RESUMO
The neuroendocrine system of crustaceans is complex and regulates many processes, such as development, growth, reproduction, osmoregulation, behavior, and metabolism. Once stimulated, crustaceans' neuroendocrine tissues modulate the release of monoamines, ecdysteroids, and neuropeptides that can act as hormones or neurotransmitters. Over a few decades, research has unraveled some mechanisms governing these processes, substantially contributing to understanding crustacean physiology. More aspects of crustacean neuroendocrinology are being comprehended with molecular biology, transcriptome, and genomics analyses. Hence, these studies will also significantly enhance the ability to cultivate decapods, such as crabs and shrimps, used as human food sources. In this review, current knowledge on crustacean endocrinology is updated with new findings about crustacean hormones, focusing mainly on the main neuroendocrine organs and their hormones and the effects of these molecules regulating metabolism, growth, reproduction, and color adaptation. New evidence about vertebrate-type hormones found in crustaceans is included and discussed. Finally, this review may assist in understanding how the emerging chemicals of environmental concern can potentially impair and disrupt crustacean's endocrine functions and their physiology.
Assuntos
Crustáceos , Sistemas Neurossecretores , Animais , Crustáceos/fisiologia , Crustáceos/metabolismo , Neuropeptídeos/metabolismo , Sistemas Neurossecretores/fisiologia , Sistemas Neurossecretores/metabolismo , Reprodução/fisiologiaRESUMO
Exploring the relationship between exercise inflammation and the peripheral neuroendocrine system is essential for understanding how acute or repetitive bouts of exercise can contribute to skeletal muscle adaption. In severe damage, some evidence demonstrates that peripheral neuroendocrine receptors might contribute to inflammatory resolution, supporting the muscle healing process through myogenesis. In this sense, the current study aimed to evaluate two classic peripheral neuronal receptors along with skeletal muscle inflammation and adaptation parameters in triceps brachii after exercise. We euthanized C57BL (10 to 12 weeks old) male mice before, and one, two, and three days after a downhill running protocol. The positive Ly6C cells, along with interleukin-6 (IL-6), nuclear factor kappa B (NF-κB), glucocorticoid receptor (GR), α7 subunits of the nicotinic acetylcholine receptor (nAChRs), and myonuclei accretion were analyzed. Our main results demonstrated that nAChRs increased with the inflammatory and myonuclei accretion responses regardless of NF-κB and GR protein expression. These results indicate that increased nAChR may contribute to skeletal muscle adaption after downhill running in mice.
Assuntos
Inflamação/fisiopatologia , Sistemas Neurossecretores/fisiopatologia , Condicionamento Físico Animal/fisiologia , Corrida/fisiologia , Animais , Inflamação/metabolismo , Interleucina-6/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Músculo Esquelético/metabolismo , Músculo Esquelético/fisiopatologia , NF-kappa B/metabolismo , Sistemas Neurossecretores/metabolismo , Receptores de Glucocorticoides/metabolismo , Receptores Nicotínicos/metabolismoRESUMO
Here, we report the participation of N-methyl-D-aspartate (NMDA) glutamate receptor in the mediation of cardiovascular and circulating vasopressin responses evoked by a hemorrhagic stimulus. In addition, once NMDA receptor activation is a prominent mechanism involved in nitric oxide (NO) synthesis in the brain, we investigated whether control of hemorrhagic shock by NMDA glutamate receptor was followed by changes in NO synthesis in brain supramedullary structures involved in cardiovascular and neuroendocrine control. Thus, we observed that intraperitoneal administration of the selective NMDA glutamate receptor antagonist dizocilpine maleate (MK801, 0.3 mg/kg) delayed and reduced the magnitude of hemorrhage-induced hypotension. Besides, hemorrhage induced a tachycardia response in the posthemorrhage period (i.e., recovery period) in control animals, and systemic treatment with MK801 caused a bradycardia response during hemorrhagic shock. Hemorrhagic stimulus increased plasma vasopressin levels during the recovery period and NMDA receptor antagonism increased concentration of this hormone during both the hemorrhage and postbleeding periods in relation to control animals. Moreover, hemorrhagic shock caused a decrease in NOx levels in the paraventricular nucleus of the hypothalamus (PVN), amygdala, bed nucleus of the stria terminalis (BNST), and ventral periaqueductal gray matter (vPAG). Nevertheless, treatment with MK801 did not affect these effects. Taken together, these results indicate that the NMDA glutamate receptor is involved in the hemorrhagic shock by inhibiting circulating vasopressin release. Our data also suggest a role of the NMDA receptor in tachycardia, but not in the decreased NO synthesis in the brain evoked by hemorrhage.
