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1.
Front Behav Neurosci ; 17: 1285557, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-38025390
3.
Mech Ageing Dev ; 211: 111798, 2023 04.
Artículo en Inglés | MEDLINE | ID: mdl-36907251

RESUMEN

Endocrine, nervous, and immune systems work coordinately to maintain the global homeostasis of the organism. They show sex differences in their functions that, in turn, contribute to sex differences beyond reproductive function. Females display a better control of the energetic metabolism and improved neuroprotection and have more antioxidant defenses and a better inflammatory status than males, which is associated with a more robust immune response than that of males. These differences are present from the early stages of life, being more relevant in adulthood and influencing the aging trajectory in each sex and may contribute to the different life lifespan between sexes.


Asunto(s)
Longevidad , Caracteres Sexuales , Femenino , Masculino , Humanos , Sistema Endocrino , Antioxidantes
4.
Int J Mol Sci ; 23(6)2022 Mar 14.
Artículo en Inglés | MEDLINE | ID: mdl-35328539

RESUMEN

Weight gain is a hallmark of decreased estradiol (E2) levels because of menopause or following surgical ovariectomy (OVX) at younger ages. Of note, this weight gain tends to be around the abdomen, which is frequently associated with impaired metabolic homeostasis and greater cardiovascular risk in both rodents and humans. However, the molecular underpinnings and the neuronal basis for these effects remain to be elucidated. The aim of this study is to elucidate whether the kappa-opioid receptor (k-OR) system is involved in mediating body weight changes associated with E2 withdrawal. Here, we document that body weight gain induced by OVX occurs, at least partially, in a k-OR dependent manner, by modulation of energy expenditure independently of food intake as assessed in Oprk1-/-global KO mice. These effects were also observed following central pharmacological blockade of the k-OR system using the k-OR-selective antagonist PF-04455242 in wild type mice, in which we also observed a decrease in OVX-induced weight gain associated with increased UCP1 positive immunostaining in brown adipose tissue (BAT) and browning of white adipose tissue (WAT). Remarkably, the hypothalamic mTOR pathway plays an important role in regulating weight gain and adiposity in OVX mice. These findings will help to define new therapies to manage metabolic disorders associated with low/null E2 levels based on the modulation of central k-OR signaling.


Asunto(s)
Ingestión de Alimentos , Receptores Opioides kappa , Tejido Adiposo Pardo/metabolismo , Animales , Peso Corporal , Metabolismo Energético , Estrógenos/metabolismo , Femenino , Humanos , Ratones , Obesidad/tratamiento farmacológico , Obesidad/etiología , Obesidad/metabolismo , Ovariectomía/efectos adversos , Receptores Opioides kappa/metabolismo , Serina-Treonina Quinasas TOR/metabolismo , Aumento de Peso
5.
Artículo en Inglés | MEDLINE | ID: mdl-34202073

RESUMEN

Eating behaviour is characterised by a solid balance between homeostatic and hedonic regulatory mechanisms at the central level and highly influenced by peripheral signals. Among these signals, those generated by the gut microbiota have achieved relevance in recent years. Despite this complex regulation, under certain circumstances eating behaviour can be deregulated becoming addictive. Although there is still an ongoing debate about the food addiction concept, studies agree that patients with eating addictive behaviour present similar symptoms to those experienced by drug addicts, by affecting central areas involved in the control of motivated behaviour. In this context, this review tries to summarise the main data regarding the role of the gut microbiome in eating behaviour and how a gut dysbiosis can be responsible for a maladaptive behaviour such as "food addiction".


Asunto(s)
Conducta Adictiva , Adicción a la Comida , Microbioma Gastrointestinal , Disbiosis , Conducta Alimentaria , Humanos , Obesidad
6.
Cell Rep ; 34(11): 108851, 2021 03 16.
Artículo en Inglés | MEDLINE | ID: mdl-33730574

RESUMEN

Devil facial tumor disease (DFTD) and its lack of available therapies are propelling the Tasmanian devil population toward extinction. This study demonstrates that cholesterol homeostasis and carbohydrate energy metabolism sustain the proliferation of DFTD cells in a cell-type-dependent manner. In addition, we show that the liver-X nuclear receptor-ß (LXRß), a major cholesterol cellular sensor, and its natural ligand 24S-hydroxycholesterol promote the proliferation of DFTD cells via a metabolic switch toward aerobic glycolysis. As a proof of concept of the role of cholesterol homeostasis on DFTD proliferation, we show that atorvastatin, an FDA-approved statin-drug subtype used against human cardiovascular diseases that inhibits cholesterol synthesis, shuts down DFTD energy metabolism and prevents tumor growth in an in vivo DFTD-xenograft model. In conclusion, we show that intervention against cholesterol homeostasis and carbohydrate-dependent energy metabolism by atorvastatin constitutes a feasible biochemical treatment against DFTD, which may assist in the conservation of the Tasmanian devil.


Asunto(s)
Colesterol/metabolismo , Neoplasias Faciales/metabolismo , Neoplasias Faciales/veterinaria , Homeostasis , Inhibidores de Hidroximetilglutaril-CoA Reductasas/farmacología , Receptores X del Hígado/metabolismo , Marsupiales/metabolismo , Aerobiosis/efectos de los fármacos , Animales , Atorvastatina/farmacología , Proliferación Celular/efectos de los fármacos , Neoplasias Faciales/patología , Femenino , Glucólisis/efectos de los fármacos , Humanos , Ratones Endogámicos BALB C , Ratones Desnudos , Oxiesteroles/farmacología , Transducción de Señal/efectos de los fármacos , Ensayos Antitumor por Modelo de Xenoinjerto
7.
iScience ; 24(2): 102071, 2021 Feb 19.
Artículo en Inglés | MEDLINE | ID: mdl-33554072

RESUMEN

Excessive consumption of high-fructose diets is associated with insulin resistance, obesity, and non-alcoholic fatty liver disease (NAFLD). However, fructose differentially affects hepatic regulation of lipogenesis in males and females. Hence, additional studies are necessary in order to find strategies taking gender disparities in fructose-induced liver damage into consideration. Although the eighth member of facilitated glucose transporters (GLUT8) has been linked to fructose-induced macrosteatosis in female mice, its contribution to the inflammatory state of NAFLD remains to be elucidated. Combining pharmacological, biochemical, and proteomic approaches, we evaluated the preventive effect of targeted liver GLUT8 silencing on liver injury in a mice female fructose-induced non-alcoholic steatohepatitis female mouse model. Liver GLUT8-knockdown attenuated fructose-induced ER stress, recovered liver inflammation, and dramatically reduced fatty acid content, in part, via the omega oxidation. Therefore, this study links GLUT8 with liver inflammatory response and suggests GLUT8 as a potential target for the prevention of NAFLD.

8.
Int J Mol Sci ; 21(24)2020 Dec 09.
Artículo en Inglés | MEDLINE | ID: mdl-33316927

RESUMEN

Since its discovery twenty-five years ago, the fat-derived hormone leptin has provided a revolutionary framework for studying the physiological role of adipose tissue as an endocrine organ. Leptin exerts pleiotropic effects on many metabolic pathways and is tightly connected with the liver, the major player in systemic metabolism. As a consequence, understanding the metabolic and hormonal interplay between the liver and adipose tissue could provide us with new therapeutic targets for some chronic liver diseases, an increasing problem worldwide. In this review, we assess relevant literature regarding the main metabolic effects of leptin on the liver, by direct regulation or through the central nervous system (CNS). We draw special attention to the contribution of leptin to the non-alcoholic fatty liver disease (NAFLD) pathogenesis and its progression to more advanced stages of the disease as non-alcoholic steatohepatitis (NASH). Likewise, we describe the contribution of leptin to the liver regeneration process after partial hepatectomy, the mainstay of treatment for certain hepatic malignant tumors.


Asunto(s)
Leptina/metabolismo , Regeneración Hepática , Hígado/metabolismo , Enfermedad del Hígado Graso no Alcohólico/metabolismo , Tejido Adiposo/metabolismo , Animales , Humanos , Hígado/fisiología
9.
Cells ; 9(9)2020 08 21.
Artículo en Inglés | MEDLINE | ID: mdl-32839401

RESUMEN

GH (growth hormone) secretion/action is modulated by alterations in energy homeostasis, such as malnutrition and obesity. Recent data have uncovered the mechanism by which hypothalamic neurons sense nutrient bioavailability, with a relevant contribution of AMPK (AMP-activated protein kinase) and mTOR (mammalian Target of Rapamycin), as sensors of cellular energy status. However, whether central AMPK-mediated lipid signaling and mTOR participate in the regulation of pituitary GH secretion remains unexplored. We provide herein evidence for the involvement of hypothalamic AMPK signaling, but not hypothalamic lipid metabolism or CPT-1 (carnitine palmitoyltransferase I) activity, in the regulation of GH stimulatory responses to the two major elicitors of GH release in vivo, namely GHRH (growth hormone-releasing hormone) and ghrelin. This effect appeared to be GH-specific, as blocking of hypothalamic AMPK failed to influence GnRH (gonadotropin-releasing hormone)-induced LH (luteinizing hormone) secretion. Additionally, central mTOR inactivation did not alter GH responses to GHRH or ghrelin, nor this blockade affected LH responses to GnRH in vivo. In sum, we document here for the first time the indispensable and specific role of preserved central AMPK, but not mTOR, signaling, through a non-canonical lipid signaling pathway, for proper GH responses to GHRH and ghrelin in vivo.


Asunto(s)
Proteínas Quinasas Activadas por AMP/metabolismo , Ghrelina/metabolismo , Hormona Liberadora de Hormona del Crecimiento/metabolismo , Animales , Humanos , Masculino , Ratas , Ratas Sprague-Dawley , Transducción de Señal
10.
Mol Cell Endocrinol ; 497: 110508, 2019 11 01.
Artículo en Inglés | MEDLINE | ID: mdl-31319096

RESUMEN

In an obesity pandemic context, eating disorders (ED) have arisen as serious illnesses associated with severe disturbances and has a clear gender dependent bias. In this manuscript, we provide an overview of the oestrogen role in the homeostatic and hedonic control of food intake. We draw attention to the role of oestrogens in the various reward processes and their possible implication in the development of ED, a condition much more common in women. In here, we have summarized the most relevant studies conducted in animal models over the last few years. In particular, we want to emphasize on the importance of continuing thorough investigations in female animal models. We believe that understanding the molecular mechanisms that regulate gender differences in food intake may provide new potential targets for ED treatment.


Asunto(s)
Trastorno por Atracón/fisiopatología , Conducta Alimentaria/fisiología , Homeostasis , Filosofía , Caracteres Sexuales , Metabolismo Energético , Femenino , Humanos , Masculino
11.
Eur Eat Disord Rev ; 26(6): 551-568, 2018 11.
Artículo en Inglés | MEDLINE | ID: mdl-30280451

RESUMEN

Central and peripheral signals regulating energy homeostasis interact tightly with neuronal pathways to modulate the hedonic component of food intake. Dysregulation of these interactions could explain the development of binge eating disorder (BED) and/or obesity and the increasing incidence of food addiction. In this review, we have highlighted the crucial role of peripheral hormones, such as leptin and ghrelin, among others, in these nonhomeostatic pathways. We have also emphasised the relevance of central cannabinoid pathway and lateral hypothalamus, with orexin and melanin-concentrating hormone neurons, as the critical hub controlling motivation and reward. Throughout the manuscript, we have focused on mechanisms learned from animal models of BED/food addiction in order to understand how these peripheral signals can modulate the motivation to eat. Understanding these mechanisms could help us to develop new treatment options for BED and/or obesity.


Asunto(s)
Adipoquinas/fisiología , Tracto Gastrointestinal/fisiología , Homeostasis/fisiología , Transducción de Señal/fisiología , Animales , Trastorno por Atracón/fisiopatología , Modelos Animales de Enfermedad , Ingestión de Alimentos/fisiología
12.
Nutrients ; 10(1)2018 Jan 11.
Artículo en Inglés | MEDLINE | ID: mdl-29324652

RESUMEN

The feeding process is required for basic life, influenced by environment cues and tightly regulated according to demands of the internal milieu by regulatory brain circuits. Although eating behaviour cannot be considered "addictive" under normal circumstances, people can become "addicted" to this behaviour, similarly to how some people are addicted to drugs. The symptoms, cravings and causes of "eating addiction" are remarkably similar to those experienced by drug addicts, and both drug-seeking behaviour as eating addiction share the same neural pathways. However, while the drug addiction process has been highly characterised, eating addiction is a nascent field. In fact, there is still a great controversy over the concept of "food addiction". This review aims to summarize the most relevant animal models of "eating addictive behaviour", emphasising binge eating disorder, that could help us to understand the neurobiological mechanisms hidden under this behaviour, and to improve the psychotherapy and pharmacological treatment in patients suffering from these pathologies.


