scholarly journals GLP-1 Suppresses Feeding Behaviors and Modulates Neuronal Electrophysiological Properties in Multiple Brain Regions

2021 ◽  
Vol 14 ◽  
Author(s):  
Xin-Yi Chen ◽  
Lei Chen ◽  
Wu Yang ◽  
An-Mu Xie
Keyword(s):  
Food Intake ◽  
Neuronal Excitability ◽  
Functional Organization ◽  
Brain Regions ◽  
Future Research ◽  
Cellular Mechanisms ◽  
Feeding Behaviors ◽  
Gabaergic Neurotransmission ◽  
Electrophysiological Properties ◽  
Glucagon Like Peptide 1

The glucagon-like peptide-1 (GLP-1) plays important roles in the regulation of food intake and energy metabolism. Peripheral or central GLP-1 suppresses food intake and reduces body weight. The electrophysiological properties of neurons in the mammalian central nervous system reflect the neuronal excitability and the functional organization of the brain. Recent studies focus on elucidating GLP-1-induced suppression of feeding behaviors and modulation of neuronal electrophysiological properties in several brain regions. Here, we summarize that activation of GLP-1 receptor (GLP-1R) suppresses food intake and induces postsynaptic depolarization of membrane potential and/or presynaptic modulation of glutamatergic or GABAergic neurotransmission in brain nuclei located within the medulla oblongata, pons, mesencephalon, diencephalon, and telencephalon. This review may provide a background to guide future research about the cellular mechanisms of GLP-1-induced feeding inhibition.

Glucagon-like peptide 1-(7–36) amide acts at lateral and medial hypothalamic sites to suppress feeding in rats

2003 ◽  
Vol 284 (6) ◽  
pp. R1427-R1435 ◽  
Author(s):  
Rafael R. Schick ◽  
Jens P. Zimmermann ◽  
Thomas vorm Walde ◽  
Volker Schusdziarra
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Effective Dose ◽  
Ventromedial Hypothalamus ◽  
Brain Regions ◽  
Central Administration ◽  
Minimal Effective Dose ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Fasted Rats

Glucagon-like peptide 1-(7–36) amide (GLP-1) potently inhibits rat feeding behavior after central administration. Because third ventricular injection of GLP-1 appeared to be less effective than lateral ventricular injection, we have reexamined this issue. In addition, we attempted to identify brain regions other than the paraventricular nucleus of the hypothalamus that are sensitive toward GLP-1-induced feeding suppression. Finally, we examined the local role of endogenous GLP-1 by specific GLP-1 receptor blockade. After lateral ventricular injection, GLP-1 significantly inhibited food intake of 24-h-fasted rats in a dose-dependent fashion with a minimal effective dose of 1 μg. After third ventricular injection, GLP-1 (1 μg) was similarly effective in suppressing food intake, which extends previous findings. Intracerebral microinjections of GLP-1 significantly suppressed food intake in the lateral (LH), dorsomedial (DMH), and ventromedial hypothalamus (VMH), but not in the medial nucleus of the amygdala. The minimal effective dose of GLP-1 was 0.3 μg at LH sites and 1 μg at DMH or VMH sites. LH microinjections of exendin-(9–39) amide, a GLP-1 receptor antagonist, at 1 or 2.5 μg did not alter feeding behavior in 24-h-fasted rats. In satiated animals, however, a single LH injection of 1 μg exendin-(9–39) amide significantly augmented food intake, but only during the first 20 min (0.6 vs. 0.1 g). With three repeated injections of 2.5 μg exendin-(9–39) amide every 20 min, 1-h food intake was significantly increased by 300%. These data strongly support and extend the concept of GLP-1 as a physiological regulator of food intake in the hypothalamus.

scholarly journals Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ashley E. Smith ◽  
Kehinde O. Ogunseye ◽  
Julia N. DeBenedictis ◽  
Joanna Peris ◽  
James M. Kasper ◽  
...  
Keyword(s):  
Food Intake ◽  
Glutamate Release ◽  
Caloric Intake ◽  
Brain Regions ◽  
Gamma Aminobutyric Acid ◽  
Palatable Food ◽  
Feeding Behaviors ◽  
Brain Nuclei ◽  
Glutamatergic Signaling ◽  
Tracing Techniques

AbstractFood intake is a complex behavior regulated by discrete brain nuclei that integrate homeostatic nutritional requirements with the hedonic properties of food. Homeostatic feeding (i.e. titration of caloric intake), is typically associated with hypothalamic brain nuclei, including the paraventricular nucleus of the hypothalamus (PVN). Hedonic feeding is driven, in part, by the reinforcing properties of highly palatable food (HPF), which is mediated by the nucleus accumbens (NAc). Dysregulation of homeostatic and hedonic brain nuclei can lead to pathological feeding behaviors, namely overconsumption of highly palatable food (HPF), that may drive obesity. Both homeostatic and hedonic mechanisms of food intake have been attributed to several brain regions, but the integration of homeostatic and hedonic signaling to drive food intake is less clear, therefore we aimed to identify the neuroanatomical, functional, and behavioral features of a novel PVN → NAc circuit. Using viral tracing techniques, we determined that PVN → NAc has origins in the parvocellular PVN, and that PVN → NAc neurons express VGLUT1, a marker of glutamatergic signaling. Next, we pharmacogenetically stimulated PVN → NAc neurons and quantified both gamma-aminobutyric acid (GABA) and glutamate release and phospho-cFos expression in the NAc and observed a robust and significant increase in extracellular glutamate and phospho-cFos expression. Finally, we pharmacogenetically stimulated PVN → NAc which decreased intake of highly palatable food, demonstrating that this glutamatergic circuitry regulates aspects of feeding.

scholarly journals Effects of glucagon-like peptide 1 on appetite and body weight: focus on the CNS

2013 ◽  
Vol 221 (1) ◽  
pp. T1-T16 ◽  
Author(s):  
L van Bloemendaal ◽  
J S ten Kulve ◽  
S E la Fleur ◽  
R G Ijzerman ◽  
M Diamant
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Physiological Role ◽  
Brain Regions ◽  
Gastric Distension ◽  
Cns Activity ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The delivery of nutrients to the gastrointestinal tract after food ingestion activates the secretion of several gut-derived mediators, including the incretin hormone glucagon-like peptide 1 (GLP-1). GLP-1 receptor agonists (GLP-1RA), such as exenatide and liraglutide, are currently employed successfully in the treatment of patients with type 2 diabetes mellitus. GLP-1RA improve glycaemic control and stimulate satiety, leading to reductions in food intake and body weight. Besides gastric distension and peripheral vagal nerve activation, GLP-1RA induce satiety by influencing brain regions involved in the regulation of feeding, and several routes of action have been proposed. This review summarises the evidence for a physiological role of GLP-1 in the central regulation of feeding behaviour and the different routes of action involved. Also, we provide an overview of presently available data on pharmacological stimulation of GLP-1 pathways leading to alterations in CNS activity, reductions in food intake and weight loss.

scholarly journals Computational models of category-selective brain regions enable high-throughput tests of selectivity

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
N. Apurva Ratan Murty ◽  
Pouya Bashivan ◽  
Alex Abate ◽  
James J. DiCarlo ◽  
Nancy Kanwisher
Keyword(s):  
Computational Models ◽  
Functional Organization ◽  
Brain Regions ◽  
Human Cognition ◽  
Future Research ◽  
Domain Specific ◽  
Face Area ◽  
Extrastriate Body Area ◽  
Cortical Regions ◽  
The Brain

AbstractCortical regions apparently selective to faces, places, and bodies have provided important evidence for domain-specific theories of human cognition, development, and evolution. But claims of category selectivity are not quantitatively precise and remain vulnerable to empirical refutation. Here we develop artificial neural network-based encoding models that accurately predict the response to novel images in the fusiform face area, parahippocampal place area, and extrastriate body area, outperforming descriptive models and experts. We use these models to subject claims of category selectivity to strong tests, by screening for and synthesizing images predicted to produce high responses. We find that these high-response-predicted images are all unambiguous members of the hypothesized preferred category for each region. These results provide accurate, image-computable encoding models of each category-selective region, strengthen evidence for domain specificity in the brain, and point the way for future research characterizing the functional organization of the brain with unprecedented computational precision.

scholarly journals The primary cilium is required for MC4R control of food intake and body weight

2020 ◽  
Author(s):  
Yi Wang ◽  
Adelaide Bernard ◽  
Fanny Comblain ◽  
Xinyu Yue ◽  
Christophe Paillart ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Adenylyl Cyclase ◽  
Energy Homeostasis ◽  
Primary Cilia ◽  
Critical Role ◽  
Brain Regions ◽  
Cyclase Activity ◽  
Adenylyl Cyclase Activity ◽  
Cellular Mechanisms

AbstractThe Melanocortin-4 Receptor (MC4R) plays a critical role in the long-term regulation of energy homeostasis and mutations in MC4R are the most common cause of monogenic obesity. However, the precise molecular and cellular mechanisms underlying the maintenance of energy balance within MC4R expressing neurons are unknown. We recently reported that MC4R localizes to primary cilia, a cellular organelle that allows for partitioning of incoming cellular signals, raising the question of whether MC4R functions there. Here, using mouse genetic approaches, we found that cilia are required specifically on MC4R-expressing neurons to restrain feeding behavior. Moreover, these cilia were critical for pharmacological activators of MC4R to exert an anorexigenic effect. MC4R is expressed in multiple brain regions. Using targeted deletion of primary cilia, we found that cilia in the paraventricular nucleus (PVN) of the hypothalamus are essential to restrict food intake. MC4R activation increases adenylyl cyclase activity. Like removing cilia, inhibiting adenylyl cyclase activity in the cilia of MC4R-expressing neurons of the PVN caused hyperphagia and obesity. Thus, MC4R signals via cilia of PVN neurons to control food intake and body weight. We propose that defects in ciliary localization of MC4R cause obesity in human inherited obesity syndromes and ciliopathies.

The Social Neuroscience of Cooperation

2018 ◽  
Author(s):  
Jay Joseph Van Bavel
Keyword(s):  
Theoretical Models ◽  
Brain Regions ◽  
Review Literature ◽  
Social Neuroscience ◽  
Future Research ◽  
A Value ◽  
Group Cooperation ◽  
Neural Processes ◽  
The Social ◽  
Cooperative Decision Making

We review literature from several fields to describe common experimental tasks used to measure human cooperation as well as the theoretical models that have been used to characterize cooperative decision-making, as well as brain regions implicated in cooperation. Building on work in neuroeconomics, we suggest a value-based account may provide the most powerful understanding the psychology and neuroscience of group cooperation. We also review the role of individual differences and social context in shaping the mental processes that underlie cooperation and consider gaps in the literature and potential directions for future research on the social neuroscience of cooperation. We suggest that this multi-level approach provides a more comprehensive understanding of the mental and neural processes that underlie the decision to cooperate with others.

Dorsal Horn Pain Mechanisms

2019 ◽  
pp. 444-469 ◽  
Author(s):  
Hanns Ulrich Zeilhofer ◽  
Robert Ganley
Keyword(s):  
Dorsal Horn ◽  
Neuronal Excitability ◽  
Functional Organization ◽  
Synaptic Integration ◽  
Synaptic Efficacy ◽  
Pain Mechanisms ◽  
Pain Pathway ◽  
Pathological Pain ◽  
The Subject ◽  
Equivalent Structure

The spinal dorsal horn and its equivalent structure in the brainstem constitute the first sites of synaptic integration in the pain pathway. A huge body of literature exists on alterations in spinal nociceptive signal processing that contribute to the generation of exaggerated pain states and hence to what is generally known as “central sensitization.” Such mechanisms include changes in synaptic efficacy or neuronal excitability, which can be evoked by intense nociceptive stimulation or by inflammatory or neuropathic insults. Some of these changes cause alterations in the functional organization of dorsal horn sensory circuits, leading to abnormal pathological pain sensations. This article reviews the present state of this knowledge. It does not cover the contributions of astrocytes and microglia in detail as their functions are the subject of a separate chapter.

scholarly journals Metacognition: ideas and insights from neuro- and educational sciences

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Damien S. Fleur ◽  
Bert Bredeweg ◽  
Wouter van den Bos
Keyword(s):  
Cognitive Neuroscience ◽  
Large Body ◽  
Brain Regions ◽  
Metacognitive Knowledge ◽  
Future Research ◽  
Metacognitive Control ◽  
Domain Generality ◽  
Entry Points ◽  
Control Research ◽  
Educational Sciences

AbstractMetacognition comprises both the ability to be aware of one’s cognitive processes (metacognitive knowledge) and to regulate them (metacognitive control). Research in educational sciences has amassed a large body of evidence on the importance of metacognition in learning and academic achievement. More recently, metacognition has been studied from experimental and cognitive neuroscience perspectives. This research has started to identify brain regions that encode metacognitive processes. However, the educational and neuroscience disciplines have largely developed separately with little exchange and communication. In this article, we review the literature on metacognition in educational and cognitive neuroscience and identify entry points for synthesis. We argue that to improve our understanding of metacognition, future research needs to (i) investigate the degree to which different protocols relate to the similar or different metacognitive constructs and processes, (ii) implement experiments to identify neural substrates necessary for metacognition based on protocols used in educational sciences, (iii) study the effects of training metacognitive knowledge in the brain, and (iv) perform developmental research in the metacognitive brain and compare it with the existing developmental literature from educational sciences regarding the domain-generality of metacognition.

scholarly journals Social exclusion increases the executive function of attention networks

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Huoyin Zhang ◽  
Shiyunmeng Zhang ◽  
Jiachen Lu ◽  
Yi Lei ◽  
Hong Li
Keyword(s):  
Social Exclusion ◽  
Executive Control ◽  
Brain Regions ◽  
Negative Influence ◽  
Future Research ◽  
Research Attention ◽  
Attention Network ◽  
Attention Networks ◽  
The Social ◽  
And Control

AbstractPrevious studies in humans have shown that brain regions activating social exclusion overlap with those related to attention. However, in the context of social exclusion, how does behavioral monitoring affect individual behavior? In this study, we used the Cyberball game to induce the social exclusion effect in a group of participants. To explore the influence of social exclusion on the attention network, we administered the Attention Network Test (ANT) and compared results for the three subsystems of the attention network (orienting, alerting, and executive control) between exclusion (N = 60) and inclusion (N = 60) groups. Compared with the inclusion group, the exclusion group showed shorter overall response time and better executive control performance, but no significant differences in orienting or alerting. The excluded individuals showed a stronger ability to detect and control conflicts. It appears that social exclusion does not always exert a negative influence on individuals. In future research, attention to network can be used as indicators of social exclusion. This may further reveal how social exclusion affects individuals' psychosomatic mechanisms.

Sign in / Sign up

Export Citation Format

Share Document