Receptores de Melatonina/antagonistas & inhibidores , Receptores Tipo II del Factor de Necrosis Tumoral/deficiencia , Receptores Tipo II del Factor de Necrosis Tumoral/genética , Factor de Transcripción STAT3/antagonistas & inhibidores , Factor de Transcripción STAT3/deficiencia , Factor de Transcripción STAT3/genética , Triptaminas/farmacología , Tirfostinos/farmacología
3.
Neuropharmacology ; 99: 187-95, 2015 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-26188145

RESUMEN

Stopping the ischemic cascade by targeting its components is a potential strategy for acute ischemic stroke treatment. During ischemia and especially over reperfusion, oxidative stress plays a major role in causing neuronal cell death. Melatonin has been previously reported to provide neuroprotective effects in in vivo models of stroke by a mechanism that implicates melatonin receptors. In this context, this study was planned to test the potential neuroprotective effects of the novel melatonin MT1/MT2 receptor agonist, Neu-P11, against brain ischemia in in vitro and in vivo models, and to elucidate its underlying mechanism of action. Neu-P11 proved to be a good antioxidant, to protect against glutamate-induced excitotoxicity and oxygen and glucose deprivation in hippocampal slices, and to reduce infarct volume in an in vivo stroke model. Regarding its mechanism of action, the protective effect of Neu-P11 was reverted by luzindole (melatonin receptor antagonist), AG490 (JAK2 inhibitor), LY294002 (PI3/AKT inhibitor) and PD98059 (MEK/ERK1/2 inhibitor). In conclusion, Neu-P11 affords neuroprotection against brain ischemia in in vitro and in vivo models by activating a pro-survival signaling pathway that involves melatonin receptors, JAK/STAT, PI3K/Akt and MEK/ERK1/2.


Asunto(s)
Isquemia Encefálica/tratamiento farmacológico , Indoles/farmacología , Fármacos Neuroprotectores/farmacología , Piranos/farmacología , Animales , Antioxidantes/farmacología , Encéfalo/efectos de los fármacos , Encéfalo/patología , Encéfalo/fisiopatología , Isquemia Encefálica/patología , Isquemia Encefálica/fisiopatología , Hipoxia de la Célula/efectos de los fármacos , Hipoxia de la Célula/fisiología , Línea Celular Tumoral , Modelos Animales de Enfermedad , Evaluación Preclínica de Medicamentos , Glucosa/deficiencia , Humanos , Masculino , Melatonina/análogos & derivados , Ratones Endogámicos C57BL , Distribución Aleatoria , Ratas Sprague-Dawley , Receptores de Melatonina/agonistas , Receptores de Melatonina/antagonistas & inhibidores , Receptores de Melatonina/metabolismo , Técnicas de Cultivo de Tejidos
4.
Anim Reprod Sci ; 153: 13-21, 2015 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-25578503

RESUMEN

Previously we reported increased umbilical artery blood flow in ewes supplemented with melatonin from mid- to late-pregnancy, while maternal nutrient restriction decreased uterine artery blood flow. To further unravel these responses, this study was designed to assess placental cell proliferation and vascularity following supplementation with melatonin or maternal nutrient restriction. For the first experiment, 31 primiparous ewes were supplemented with 5mg of melatonin per day (MEL) or no melatonin (CON) and allocated to receive 100% (adequate fed; ADQ) or 60% (restricted; RES) of their nutrient requirements from day 50 to 130 of gestation. To examine melatonin receptor dependent effects, a second experiment was designed utilizing 14 primiparous ewes infused with vehicle, melatonin, or luzindole (melatonin receptor 1 and 2 antagonist) from day 62 to 90 of gestation. For experiment 1, caruncle concentrations of RNA were increased in MEL-RES compared to CON-RES. Caruncle capillary area density and average capillary cross-sectional area were decreased in MEL-RES compared to CON-RES. Cotyledon vascularity was not different across dietary treatments. For experiment 2, placental cellular proliferation and vascularity were not affected by infusion treatment. In summary, melatonin interacted with nutrient restriction to alter caruncle vascularity and RNA concentrations during late pregnancy. Although melatonin receptor antagonism alters feto-placental blood flow, these receptor dependent responses were not observed in placental vascularity. Moreover, placental vascularity measures do not fully explain the alterations in uteroplacental blood flow.


Asunto(s)
Privación de Alimentos/fisiología , Fenómenos Fisiologicos Nutricionales Maternos , Melatonina/farmacología , Placenta/irrigación sanguínea , Placenta/citología , Preñez , Ovinos/fisiología , Fenómenos Fisiológicos Nutricionales de los Animales , Animales , Vasos Sanguíneos/citología , Vasos Sanguíneos/efectos de los fármacos , Restricción Calórica/veterinaria , Recuento de Células , Proliferación Celular/efectos de los fármacos , Femenino , Antagonistas de Hormonas/farmacología , Placenta/efectos de los fármacos , Embarazo , Preñez/efectos de los fármacos , Receptores de Melatonina/antagonistas & inhibidores
5.
Brain Res ; 1557: 34-42, 2014 Apr 04.
Artículo en Inglés | MEDLINE | ID: mdl-24560601

RESUMEN

Melatonin is involved in various neuronal functions such as circadian rhythmicity and thermoregulation. Melatonin has a wide range of pharmacologically effective concentration levels from the nanomolar to millimolar levels. Recently, the antiepileptic effect of high dose melatonin has been the focus of clinical studies; however, its detailed mechanism especially in relation to neurotransmitter release and synaptic transmission remains unclear. We studied the effect of melatonin at high concentrations on the neurotransmitter release by monitoring norepinephrine release in PC12 cells, and excitatory postsynaptic potential in rat hippocampal slices. Melatonin inhibits the 70mM K(+)-induced Ca(2+) increase at millimolar levels without effect on bradykinin-triggered Ca(2+) increase in PC12 cells. Melatonin (1mM) did not affect A2A adenosine receptor-evoked cAMP production, and classical melatonin receptor antagonists did not reverse the melatonin-induced inhibitory effect, suggesting G-protein coupled receptor independency. Melatonin inhibits the 70mM K(+)-induced norepinephrine release at a similar effective concentration range in PC12 cells. We confirmed that melatonin (100µM) inhibits excitatory synaptic transmission of the hippocampal Schaffer collateral pathway with the decrease in basal synaptic transmission and the increase in paired pulse ratio. These results show that melatonin inhibits neurotransmitter release through the blocking of voltage-sensitive Ca(2+) channels and suggest a possible mechanism for the antiepileptic effect of melatonin.


Asunto(s)
Bloqueadores de los Canales de Calcio/farmacología , Hipocampo/efectos de los fármacos , Melatonina/farmacología , Animales , Calcio/metabolismo , Canales de Calcio/metabolismo , AMP Cíclico/metabolismo , Estimulación Eléctrica , Potenciales Postsinápticos Excitadores/efectos de los fármacos , Células HEK293 , Hipocampo/fisiología , Humanos , Técnicas In Vitro , Potenciales de la Membrana/efectos de los fármacos , Potenciales de la Membrana/fisiología , Norepinefrina/metabolismo , Células PC12 , Técnicas de Placa-Clamp , Ratas , Ratas Sprague-Dawley , Receptor de Adenosina A2A/metabolismo , Receptores de Melatonina/agonistas , Receptores de Melatonina/antagonistas & inhibidores , Receptores de Melatonina/metabolismo , Transmisión Sináptica/efectos de los fármacos , Transmisión Sináptica/fisiología
6.
Curr Opin Psychiatry ; 26(6): 566-71, 2013 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-24060916

RESUMEN

PURPOSE OF REVIEW: The present review provides a conceptual introduction to sleep and circadian research in psychiatric illness, and discusses recent experimental and intervention findings in this area. RECENT FINDINGS: In this review, studies published since January 2011 on circadian disturbance and psychiatric illness have been summarized. SUMMARY: Exciting new results have increasingly utilized objective and validated instruments to measure the circadian system in experimental studies. Since 2011, treatment research has still predominantly utilized self-report measures as outcome variables. However, research in the treatment domain for sleep/circadian disturbances comorbid with psychiatric illness has advanced the field in its work to broaden the validation of existing sleep treatments to additional patient populations with comorbid sleep/circadian disruptions and address how to increase access to and affordability of treatment for sleep and circadian dysfunction for patients with psychiatric disorders, and how to combine psychosocial treatments with psychopharmacology to optimize treatment outcomes.


Asunto(s)
Ritmo Circadiano , Trastornos Mentales/complicaciones , Trastornos del Inicio y del Mantenimiento del Sueño/complicaciones , Antidepresivos/uso terapéutico , Humanos , Trastornos Mentales/fisiopatología , Trastornos Mentales/terapia , Psicoterapia/métodos , Receptores de Melatonina/antagonistas & inhibidores , Factores de Riesgo , Trastornos del Inicio y del Mantenimiento del Sueño/fisiopatología , Trastornos del Inicio y del Mantenimiento del Sueño/terapia , Cronoterapia de la Fase del Sueño
7.
Biol Reprod ; 89(2): 40, 2013 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-23782836

RESUMEN

Dietary melatonin supplementation from mid- to late gestation increases umbilical artery blood flow and causes disproportionate fetal growth. Melatonin receptors have been described throughout the cardiovascular system; however, there is a paucity of data on the function of placental melatonin receptors. The objectives of the current experiment were to determine fetal descending aorta blood flow, umbilical artery blood flow, and placental and fetal development following a 4-wk uterine infusion of melatonin (MEL), melatonin receptor 1 and 2 antagonist (luzindole; LUZ), or vehicle (CON) from Day 62 to Day 90 of gestation. After 4 wk of infusion, umbilical artery blood flow and umbilical artery blood flow relative to placentome weight were increased (P < 0.05) in MEL- versus CON- and LUZ-infused dams. Fetal descending aorta blood flow was increased (P < 0.05) in MEL- versus CON- and LUZ-infused dams, while fetal descending aorta blood flow relative to fetal weight was increased in MEL- versus CON-infused dams and decreased in LUZ- versus CON-infused dams. Following the 4-wk infusion, we observed an increase in placental efficiency (fetal-placentome weight ratio) in MEL- versus LUZ-infused dams. The increase in umbilical artery blood flow due to chronic uterine melatonin infusion is potentiated by an increased fetal cardiac output through the descending aorta. Moreover, melatonin receptor antagonism decreased fetal descending aorta blood flow relative to fetal weight. Therefore, melatonin receptor activation may partially mediate the observed increase in fetal blood flow following dietary melatonin supplementation.


Asunto(s)
Hemodinámica/efectos de los fármacos , Melatonina/farmacología , Placenta/efectos de los fármacos , Receptores de Melatonina/antagonistas & inhibidores , Flujo Sanguíneo Regional/efectos de los fármacos , Triptaminas/farmacología , Animales , Femenino , Feto/irrigación sanguínea , Placenta/irrigación sanguínea , Embarazo , Flujo Sanguíneo Regional/fisiología , Ovinos , Arterias Umbilicales/efectos de los fármacos , Arterias Umbilicales/fisiología , Útero/irrigación sanguínea , Útero/efectos de los fármacos
8.
J Physiol Pharmacol ; 60 Suppl 7: 47-56, 2009 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-20388945

RESUMEN

This review summarizes the involvement of centrally and peripherally applied melatonin, a major hormone of pineal gland, in the mechanism of gastric mucosal integrity, gastroprotection and ulcer healing. Melatonin was originally shown to attenuate gastric mucosal lesions but the controversy exists in the literature as to whether melatonin derived from the pineal gland, considered as the major source of this indole or rather that locally generated from L-tryptophan within gastric mucosa, plays predominant role in the mechanism of gastrointestinal integrity. Both, intragastric (i.g.) and intracerebroventricular (i.c.v.) administration of melatonin and its precursor, L-tryptophan to rats without or with removed pineal gland by pinealectomy attenuates in the dose-dependent manner the formation of on gastric lesions induced by topical irritants and water immersion restraint stress (WRS). Melatonin accelerated the gastric ulcer healing and this was accompanied by the rise in gastric blood flow (GBF), the plasma melatonin and gastrin levels, the mucosal generation of PGE(2) and luminal NO content. Pinealectomy, which suppresses the plasma melatonin levels, markedly aggravated the gastric lesions induced by WRS. Concurrent supplementation of pinealectomized animals with melatonin or L-tryptophan, the melatonin precursor, attenuated the lesions induced by WRS. Treatment with luzindole, an antagonist of Mel(2) receptors, or with L-NNA, the NO-synthase inhibitor, significantly attenuated melatonin- and L-tryptophan-induced protection and the acceleration of ulcer healing and the accompanying increase in the GBF and luminal content of NO. We conclude that 1) exogenous melatonin and that released from the L-tryptophan attenuate lesions induced by topical irritant such as ethanol and WRS via interaction with MT(2) receptors and due to an enhancement of gastric microcirculation, probably mediated by NO and PG derived from cNOS, iNOS and COX-2 overexpression and activity, and 2) the pineal gland plays an important role in the limitation of WRS-induced gastric lesions and acceleration of ulcer healing via releasing melatonin predominately at night time, that exerts gastroprotective and ulcer healing actions.


Asunto(s)
Mucosa Gástrica/fisiología , Mucosa Gástrica/fisiopatología , Tracto Gastrointestinal/fisiología , Tracto Gastrointestinal/fisiopatología , Melatonina/fisiología , Gastropatías/prevención & control , Animales , Mucosa Gástrica/irrigación sanguínea , Mucosa Gástrica/metabolismo , Tracto Gastrointestinal/irrigación sanguínea , Humanos , Peroxidación de Lípido , Melatonina/biosíntesis , Melatonina/sangre , Óxido Nítrico Sintasa/antagonistas & inhibidores , Óxido Nítrico Sintasa/metabolismo , Especificidad de Órganos , Glándula Pineal/fisiología , Prostaglandina-Endoperóxido Sintasas/metabolismo , Isoformas de Proteínas/antagonistas & inhibidores , Isoformas de Proteínas/fisiología , Receptores de Melatonina/antagonistas & inhibidores , Receptores de Melatonina/fisiología , Gastropatías/fisiopatología , Triptófano/metabolismo , Cicatrización de Heridas
9.
J Neurophysiol ; 94(2): 968-78, 2005 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-15817645

RESUMEN

To investigate the physiological effects of melatonin receptors in the Xenopus tectum, we have used the fluorescent indicator Fluo-4 AM to monitor calcium dynamics of cells in tectal slices. Bath application of KCl elicited fluorescence increases that were reduced by melatonin. This effect was stronger at the end of the light period than at the end of the dark period. Melatonin increased gamma-aminobutyric acid-C (GABA(C))-receptor activity, as demonstrated by the ability of the GABA(C)-receptor antagonists, picrotoxin and TPMPA, to abolish the effects of melatonin. In contrast, neither the GABA(A)-receptor antagonist bicuculline nor the GABA(B)-receptor antagonist CGP 35348 diminished the effects of melatonin. RT-PCR analyses revealed expression of the 3 known melatonin receptors, MT1 (Mel1(a)), MT2 (Mel1(b)), and Mel1(c). Because the effect of melatonin on tectal calcium increases was antagonized by an MT2-selective antagonist, 4-P-PDOT, we performed Western blot analyses with an antibody to the MT2 receptor; the data indicate that the MT2 receptor is expressed primarily as a dimeric complex and is glycosylated. The receptor is present in higher amounts at the end of the light period than at the end of the dark period, in a pattern complementary to the changes in melatonin levels, which are higher during the night than during the day. These results imply that melatonin, acting by MT2 receptors, modulates GABA(C) receptor activity in the optic tectum and that this effect is influenced by the light-dark cycle.


