scholarly journals A temperature-regulated circuit for feeding behavior

2021 ◽  
Author(s):  
Shaowen Qian ◽  
Sumei Yan ◽  
Ruiqi Pang ◽  
Jing Zhang ◽  
Kai Liu ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Hypothalamic Nucleus ◽  
Galanin Receptor ◽  
Neuronal Populations ◽  
Lateral Parabrachial Nucleus ◽  
Apelin Receptor ◽  
Feeding Center

Abstract Both rodents and primates have evolved to orchestrate food intake to maintain thermal homeostasis in coping with ambient temperature challenges. However, the mechanisms underlying temperature-coordinated feeding behavior are rarely reported. Here we found that a non-canonical feeding center, the anteroventral and periventricular portions of medial preoptic area (apMPOA) responded to altered dietary states. Two neighboring but distinct apMPOA neurons mediated feeding in receiving anatomical inputs from external and dorsal subnuclei of lateral parabrachial nucleus (LPB). While both populations are glutamatergic, the arcuate nucleus (ARC)-projecting neurons in apMPOA can sense low temperature and promote food intake. The other type, the paraventricular hypothalamic nucleus (PVH)-projecting neurons in apMPOA are primarily sensitive to high temperature and suppress food intake. Cutting off both pathways can eliminate the temperature-dependence of feeding. Further projection-specific RNA sequencing identified that the two neuronal populations were molecularly marked by galanin receptor and apelin receptor. These findings reveal an unrecognized cell populations and circuits of apMPOA that orchestrates feeding behavior against thermal challenges.

Hypothalamic mapping of orexigenic action and Fos-like immunoreactivity following relaxin-3 administration in male Wistar rats

2007 ◽  
Vol 292 (3) ◽  
pp. E913-E919 ◽  
Author(s):  
B. M. McGowan ◽  
S. A. Stanley ◽  
N. E. White ◽  
A. Spangeus ◽  
M. Patterson ◽  
...  
Keyword(s):  
Food Intake ◽  
Supraoptic Nucleus ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Disulphide Bonds ◽  
Hypothalamic Nuclei ◽  
Relaxin Family ◽  
Male Wistar Rats ◽  
Additional Support ◽  
G Protein Coupled

The insulin superfamily, characterized by common disulphide bonds, includes not only insulin but also insulin-like peptides such as relaxin-1 and relaxin-3. The actions of relaxin-3 are largely unknown, but recent work suggests a role in regulation of food intake. Relaxin-3 mRNA is highly expressed in the nucleus incertus, which has extensive projections to the hypothalamus, and relaxin immunoreactivity is present in several hypothalamic nuclei. In the rat, relaxin-3 binds and activates both relaxin family peptide receptor 1, which also binds relaxin-1, and a previously orphaned G protein-coupled receptor, RXFP3. These receptors are extensively expressed in the hypothalamus. The aims of these studies were twofold: 1) map the hypothalamic site(s) of the orexigenic action of relaxin-3 and 2) examine the site(s) of neuronal activation following central relaxin-3 administration. After microinjection into hypothalamic sites, human relaxin-3 (H3; 180 pmol) significantly stimulated 0- to 1-h food intake in the supraoptic nucleus (SON), arcuate nucleus (ARC), and the anterior preoptic area (APOA) [SON 0.4 ± 0.2 (vehicle) vs. 2.9 ± 0.5 g (H3), P < 0.001; ARC 0.7 ± 0.3 (vehicle) vs. 2.7 ± 0.2 g (H3), P < 0.05; and APOA 0.8 ± 0.1 (vehicle) vs. 2.2 ± 0.2 g (H3), P < 0.05]. Cumulative food intake was significantly increased ≤8 h following administration into the SON and 4 h into the APOA. A significant increase in Fos-like immunoreactivity was seen in the SON following central relaxin-3 administration. Relaxin-3 stimulates feeding in several hypothalamic nuclei, and these studies provide additional support for relaxin-3 as an important peptide in appetite regulation.

scholarly journals Inhibition of Hypothalamic MCT4 and MCT1–MCT4 Expressions Affects Food Intake and Alters Orexigenic and Anorexigenic Neuropeptide Expressions

2019 ◽  
Vol 57 (2) ◽  
pp. 896-909 ◽  
Author(s):  
Roberto Elizondo-Vega ◽  
Karina Oyarce ◽  
Magdiel Salgado ◽  
María José Barahona ◽  
Antonia Recabal ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Arcuate Nucleus ◽  
Third Ventricle ◽  
Monocarboxylate Transporters ◽  
Energy Status ◽  
Eating Rate ◽  
Behavior Regulation ◽  
Cellular Processes ◽  
Complex Process

Abstract Feeding behavior regulation is a complex process, which depends on the central integration of different signals, such as glucose, leptin, and ghrelin. Recent studies have shown that glial cells known as tanycytes that border the basal third ventricle (3V) detect glucose and then use glucose-derived signaling to inform energy status to arcuate nucleus (ARC) neurons to regulate feeding behavior. Monocarboxylate transporters (MCT) 1 and MCT4 are localized in the cellular processes of tanycytes, which could facilitate monocarboxylate release to orexigenic and anorexigenic neurons. We hypothesize that MCT1 and MCT4 inhibitions could alter the metabolic communication between tanycytes and ARC neurons, affecting feeding behavior. We have previously shown that MCT1 knockdown rats eat more and exhibit altered satiety parameters. Here, we generate MCT4 knockdown rats and MCT1–MCT4 double knockdown rats using adenovirus-mediated transduction of a shRNA into the 3V. Feeding behavior was evaluated in MCT4 and double knockdown animals, and neuropeptide expression in response to intracerebroventricular glucose administration was measured. MCT4 inhibition produced a decrease in food intake, contrary to double knockdown. MCT4 inhibition was accompanied by a decrease in eating rate and mean meal size and an increase in mean meal duration, parameters that are not changed in the double knockdown animals with exception of eating rate. Finally, we observed a loss in glucose regulation of orexigenic neuropeptides and abnormal expression of anorexigenic neuropeptides in response to fasting when these transporters are inhibited. Taken together, these results indicate that MCT1 and MCT4 expressions in tanycytes play a role in feeding behavior regulation.

