scholarly journals Studying the central control of food intake and obesity in rats

2009 ◽  
Vol 22 (1) ◽  
pp. 163-171 ◽  
Author(s):  
Eliane Beraldi Ribeiro

The central nervous system regulates energy intake and expenditure through a complex network of neurotransmitters and neuromodulators. It is of great interest to understand the relevance of these systems to the physiological control of energy balance and to the disturbances of obesity. The present paper discusses some of the methods to address this field used at the laboratory of Endocrine Physiology of Universidade Federal de São Paulo. Initially, different experimental models of rat obesity are presented, namely the hypothalamic induced monosodium glutamate model, the Zucker genetic model, and the dietary model. The principles of brain microdialysis are also presented, the technique applied to obtain representative samples of the extracellular fluid of brain sites involved in feeding control. The microdialysate levels of serotonin, an important anorexigenic neurotransmitter, are determined by HPLC with electrochemical detection. The immunoblot technique (Western blot) is used to determine hypothalamic levels of proteins relevant to the anorexigenic effect of serotonin and to analyze the acute activation of the insulin signaling cascade in the hypothalamus. The final section addresses the potential applications of proteomics in the study of the central control of feeding.

1996 ◽  
Vol 54 (2) ◽  
pp. 331-334 ◽  
Author(s):  
L. A. V Peireira ◽  
M. A. Cruz-Höfling ◽  
M. S. J. Dertkigil ◽  
D. L. Graça

The integrity of myelin sheaths is maintained by oligodendrocytes and Schwann cells respectively in the central nervous system (CNS) and in the peripheral nervous system. The process of demyelination consisting of the withdrawal of myelin sheaths from their axons is a characteristic feature of multiple sclerosis, the most common human demyelinating disease. Many experimental models have been designed to study the biology of demyelination and remyelination (repair of the lost myelin) in the CNS, due to the difficulties in studying human material. In the ethidium bromide (an intercalating gliotoxic drug) model of demyelination, CNS remyelination may be carried out by surviving oligodendrocytes and/or by cells differentiated from the primitive cell lines or either by Schwann cells that invade the CNS. However, some factors such as the age of the experimental animals, intensity and time of exposure to the intercalating chemical and the topography of the lesions have marked influence on the repair of the tissue.


2021 ◽  
Vol 22 (10) ◽  
pp. 5401
Author(s):  
Marta Dziewięcka ◽  
Mirosława Pawlyta ◽  
Łukasz Majchrzycki ◽  
Katarzyna Balin ◽  
Sylwia Barteczko ◽  
...  

Interest in graphene oxide nature and potential applications (especially nanocarriers) has resulted in numerous studies, but the results do not lead to clear conclusions. In this paper, graphene oxide is obtained by multiple synthesis methods and generally characterized. The mechanism of GO interaction with the organism is hard to summarize due to its high chemical activity and variability during the synthesis process and in biological buffers’ environments. When assessing the biocompatibility of GO, it is necessary to take into account many factors derived from nanoparticles (structure, morphology, chemical composition) and the organism (species, defense mechanisms, adaptation). This research aims to determine and compare the in vivo toxicity potential of GO samples from various manufacturers. Each GO sample is analyzed in two concentrations and applied with food. The physiological reactions of an easy model Acheta domesticus (cell viability, apoptosis, oxidative defense, DNA damage) during ten-day lasting exposure were observed. This study emphasizes the variability of the GO nature and complements the biocompatibility aspect, especially in the context of various GO-based experimental models. Changes in the cell biomarkers are discussed in light of detailed physicochemical analysis.


Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 566
Author(s):  
Jae-Geun Lee ◽  
Hyun-Ju Cho ◽  
Yun-Mi Jeong ◽  
Jeong-Soo Lee

The microbiota–gut–brain axis (MGBA) is a bidirectional signaling pathway mediating the interaction of the microbiota, the intestine, and the central nervous system. While the MGBA plays a pivotal role in normal development and physiology of the nervous and gastrointestinal system of the host, its dysfunction has been strongly implicated in neurological disorders, where intestinal dysbiosis and derived metabolites cause barrier permeability defects and elicit local inflammation of the gastrointestinal tract, concomitant with increased pro-inflammatory cytokines, mobilization and infiltration of immune cells into the brain, and the dysregulated activation of the vagus nerve, culminating in neuroinflammation and neuronal dysfunction of the brain and behavioral abnormalities. In this topical review, we summarize recent findings in human and animal models regarding the roles of the MGBA in physiological and neuropathological conditions, and discuss the molecular, genetic, and neurobehavioral characteristics of zebrafish as an animal model to study the MGBA. The exploitation of zebrafish as an amenable genetic model combined with in vivo imaging capabilities and gnotobiotic approaches at the whole organism level may reveal novel mechanistic insights into microbiota–gut–brain interactions, especially in the context of neurological disorders such as autism spectrum disorder and Alzheimer’s disease.