Assuntos
Bradicardia/induzido quimicamente , Sistema Cardiovascular/metabolismo , Maleato de Dizocilpina/administração & dosagem , Choque Hemorrágico/metabolismo , Vasopressinas/sangue , Animais , Bradicardia/sangue , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Sistema Cardiovascular/efeitos dos fármacos , Modelos Animais de Doenças , Maleato de Dizocilpina/efeitos adversos , Injeções Intraperitoneais , Masculino , Sistemas Neurossecretores/efeitos dos fármacos , Sistemas Neurossecretores/metabolismo , Óxido Nítrico/metabolismo , Ratos , Ratos Wistar , Receptores de N-Metil-D-Aspartato/antagonistas & inibidores , Receptores de N-Metil-D-Aspartato/metabolismoRESUMO
The Wistar audiogenic rat (WAR) strain is used as an animal model of epilepsy, which when submitted to acute acoustic stimulus presents tonic-clonic seizures, mainly dependent on brainstem (mesencephalic) structures. However, when WARs are exposed to chronic acoustic stimuli (audiogenic kindling-AK), they usually present tonic-clonic seizures, followed by limbic seizures, after recruitment of forebrain structures such as the cortex, hippocampus and amygdala. Although some studies have reported that hypothalamic-hypophysis function is also altered in WAR through modulating vasopressin (AVP) and oxytocin (OXT) secretion, the role of these neuropeptides in epilepsy still is controversial. We analyzed the impact of AK and consequent activation of mesencephalic neurocircuits and the recruitment of forebrain limbic (LiR) sites on the hypothalamic-neurohypophysial system and expression of Avpr1a and Oxtr in these structures. At the end of the AK protocol, nine out of 18 WARs presented LiR. Increases in both plasma vasopressin and oxytocin levels were observed in WAR when compared to Wistar rats. These results were correlated with an increase in the expressions of heteronuclear (hn) and messenger (m) RNA for Oxt in the paraventricular nucleus (PVN) in WARs submitted to AK that presented LiR. In the paraventricular nucleus, the hnAvp and mAvp expressions increased in WARs with and without LiR, respectively. There were no significant differences in Avp and Oxt expression in supraoptic nuclei (SON). Also, there was a reduction in the Avpr1a expression in the central nucleus of the amygdala and frontal lobe in the WAR strain. In the inferior colliculus, Avpr1a expression was lower in WARs after AK, especially those without LiR. Our results indicate that both AK and LiR in WARs lead to changes in the hypothalamic-neurohypophysial system and its receptors, providing a new molecular basis to better understaind epilepsy.
Assuntos
Epilepsia Reflexa , Hipotálamo/metabolismo , Excitação Neurológica/fisiologia , Sistemas Neurossecretores/metabolismo , Neuro-Hipófise/metabolismo , Estimulação Acústica , Animais , Modelos Animais de Doenças , Epilepsia Reflexa/genética , Epilepsia Reflexa/metabolismo , Epilepsia Reflexa/patologia , Epilepsia Reflexa/fisiopatologia , Regulação da Expressão Gênica , Hipocampo/metabolismo , Hipocampo/patologia , Hipocampo/fisiopatologia , Hipotálamo/patologia , Hipotálamo/fisiopatologia , Excitação Neurológica/patologia , Masculino , Sistemas Neurossecretores/patologia , Sistemas Neurossecretores/fisiopatologia , Ocitocina/sangue , Ocitocina/genética , Ocitocina/metabolismo , Neuro-Hipófise/patologia , Neuro-Hipófise/fisiopatologia , Ratos , Ratos Wistar , Convulsões/genética , Convulsões/metabolismo , Convulsões/fisiopatologia , Convulsões/psicologia , Vasopressinas/sangue , Vasopressinas/genética , Vasopressinas/metabolismoRESUMO
Sepsis promotes an inflammatory state in the central nervous system (CNS) that may cause autonomic, cognitive, and endocrine changes. Microglia, a resident immune cell of the CNS, is activated in several brain regions during sepsis, suggesting its participation in the central alterations observed in this disease. In this study, we aimed to investigate the role of microglial activation in the neuroendocrine system functions during systemic inflammation. Wistar rats received an intracerebroventricular injection of the microglial activation inhibitor minocycline (100 µg/animal), shortly before sepsis induction by cecal ligation and puncture. At 6 and 24 h after surgery, hormonal parameters, central and peripheral inflammation, and markers of apoptosis and synaptic function in the hypothalamus were analyzed. The administration of minocycline decreased the production of inflammatory mediators and the expression of cell death markers, especially in the late phase of sepsis (24 h). With respect to the endocrine parameters, microglial inhibition caused a decrease in oxytocin and an increase in corticosterone and vasopressin plasma levels in the early phase of sepsis (6 h), while in the late phase, we observed decreased oxytocin and increased ACTH and corticosterone levels compared to septic animals that did not receive minocycline. Prolactin levels were not affected by minocycline administration. The results indicate that microglial activation differentially modulates the secretion of several hormones and that this process is associated with inflammatory mediators produced both centrally and peripherally.
Assuntos
Corticosterona/sangue , Microglia/metabolismo , Ocitocina/sangue , Sepse/metabolismo , Vasopressinas/sangue , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Modelos Animais de Doenças , Masculino , Microglia/efeitos dos fármacos , Minociclina/farmacologia , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Sistemas Neurossecretores/metabolismo , Ratos , Ratos WistarRESUMO
Stress is a condition that maintains the homeostasis of the organism through the activation of different neuroendocrine pathways and secretion of a wide array of chemical mediators, including corticotropin-releasing hormone (CRH), neurotransmitters and glucocorticoids hormones. These molecules fulfill important physiological functions, but under stressful conditions, they can induce or aggravate a pathological state depending on type, severity and duration of stress. For this reason, the search for compounds that modulate the activity of the neuroendocrine pathways is crucial for the control of diseases associated with stressful situations. Bovine lactoferrin (bLf) is an iron-binding multifunctional glycoprotein that exhibits modulatory properties on the neuroendocrine system. Bovine lactoferrin affects the production and secretion of neuroendocrine components of the hypothalamus-pituitary-adrenal (HPA) axis. Neuroendocrine mechanisms of bLf entail either the down- or up-modulation of adrenal corticosteroids via HPA pathway activation, nitric oxide (NO) generation and opioid nervous system pathway activation. This manuscript is focused on reviewing the current contributions of bLf modulatory actions on the response of hormones, neurotransmitters involved in stress and behavior. Sustained use of drugs for stress-associated dysfunctions loses efficacy and requires the dose increase by tolerance and drug dependence. Therefore, bLf may be included as a therapeutic and/or adjunctive agent of drugbased therapies for the treatment of stress-associated emotional-disturbances.
Assuntos
Lactoferrina , Estresse Fisiológico , Sistema Hipotálamo-Hipofisário/metabolismo , Lactoferrina/metabolismo , Sistemas Neurossecretores/metabolismo , Sistema Hipófise-Suprarrenal/metabolismoRESUMO
The hypothalamic neuropeptides of the vasopressin-oxytocin family (and their homologs for non-mammalian species) are key modulators of the Social Brain Network, acting via specific receptors reported in all the nuclei of this network. Different conclusive examples have proven the context-dependency actions of hypothalamic nonapeptides on social behavior in several vertebrate taxa. Teleost fishes provide endless possibilities of experimental model systems to explore the underlying mechanisms of nonapeptide actions on social behavior given that they are the most diverse group of vertebrates. Although it has been difficult to identify commonalities of nonapeptide actions across species, indisputable evidence in many teleost species have demonstrated a clear role of vasotocin in the modulation of aggressive and sexual behaviors. Though Neotropical South American fish contribute an important percentage of teleost diversity, most native species remain unexplored as model systems for the study of the neuroendocrine bases of social behavior. In this review, we will revise recent data on the two model systems of Neotropical fish, South American cichlids and weakly electric fish that have contributed to this issue.
Assuntos
Comportamento Agonístico/efeitos dos fármacos , Peixes/fisiologia , Vasotocina/farmacologia , Animais , Modelos Biológicos , Sistemas Neurossecretores/metabolismo , Comportamento SocialRESUMO
Many diseases result from programming effects in utero. This chapter describes recent advances in proteomic studies which have improved our understanding of the underlying pathophysiological pathways in the major psychiatric disorders, resulting in the development of potential novel biomarker tests. Such tests should be based on measurement of blood-based proteins given the ease of accessibility of this medium and the known connections between the periphery and the central nervous system. Most importantly, emerging biomarker tests should be developed on lab-on-a-chip and other handheld devices to enable point-of-care use. This should help to identify individuals with psychiatric disorders much sooner than ever before, which will allow more rapid treatment options for the best possible patient outcomes.