Asunto(s)
Calcio/metabolismo , Neuronas/efectos de los fármacos , Receptores de GABA-A/fisiología , Receptores de Melatonina/fisiología , Techo del Mesencéfalo/citología , Compuestos de Anilina/metabolismo , Animales , Bicuculina/farmacología , Northern Blotting/métodos , Western Blotting/métodos , Química Encefálica/efectos de los fármacos , Ritmo Circadiano/efectos de los fármacos , Ritmo Circadiano/fisiología , Diagnóstico por Imagen/métodos , Relación Dosis-Respuesta a Droga , Interacciones Farmacológicas , Agonistas del GABA/farmacología , Antagonistas del GABA/farmacología , Técnicas In Vitro , Melatonina/metabolismo , Melatonina/farmacología , Modelos Neurológicos , Neuronas/metabolismo , Neuronas/efectos de la radiación , Toxina del Pertussis/farmacología , Cloruro de Potasio/farmacología , ARN Mensajero/biosíntesis , Radioinmunoensayo/métodos , Receptores de Melatonina/agonistas , Receptores de Melatonina/antagonistas & inhibidores , Receptores de Melatonina/genética , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa/métodos , Tetrahidronaftalenos/farmacología , Xantenos/metabolismo , Xenopus laevis
10.
J Neurochem ; 90(3): 559-66, 2004 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-15255933

RESUMEN

Melatonin is the pineal hormone that acts via a pertussis toxin-sensitive G-protein to inhibit adenylate cyclase. However, the intracellular signalling effects of melatonin are not completely understood. Melatonin receptors are mainly present in the suprachiasmatic nucleus (SCN) and pars tuberalis of both humans and rats. The SCN directly controls, amongst other mechanisms, the circadian rhythm of plasma glucose concentration. In this study, using immunoprecipitation and immunoblotting, we show that melatonin induces rapid tyrosine phosphorylation and activation of the insulin receptor beta-subunit tyrosine kinase (IR) in the rat hypothalamic suprachiasmatic region. Upon IR activation, tyrosine phosphorylation of IRS-1 was detected. In addition, melatonin induced IRS-1/PI3-kinase and IRS-1/SHP-2 associations and downstream AKT serine phosphorylation and MAPK (mitogen-activated protein kinase) phosphorylation, respectively. These results not only indicate a new signal transduction pathway for melatonin, but also a potential cross-talk between melatonin and insulin.


Asunto(s)
Hipotálamo/efectos de los fármacos , Hipotálamo/metabolismo , Melatonina/farmacología , Proteínas Tirosina Quinasas/metabolismo , Animales , Relación Dosis-Respuesta a Droga , Inyecciones Intraventriculares , Insulina/farmacología , Proteínas Sustrato del Receptor de Insulina , Péptidos y Proteínas de Señalización Intracelular , Masculino , Proteína Quinasa 1 Activada por Mitógenos/efectos de los fármacos , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Fosfoproteínas/efectos de los fármacos , Fosfoproteínas/metabolismo , Fosforilación/efectos de los fármacos , Unión Proteica/efectos de los fármacos , Proteínas Serina-Treonina Quinasas/efectos de los fármacos , Proteínas Serina-Treonina Quinasas/metabolismo , Proteína Tirosina Fosfatasa no Receptora Tipo 11 , Proteínas Tirosina Fosfatasas/metabolismo , Proteínas Tirosina Quinasas/efectos de los fármacos , Proteínas Proto-Oncogénicas/efectos de los fármacos , Proteínas Proto-Oncogénicas/metabolismo , Proteínas Proto-Oncogénicas c-akt , Ratas , Ratas Wistar , Receptores de Melatonina/antagonistas & inhibidores , Receptores de Melatonina/metabolismo , Tetrahidronaftalenos/farmacología , Triptaminas/farmacología
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