Feeding responses of rats with dorsomedial hypothalamic lesions given ip 2DG or glucose

1978 ◽  
Vol 235 (3) ◽  
pp. R168-R174
Author(s):  
L. L. Bellinger ◽  
L. L. Bernardis ◽  
S. Brooks
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Food Consumption ◽  
The Other ◽  
Hypothalamic Nucleus ◽  
Saline Control ◽  
Other Hand ◽  
Dorsomedial Hypothalamic Nucleus ◽  
Pass Through ◽  
Bilateral Lesions

The glucoprivation effects of 2-deoxy-D-glucose (2DG) on feeding behavior were studied in rats with bilateral lesions of the dorsomedial hypothalamic nucleus (DMN) and sham-operated controls. The lesioned and sham-operated rats were injected intraperitoneally with 2DG (5% wt/vol) at doses of either 150 mg/kg, 300 mg/kg, or 500 mg/kg, or with saline ("control days"). At all doses significantly more sham-operated rats ate and showed an increased food consumption during the first few hours after 2DG injection when compared to saline control days. However, their 24-h food consumption was normal or less than normal, depending on the dose of 2DG. On the other hand, rats with DMN lesions (DMN-L) did not increase their food consumption during the 4 h after the injection at any of the 2DG doses. In a second experiment DMN-L and sham-operated controls were injected intraperitoneally with glucose (1.36 g/kg body wt or 2.72 g/kg body wt) or saline after an overnight fast. Glucose loads, compared to saline injections, significantly depressed the controls' food consumption only during the first hour of refeeding. On the other hand, glucose injections did not depress food intake of the DMN-L rats. It is suggested that DMN lesions may have either destroyed glucoreceptors in the DMN that monitor glucose or the glucoprivation effects caused by 2DG and/or glucoreceptive pathways that pass through the DMN.

scholarly journals Arcuate nucleus and lateral hypothalamic CART neurons in the mouse brain exert opposing effects on energy expenditure

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Aitak Farzi ◽  
Jackie Lau ◽  
Chi Kin Ip ◽  
Yue Qi ◽  
Yan-Chuan Shi ◽  
...  
Keyword(s):  
Physical Activity ◽  
Food Intake ◽  
Energy Expenditure ◽  
Lateral Hypothalamus ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Neuronal Populations ◽  
Neuron Activation ◽  
Important Regulator ◽  
Opposing Effects

Cocaine- and amphetamine-regulated transcript (CART) is widely expressed in the hypothalamus and an important regulator of energy homeostasis; however, the specific contributions of different CART neuronal populations to this process are not known. Here, we show that depolarization of mouse arcuate nucleus (Arc) CART neurons via DREADD technology decreases energy expenditure and physical activity, while it exerts the opposite effects in CART neurons in the lateral hypothalamus (LHA). Importantly, when stimulating these neuronal populations in the absence of CART, the effects were attenuated. In contrast, while activation of CART neurons in the LHA stimulated feeding in the presence of CART, endogenous CART inhibited food intake in response to Arc CART neuron activation. Taken together, these results demonstrate anorexigenic but anabolic effects of CART upon Arc neuron activation, and orexigenic but catabolic effects upon LHA-neuron activation, highlighting the complex and nuclei-specific functions of CART in controlling feeding and energy homeostasis.

A comparison of brain angiotensin II receptors during lactation and diestrus of the estrous cycle in the rat

1999 ◽  
Vol 277 (3) ◽  
pp. R904-R909 ◽  
Author(s):  
Robert C. Speth ◽  
William T. Barry ◽  
M. Susan Smith ◽  
Kevin L. Grove
Keyword(s):  
Receptor Binding ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Renin Angiotensin System ◽  
Hypothalamic Nucleus ◽  
Ang Ii ◽  
Hypothalamic Area ◽  
Angiotensin System ◽  
Dorsomedial Hypothalamic Nucleus ◽  
The Brain

During lactation there are many dramatic alterations in the hypothalamic-pituitary (HP) axis, as well as an increased demand for food and water. The renin-angiotensin system (RAS) is one of the major mediators of the HP axis. This study examined the receptors for ANG II in the rat brain during lactation and diestrus. Compared with diestrus, lactating rats had significant decreases in ANG II receptor binding in several forebrain regions, most notably in the arcuate nucleus/median eminence, dorsomedial hypothalamic nucleus (DMH), and lateral hypothalamic area (LHA). In contrast, there was an increase in ANG II receptor binding in the preoptic area during lactation. These significant changes in ANG II binding in the brain during lactation support the hypothesis that changes in the RAS may contribute to the dramatic changes in the HP axis during lactation. In addition, the significant reduction in ANG II binding in the DMH and LHA may be indicative of a role in the regulation of food intake, a function only recently associated with the RAS.

scholarly journals 5-HT recruits distinct neurocircuits to inhibit hunger-driven and non-hunger-driven feeding

2021 ◽  
Author(s):  
Yanlin He ◽  
Xing Cai ◽  
Hailan Liu ◽  
Krisitine M. Conde ◽  
Pingwen Xu ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Ventral Tegmental Area ◽  
Arcuate Nucleus ◽  
Outward Current ◽  
Raphe Nucleus ◽  
Area 5 ◽  
Parallel Circuits ