Central release of oxytocin and the ventromedial hypothalamus

2007 ◽  
Vol 35 (5) ◽  
pp. 1247-1251 ◽  
Author(s):  
N. Sabatier ◽  
I. Rowe ◽  
G. Leng
Keyword(s):  
Food Intake ◽  
Electrical Activity ◽  
Ventromedial Hypothalamus ◽  
Receptor Expression ◽  
Brain Areas ◽  
Magnocellular Neurons ◽  
Peptide Receptor ◽  
Peptide Release ◽  
The Brain ◽  
Social Behaviours

Recent studies on the regulation of social behaviours by neuropeptides indicate that it is the distribution of peptide receptor expression in particular brain areas that determines the specificity of peptide actions; and that, accordingly, peptides can evoke specific behaviours when administered centrally without temporal or spatial selectivity of administration. The release of neuropeptides at synaptic sites appears irrelevant, and in the brain, some peptides are released mainly from dendrites rather than from nerve endings. Dendritic peptide release can be long lasting, semi-independent of electrical activity, and allows the diffusion of peptides to distant targets. The peptide oxytocin regulates many behaviours; in particular, it inhibits food intake. Centrally, oxytocin is released in large amounts by the dendrites of hypothalamic magnocellular neurons. This mini-review considers the possible involvement of dendritically released oxytocin in the regulation of food intake by its actions on the ventromedial hypothalamus.

scholarly journals Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Alessio Molfino ◽  
Gianfranco Gioia ◽  
Filippo Rossi Fanelli ◽  
Alessandro Laviano
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Proinflammatory Cytokines ◽  
Adaptive Response ◽  
Energy Homeostasis ◽  
Cancer Cachexia ◽  
Behavioral Changes ◽  
Brain Areas ◽  
Functional Changes ◽  
The Brain

Inflammation characterizes the course of acute and chronic diseases and is largely responsible for the metabolic and behavioral changes occurring during the clinical journey of patients. Robust data indicate that, during cancer, functional modifications within brain areas regulating energy homeostasis contribute to the onset of anorexia, reduced food intake, and increased catabolism of muscle mass and adipose tissue. In particular, functional changes are associated with increased hypothalamic concentration of proinflammatory cytokines, which suggests that neuroinflammation may represent the adaptive response of the brain to peripheral challenges, including tumor growth. Within this conceptual framework, the vagus nerve appears to be involved in conveying alert signals to the hypothalamus, whereas hypothalamic serotonin appears to contribute to triggering catabolic signals.

Coherent Electrical Activity Between Vibrissa Sensory Areas of Cerebellum and Neocortex Is Enhanced During Free Whisking

2002 ◽  
Vol 87 (4) ◽  
pp. 2137-2148 ◽  
Author(s):  
Sean M. O'Connor ◽  
Rune W. Berg ◽  
David Kleinfeld
Keyword(s):  
Electrical Activity ◽  
Sensory Input ◽  
Field Potential ◽  
Sensory Cortex ◽  
Brain Areas ◽  
Low Coherence ◽  
Primary Sensory Cortex ◽  
High Level ◽  
The Brain ◽  
Local Field Potential Lfp

We tested if coherent signaling between the sensory vibrissa areas of cerebellum and neocortex in rats was enhanced as they whisked in air. Whisking was accompanied by 5- to 15-Hz oscillations in the mystatial electromyogram, a measure of vibrissa position, and by 5- to 20-Hz oscillations in the differentially recorded local field potential (∇LFP) within the vibrissa area of cerebellum and within the ∇LFP of primary sensory cortex. We observed that only 10% of the activity in either cerebellum or sensory neocortex was significantly phase-locked to rhythmic motion of the vibrissae; the extent of this modulation is in agreement with the results from previous single-unit measurements in sensory neocortex. In addition, we found that 40% of the activity in the vibrissa areas of cerebellum and neocortex was significantly coherent during periods of whisking. The relatively high level of coherence between these two brain areas, in comparison with their relatively low coherence with whisking per se, implies that the vibrissa areas of cerebellum and neocortex communicate in a manner that is incommensurate with whisking. To the extent that the vibrissa areas of cerebellum and neocortex communicate over the same frequency band as that used by whisking, these areas must multiplex electrical activity that is internal to the brain with activity that is that phase-locked to vibrissa sensory input.

A high-fat diet attenuates the central response to within-meal satiation signals and modifies the receptor expression of vagal afferents in mice

2009 ◽  
Vol 296 (6) ◽  
pp. R1681-R1686 ◽  
Author(s):  
Wahiba Nefti ◽  
Catherine Chaumontet ◽  
Gilles Fromentin ◽  
Daniel Tomé ◽  
Nicolas Darcel
Keyword(s):  
Food Intake ◽  
Dietary Intervention ◽  
Body Weight Gain ◽  
Receptor Expression ◽  
Vagal Afferents ◽  
Afferent Neuron ◽  
Short Term ◽  
Vagal Afferent ◽  
The Brain ◽  
Term Response

During digestion, macronutrients are sensed within the small intestine. This sensory process is dependent upon the action of gut mediators, such as cholecystokinin (CCK) or serotonin (5-HT), on vagal afferents that, in turn, convey peripheral information to the brain to influence the control of food intake. Recent studies have suggested that dietary conditions alter vagal sensitivity to CCK and 5-HT. This phenomenon may be of importance to the onset of eating disorders. The aim of the present study was thus to investigate the effects of subjecting mice to 15 days of either an HF diet (30% fat, 54% carbohydrate) or an NF diet (10% fat, 74% carbohydrate) on 1) daily and short-term food intake, 2) vagal sensitivity to peripheral anorectic factors and macronutrient loads, and 3) vagal afferent neuron receptor expression. The results indicated that compared with an NF diet, and while increasing food intake and body weight gain, an HF diet altered the short-term response to CCK-8 and intragastric macronutrient loads, while decreasing vagal activation by CCK-8 and modifying the receptor expression of vagal neurons. These findings, therefore, suggest that dietary intervention effect on food intake could be linked to changes in vagal afferent receptor profiles.

scholarly journals Effects of nicotine on homeostatic and hedonic components of food intake

2017 ◽  
Vol 235 (1) ◽  
pp. R13-R31 ◽  
Author(s):  
Andrea Stojakovic ◽  
Enma P Espinosa ◽  
Osman T Farhad ◽  
Kabirullah Lutfy
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
General Population ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Energy Homeostasis ◽  
Brain Areas ◽  
Nicotinic Acetylcholine ◽  
The Brain

Chronic tobacco use leads to nicotine addiction that is characterized by exaggerated urges to use the drug despite the accompanying negative health and socioeconomic burdens. Interestingly, nicotine users are found to be leaner than the general population. Review of the existing literature revealed that nicotine affects energy homeostasis and food consumption via altering the activity of neurons containing orexigenic and anorexigenic peptides in the brain. Hypothalamus is one of the critical brain areas that regulates energy balance via the action of these neuropeptides. The equilibrium between these two groups of peptides can be shifted by nicotine leading to decreased food intake and weight loss. The aim of this article is to review the existing literature on the effect of nicotine on food intake and energy homeostasis and report on the changes that nicotine brings about in the level of these peptides and their receptors that may explain changes in food intake and body weight induced by nicotine. Furthermore, we review the effect of nicotine on the hedonic aspect of food intake. Finally, we discuss the involvement of different subtypes of nicotinic acetylcholine receptors in the regulatory action of nicotine on food intake and energy homeostasis.

The Effects of Vitamin C Administration, Acute Food Deprivation, and Acute Food Intake on Vitamin C Levels in Different Brain Areas of Guinea Pigs

2010 ◽  
Vol 80 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Birsen Kaplan ◽  
Ferihan Çetin ◽  
Sehri Elbeg
Keyword(s):  
Food Intake ◽  
Vitamin C ◽  
Brain Stem ◽  
Food Deprivation ◽  
Guinea Pigs ◽  
Occipital Lobe ◽  
Brain Areas ◽  
Parietal Lobes ◽  
Intraperitoneal Dose ◽  
The Brain

Vitamin C is crucial for the brain. We aimed to investigate the effects of vitamin C administration following 24 hours of acute food deprivation and 24 hours of acute food intake on changes in vitamin C levels in different brain areas of guinea pigs. Vitamin C was administered as a single intraperitoneal dose (500 mg kg-1 body weight) both before acute food deprivation and before acute food intake. At the end of our study, we measured the vitamin C levels in cerebral cortex lobes, brain stem structures, hypophysis, hypothalamus, cerebellum, hippocampus, and amygdala. Vitamin C levels in the frontal and parietal lobes were found to be significantly higher in animals pretreated with vitamin C prior to 24 hours of food deprivation (p < 0.05). Temporal lobe vitamin C level was significantly lower in animals that were subjected to 24 hours of acute food intake following 24 hours of food deprivation (p < 0.05). Increased vitamin C levels were observed in the occipital lobe of all animals that received vitamin C administration (p < 0.05). Vitamin C levels in the brain stem structures such as mesencephalon and pons were significantly decreased in animals pretreated with vitamin C before normal feeding (p < 0.05). Vitamin C level in the hypothalamus was significantly increased after 24 hours of food deprivation (p < 0.05). In conclusion, different areas of the brain may differ in terms of vitamin C content during nutritional changes with or without vitamin C pretreatment, such as 24 hours of food deprivation or 24 hours of food intake following 24 hours of food deprivation. These differences may be attributed to several functions of vitamin C which may occur under these circumstances.