Asunto(s)
Conducta Animal , Bulimia/psicología , Conducta Alimentaria , Adicción a la Comida/psicología , Animales , Encéfalo/metabolismo , Encéfalo/fisiopatología , Bulimia/genética , Bulimia/metabolismo , Bulimia/fisiopatología , Señales (Psicología) , Modelos Animales de Enfermedad , Dopamina/metabolismo , Ambiente , Adicción a la Comida/genética , Adicción a la Comida/metabolismo , Adicción a la Comida/fisiopatología , Predisposición Genética a la Enfermedad , Humanos , Vías Nerviosas/metabolismo , Vías Nerviosas/fisiopatología , Péptidos Opioides/metabolismo , Factores de Riesgo , Transducción de Señal
13.
Sci Rep ; 7: 46194, 2017 04 07.
Artículo en Inglés | MEDLINE | ID: mdl-28387334

RESUMEN

During their lifetime, females are subjected to different nutritional and hormonal factors that could increase the risk of obesity and associated comorbidities. From early postnatal periods until the postmenopausal phase, exposure to over nutrition, high-energy diet and oestrogen deficiency, are considered as significant obesity risk factors in women. In this study, we assessed how key transitional life events and exposure to different nutrition influence energy homeostasis in a rat model. Specifically, we assessed the sequential exposure to postnatal over nutrition, high-fat diet (HFD) after weaning, followed later by ovariectomy (OVX; as a model of menopause). Each obesity risk factor increased significantly body weight (BW) and adiposity, with additive effects after sequential exposure. Increased energy intake in both HFD and/or OVX groups, and decreased locomotor activity and energy expenditure after OVX can explain these metabolic changes. Our study also documents decreased lipogenic pathway in mesenteric adipose tissue after HFD and/or OVX, independent of previous postnatal programming, yet only HFD evoked this effect in liver. In addition, we report an increase in the expression of the hepatic PEPCK depending on previous metabolic status. Overall, our results identify the impact of different risk factors, which will help in understanding the development of obesity in females.


Asunto(s)
Tejido Adiposo/metabolismo , Metabolismo de los Lípidos , Hígado/metabolismo , Obesidad/etiología , Obesidad/metabolismo , Animales , Composición Corporal , Dieta Alta en Grasa , Modelos Animales de Enfermedad , Ingestión de Energía , Metabolismo Energético , Femenino , Locomoción , Mesenterio , Ovariectomía , Fenotipo , Ratas , Factores de Riesgo , Factores Sexuales
14.
Cold Spring Harb Perspect Med ; 6(3): a025932, 2016 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-26931809

RESUMEN

Even though the inevitable process of aging by itself cannot be considered a disease, it is directly linked to life span and is the driving force behind all age-related diseases. It is an undisputable fact that age-associated diseases are among the leading causes of death in the world, primarily in industrialized countries. During the last several years, an intensive search of antiaging treatments has led to the discovery of a variety of drugs that promote health span and/or life extension. The biguanide compound metformin is widely used for treating people with type 2 diabetes and appears to show protection against cancer, inflammation, and age-related pathologies. Here, we summarize the recent developments about metformin use in translational aging research and discuss its role as a potential geroprotector.


Asunto(s)
Envejecimiento/efectos de los fármacos , Metformina/uso terapéutico , Envejecimiento/fisiología , Humanos , Esperanza de Vida , Investigación Biomédica Traslacional
15.
Aging (Albany NY) ; 7(4): 233-40, 2015 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-25948793

RESUMEN

Caloric restriction (CR) without malnutrition is one of the most consistent strategies for increasing mean and maximal lifespan and delaying the onset of age-associated diseases. Stress resistance is a common trait of many long-lived mutants and life-extending interventions, including CR. Indeed, better protection against heat shock and other genotoxic insults have helped explain the pro-survival properties of CR. In this study, both in vitro and in vivo responses to heat shock were investigated using two different models of CR. Murine B16F10 melanoma cells treated with serum from CR-fed rats showed lower proliferation, increased tolerance to heat shock and enhanced HSP-70 expression, compared to serum from ad libitum-fed animals. Similar effects were observed in B16F10 cells implanted subcutaneously in male C57BL/6 mice subjected to CR. Microarray analysis identified a number of genes and pathways whose expression profile were similar in both models. These results suggest that the use of an in vitro model could be a good alternative to study the mechanisms by which CR exerts its anti-tumorigenic effects.