Assuntos
Transtornos Mentais/metabolismo , Proteoma , Proteômica , Animais , Biomarcadores , Encéfalo/metabolismo , Humanos , Imunoensaio/métodos , Dispositivos Lab-On-A-Chip , Espectrometria de Massas , Transtornos Mentais/diagnóstico , Transtornos Mentais/psicologia , Sistemas Neurossecretores/metabolismo , Nervos Periféricos/metabolismo , Proteômica/métodosRESUMO
Activation of the hypothalamic-pituitary-adrenal axis (HPA) is critical for survival when the organism is exposed to a stressful stimulus. The endocannabinoid system (ECS) is currently considered an important neuromodulator involved in numerous pathophysiological processes and whose primary function is to maintain homeostasis. In the tissues constituting the HPA axis, all the components of the ECS are present and the activation of this system acts in parallel with changes in the activity of numerous neurotransmitters, including nitric oxide (NO). NO is widely distributed in the brain and adrenal glands and recent studies have shown that free radicals, and in particular NO, may play a crucial role in the regulation of stress response. Our objective was to determine the participation of the endocannabinoid and NOergic systems as probable mediators of the neuroendocrine HPA axis response to a psychophysical acute stress model in the adult male rat. Animals were pre-treated with cannabinoid receptors agonists and antagonists at central and systemic level prior to acute restraint exposure. We also performed in vitro studies incubating adrenal glands in the presence of ACTH and pharmacological compounds that modifies ECS components. Our results showed that the increase in corticosterone observed after acute restraint stress is blocked by anandamide administered at both central and peripheral level. At hypothalamic level both cannabinoid receptors (CB1 and CB2) are involved, while in the adrenal gland, anandamide has a very potent effect in suppressing ACTH-induced corticosterone release that is mainly mediated by vanilloid TRPV1 receptors. We also observed that stress significantly increased hypothalamic mRNA levels of CB1 as well as adrenal mRNA levels of TRPV1 receptor. In addition, anandamide reduced the activity of the nitric oxide synthase enzyme during stress, indicating that the anti-stress action of endocannabinoids may involve a reduction in NO production at hypothalamic and adrenal levels. In conclusion, an endogenous cannabinoid tone maintains the HPA axis in a stable basal state, which is lost with a noxious stimulus. In this case, the ECS dampens the response to stress allowing the recovery of homeostasis. Moreover, our work further contributes to in vitro evidence for a participation of the endocannabinoid system by inhibiting corticosterone release directly at the adrenal gland level.
Assuntos
Endocanabinoides/farmacologia , Receptor CB1 de Canabinoide/metabolismo , Estresse Psicológico/tratamento farmacológico , Animais , Ácidos Araquidônicos/metabolismo , Ácidos Araquidônicos/farmacologia , Encéfalo/metabolismo , Corticosterona/farmacologia , Endocanabinoides/metabolismo , Sistema Hipotálamo-Hipofisário/metabolismo , Masculino , Sistemas Neurossecretores/efeitos dos fármacos , Sistemas Neurossecretores/metabolismo , Óxido Nítrico/metabolismo , Sistema Hipófise-Suprarrenal/metabolismo , Alcamidas Poli-Insaturadas/metabolismo , Alcamidas Poli-Insaturadas/farmacologia , Ratos , Ratos Sprague-Dawley , Transdução de Sinais/fisiologia , Guanilil Ciclase Solúvel/efeitos dos fármacos , Estresse Psicológico/metabolismo , Canais de Cátion TRPV/efeitos dos fármacos , Canais de Cátion TRPV/metabolismoRESUMO
INTRODUCTION: Obesity, a serious public health problem, occurs mainly when food consumption exceeds energy expenditure. Therefore, energy balance depends on the regulation of the hunger-satiety mechanism, which involves interconnection of the central nervous system and peripheral signals from the adipose tissue, pancreas and gastrointestinal tract, generating responses in short-term food intake and long-term energy balance. Increased body fat alters the gut- and adipose-tissue-derived hormone signaling, which promotes modifications in appetite-regulating hormones, decreasing satiety and increasing hunger senses. With the failure of conventional weight loss interventions (dietary treatment, exercise, drugs and lifestyle modifications), bariatric surgeries are well-accepted tools for the treatment of severe obesity, with long-term and sustained weight loss. Bariatric surgeries may cause weight loss due to restriction/malabsorption of nutrients from the anatomical alteration of the gastrointestinal tract that decreases energy intake, but also by other physiological factors associated with better results of the surgical procedure. OBJECTIVE: This review discusses the neuroendocrine regulation of energy balance, with description of the predominant hormones and peptides involved in the control of energy balance in obesity and all currently available bariatric surgeries. CONCLUSIONS: According to the findings of our review, bariatric surgeries promote effective and sustained weight loss not only by reducing calorie intake, but also by precipitating changes in appetite control, satiation and satiety, and physiological changes in gut-, neuro- and adipose-tissue-derived hormone signaling.