scholarly journals Relaxin/insulin-like family peptide receptor 4 (Rxfp4) expressing hypothalamic neurons modulate food intake and preference in mice

2021 ◽  
Author(s):  
Jo E Lewis ◽  
Orla RM Woodward ◽  
Christopher A Smith ◽  
Alice E Adriaenssens ◽  
Lawrence Billing ◽  
...  
Keyword(s):  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Designer Drugs ◽  
Central Nucleus ◽  
Whole Body ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Peptide Receptor ◽  
The Central Nervous System ◽  
Paraventricular Thalamus

Relaxin/insulin-like-family peptide receptor-4 (RXFP4), the cognate receptor for insulin-like peptide 5 (INSL5), has previously been implicated in feeding behaviour. To explore Rxfp4 expression and physiology, we generated Rxfp4-Cre mice. Whole body chemogenetic activation (Dq) or inhibition (Di) of Rxfp4-expressing cells using designer receptors exclusively activated by designer drugs (DREADDs) altered food intake and preference. Potentially underlying this effect, Rxfp4-expressing neurons were identified in nodose and dorsal root ganglia and the central nervous system, including the ventromedial hypothalamus (VMH). Single-cell RNA-sequencing defined a cluster of VMH Rxfp4-labelled cells expressing Esr1, Tac1 and Oxtr. VMH-restricted activation of Rxfp4-expressing (RXFP4VMH) cells using AAV-Dq recapitulated the whole body Dq feeding phenotype. Viral tracing demonstrated RXFP4VMH neural projections to the bed nucleus of the stria terminalis, paraventricular hypothalamus, paraventricular thalamus, central nucleus of the amygdala and parabrachial nucleus. These findings identify hypothalamic RXFP4 signalling as a key regulator of food intake and preference.

Fit Vs Faint: Assessing Work Causation in “Idiopathic Fall” Cases

2014 ◽  
Vol 19 (5) ◽  
pp. 3-12
Author(s):  
Lorne Direnfeld ◽  
David B. Torrey ◽  
Jim Black ◽  
LuAnn Haley ◽  
Christopher R. Brigham
Keyword(s):  
Blood Flow ◽  
Electrical Activity ◽  
Loss Of Consciousness ◽  
Brain Electrical Activity ◽  
Medical Terminology ◽  
Scientific Analysis ◽  
Medical Causation ◽  
The Individual ◽  
The Brain ◽  
Current Science

Abstract When an individual falls due to a nonwork-related episode of dizziness, hits their head and sustains injury, do workers’ compensation laws consider such injuries to be compensable? Bearing in mind that each state makes its own laws, the answer depends on what caused the loss of consciousness, and the second asks specifically what happened in the fall that caused the injury? The first question speaks to medical causation, which applies scientific analysis to determine the cause of the problem. The second question addresses legal causation: Under what factual circumstances are injuries of this type potentially covered under the law? Much nuance attends this analysis. The authors discuss idiopathic falls, which in this context means “unique to the individual” as opposed to “of unknown cause,” which is the familiar medical terminology. The article presents three detailed case studies that describe falls that had their genesis in episodes of loss of consciousness, followed by analyses by lawyer or judge authors who address the issue of compensability, including three scenarios from Arizona, California, and Pennsylvania. A medical (scientific) analysis must be thorough and must determine the facts regarding the fall and what occurred: Was the fall due to a fit (eg, a seizure with loss of consciousness attributable to anormal brain electrical activity) or a faint (eg, loss of consciousness attributable to a decrease in blood flow to the brain? The evaluator should be able to fully explain the basis for the conclusions, including references to current science.

Aetiologies and anatomy of confabulation

2017 ◽  
Author(s):  
Armin Schnider
Keyword(s):  
Brain Damage ◽  
Limbic Encephalitis ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Brain Areas ◽  
Anatomical Basis ◽  
Korsakoff Syndrome ◽  
Hypoxic Brain ◽  
Degenerative Dementia ◽  
The Brain

What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.

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