1964 ◽  
Vol 41 (3) ◽  
pp. 559-572
Author(s):  
C. H. FRASER ROWELL

1. A reflex leg movement mediated by the prothoracic ganglion of Schistocerca is completely inhibited under most normal conditions but disinhibited if the ganglion is isolated from the C.N.S. 2. Progressive lesions to the C.N.S. give progressive disinhibition. The main inhibitory areas are the metathoracic, suboesophageal and mesothoracic ganglia. 3. The left and right sides of the thoracic ganglia are to some extent independent in both the transmission and reception of inhibitory signals. There is probably negative feedback between the reflex systems of the two sides of the prothoracic ganglion. 4. The inhibitory influence of a ganglion on the reflex appears to be proportional to its level of activity and to the amount of signal it is transmitting to the prothoracic ganglion. It is not constant, and is probably not mediated by a limited number of specific inhibitory tracts. 5. The general occurrence of similar mechanisms in animal nervous systems is suggested and discussed.


2012 ◽  
Vol 64 (3) ◽  
pp. 1207-1216 ◽  
Author(s):  
D. Hrncic ◽  
Aleksandra Rasic-Markovic ◽  
Jelica Bjekic-Macut ◽  
Veselinka Susic ◽  
D. Mladenovic ◽  
...  

Epilepsy is one of the leading neurological disorders and affects 1-2% of the world?s population. Generally, it is a result of an imbalance between excitatory and inhibitory phenomena in the central nervous system (CNS), but the mechanisms of its initiation and propagation still require further investigations. Experimental models represent one of the most powerful tools to better understand the mechanisms of epileptogenesis. Nitric oxide (NO) is gaseous molecule with pleiotropic physiological and pathological effects in almost all organ systems and intriguing biological relevance, especially in the CNS where it acts as a gaseous neurotransmitter. The role of NO in the generation of epilepsy is highly contradictory, since there is evidence of its anticonvulsive, as well as proconvulsive properties. Therefore, we will discuss in this review the involvement of NO-mediated signaling pathways in the mechanisms of epileptogenesis, taking into account the findings revealed in experimental studies on animal models of epilepsy.


eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Tai-Heng Chen ◽  
Jun-An Chen

Two crucial questions in neuroscience are how neurons establish individual identity in the developing nervous system and why only specific neuron subtypes are vulnerable to neurodegenerative diseases. In the central nervous system, spinal motor neurons serve as one of the best-characterized cell types for addressing these two questions. In this review, we dissect these questions by evaluating the emerging role of regulatory microRNAs in motor neuron generation in developing embryos and their potential contributions to neurodegenerative diseases such as spinal muscular atrophy (SMA). Given recent promising results from novel microRNA-based medicines, we discuss the potential applications of microRNAs for clinical assessments of SMA disease progression and treatment.


PEDIATRICS ◽  
1956 ◽  
Vol 18 (4) ◽  
pp. 604-613
Author(s):  
William L. Nyhan ◽  
Robert E. Cooke

Acute hyponatremia has been noted on seven occasions in five patients with acute infections of the central nervous system. Symptoms were those of water intoxication and the response to the administration of hypertonic saline was prompt and dramatic. The hyponatremia appears to be due to acute expansion of the extracellular fluid volume in association with antidiuresis. Frequent determinations of the concentrations of electrolytes in the serum and prophylactic limitation of water intake are recommended as possible means of reducing mortality in disease of the central nervous system.


2018 ◽  
Vol 73 (Suppl. 5) ◽  
pp. 43-52 ◽  
Author(s):  
John D. Fernstrom

The non-essential amino acid glutamate participates in numerous metabolic pathways in the body. It also performs important physiologic functions, which include a sensory role as one of the basic tastes (as monosodium glutamate [MSG]), and a role in neuronal function as the dominant excitatory neurotransmitter in the central nervous system. Its pleasant taste (as MSG) has led to its inclusion as a flavoring agent in foods for centuries. Glutamate’s neurotransmitter role was discovered only in the last 60 years. Its inclusion in foods has necessitated its safety evaluation, which has raised concerns about its transfer into the blood ultimately increasing brain glutamate levels, thereby causing functional disruptions because it is a neurotransmitter. This concern, originally raised almost 50 years ago, has led to an extensive series of scientific studies to examine this issue, conducted primarily in rodents, non-human primates, and humans. The key findings have been that (a) the ingestion of MSG in the diet does not produce appreciable increases in glutamate concentrations in blood, except when given experimentally in amounts vastly in excess of normal intake levels; and (b) the blood-brain barrier effectively restricts the passage of glutamate from the blood into the brain, such that brain glutamate levels only rise when blood glutamate concentrations are raised experimentally via non-physiologic means. These and related discoveries explain why the ingestion of MSG in the diet does not lead to an increase in brain glutamate concentrations, and thus does not produce functional disruptions in brain. This article briefly summarizes key experimental findings that evaluate whether MSG in the diet poses a threat to brain function.


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