Asunto(s)
Restricción Calórica , Carcinogénesis/metabolismo , Proteínas HSP70 de Choque Térmico/metabolismo , Respuesta al Choque Térmico/fisiología , Animales , Carcinogénesis/patología , Línea Celular Tumoral , Proliferación Celular/fisiología , Ingestión de Energía/fisiología , Masculino , Ratones , Ratas
16.
Ageing Res Rev ; 21: 1-15, 2015 May.
Artículo en Inglés | MEDLINE | ID: mdl-25625901

RESUMEN

Pre-clinical findings have provided mounting evidence that resveratrol, a dietary polyphenol, may confer health benefits and protect against a variety of medical conditions and age-related complications. However, there is no consistent evidence of an increased protection against metabolic disorders and other ailments when comparing studies in laboratory animals and humans. A number of extraneous and potential confounding variables can affect the outcome of clinical research. To date, most of the studies that have investigated the effect of resveratrol administration on patient outcomes have been limited by their sample sizes. In this review, we will survey the latest advances regarding the timing, dosage, formulation, bioavailability, toxicity of resveratrol, and resveratrol-drug interactions in human studies. Moreover, the present report focuses on the actions of resveratrol treatment in combating diseases, such as cancer, diabetes, neurodegeneration, cardiovascular disease, and other age-related ailments.


Asunto(s)
Antiinflamatorios no Esteroideos/uso terapéutico , Enfermedad Crónica/tratamiento farmacológico , Suplementos Dietéticos , Estilbenos/uso terapéutico , Envejecimiento/efectos de los fármacos , Animales , Antiinflamatorios no Esteroideos/metabolismo , Antiinflamatorios no Esteroideos/farmacología , Ensayos Clínicos como Asunto , Suplementos Dietéticos/efectos adversos , Ejercicio Físico , Humanos , Resveratrol , Estilbenos/metabolismo , Estilbenos/farmacología
17.
Sci Rep ; 4: 4855, 2014 May 06.
Artículo en Inglés | MEDLINE | ID: mdl-24798184

RESUMEN

It is currently accepted that ambient, non-genetic factors influence perinatal development and evoke structural and functional changes that may persist throughout life. Overfeeding and androgenization after birth are two of these key factors that could result in "metabolic imprinting" of neuronal circuits early in life and, thereby, increase the body weight homeostatic "set point", stimulate appetite, and result in obesity. Our aim was to determine the influence of these obesogenic factors on the response to ghrelin. We observed the expected orexigenic effect of ghrelin regardless of the nutritional or hormonal manipulations to which the animals were subjected to at early postnatal development and this effect remained intact at later stages of development. In fact, ghrelin responses increased significantly when the animals were subjected to one of the two manipulations, but not when both were combined. An increased response to ghrelin could explain the obese phenotype displayed by individuals with modified perinatal environment.


Asunto(s)
Animales Recién Nacidos/metabolismo , Animales Recién Nacidos/fisiología , Ingestión de Alimentos/fisiología , Ghrelina/metabolismo , Virilismo/fisiopatología , Animales , Apetito/fisiología , Peso Corporal/fisiología , Femenino , Obesidad/metabolismo , Obesidad/fisiopatología , Atención Posnatal/métodos , Ratas , Ratas Sprague-Dawley , Virilismo/metabolismo
18.
Diabetes Care ; 37(4): 1092-100, 2014 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-24496804

RESUMEN

OBJECTIVE Circulating markers of iron overload are associated with insulin resistance. Less is known about the impact of iron overload on adipose tissue (AT). We hypothesized that gene expression markers of iron metabolism in AT could be associated with insulin action. RESEARCH DESIGN AND METHODS The AT expression of ferroportin (SLC40A1), transferrin (TF), TF receptor (TFRC), ferritin (FT) heavy polypeptide 1 (FTH1), and FT light polypeptide (FTL) was analyzed cross-sectionally in three independent cohorts and also after weight loss-induced changes in insulin sensitivity (clamp M value) in an independent fourth cohort. RESULTS In human AT, TF mRNA and protein levels were decreased with obesity and insulin resistance in the three cohorts and were positively associated with adipogenic mRNAs and insulin action. Otherwise, FTL mRNA and protein and SLC40A1 transcripts were positively associated with BMI and negatively linked to adipogenic genes and insulin action. Bariatric surgery-induced weight loss led to increased TF and decreased TFRC, FTH1, FTL, and SLC40A1 in subcutaneous AT in parallel to improved insulin action. CONCLUSIONS These results suggest that iron overload impacts on AT in association with insulin resistance.


Asunto(s)
Resistencia a la Insulina , Proteínas de Unión a Hierro/metabolismo , Receptores de Transferrina/metabolismo , Grasa Subcutánea/metabolismo , Pérdida de Peso , Adulto , Cirugía Bariátrica , Estudios de Cohortes , Estudios Transversales , Humanos , Insulina/metabolismo , Insulina/farmacología , Masculino , Persona de Mediana Edad
19.
Int J Endocrinol ; 2013: 746281, 2013.
Artículo en Inglés | MEDLINE | ID: mdl-24298283

RESUMEN

In January 2012, Boström and colleagues identified a new muscle tissue secreted peptide, which they named irisin, to highlight its role as a messenger that comes from skeletal muscle to other parts of the body. Irisin is a cleaved and secreted fragment of FNDC5 (also known as FRCP2 and PeP), a member of fibronectin type III repeat containing gene family. Major interest in this protein arose because of its great therapeutic potential in diabetes and perhaps also therapy for obesity. Here we review the most important aspects of irisin's action and discuss its involvement in energy and metabolic homeostasis and whether the beneficial effects of exercise in these disease states could be mediated by this protein. In addition the effects of irisin at the central nervous system (CNS) are highlighted. It is concluded that although current and upcoming research on irisin is very promising it is still necessary to deepen in several aspects in order to clarify its full potential as a meaningful drug target in human disease states.

20.
Psychopharmacology (Berl) ; 229(2): 275-83, 2013 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-23624808

RESUMEN

OBJECTIVE: Recent evidence suggests that ghrelin, a peptidic hormone stimulating food intake, interacts with the dopamine signaling. This interaction has been demonstrated to modulate several effects of ghrelin, such as locomotor activity, memory, and food intake. Ghrelin increases dopamine levels in the shell of the nucleus accumbens stimulating food intake, while ablation of the ghrelin receptor attenuates the hypophagia caused by the activation of dopamine receptor 2. However, it is not known whether the orexigenic action of ghrelin is due to changes in central dopamine receptors. MATERIALS AND METHODS: We used Sprague-Dawley rats injected with different dopamine receptor agonists, antagonists, and ghrelin. RESULTS: We demonstrate that the specific central blockade of dopamine receptor 1, 2, and 3 (D1, D2, and D3, respectively) reduces the orexigenic action of ghrelin. Similarly, specific central stimulation, either singly of dopamine receptor 1 or dopamine receptors 2 and 3 simultaneously, causes a significant decrease in ghrelin-induced food intake. Co-stimulation of all three receptors (D1, D2, and D3) also led to a marked attenuation in ghrelin-induced food intake. Importantly, the reduction in ghrelin-induced feeding was not caused by malaise or any type of behavioral alteration. CONCLUSION: Taken together, these data indicate that dopamine receptors play an important role in acute stimulation of feeding behavior induced by central injection of ghrelin.


Asunto(s)
Ingestión de Alimentos/efectos de los fármacos , Ghrelina/farmacología , Receptores Dopaminérgicos/metabolismo , Análisis de Varianza , Animales , Reacción de Prevención/efectos de los fármacos , Dopaminérgicos/farmacología , Relación Dosis-Respuesta a Droga , Vías de Administración de Medicamentos , Interacciones Farmacológicas , Inyecciones Intraventriculares , Actividad Motora/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Gusto/efectos de los fármacos , Factores de Tiempo
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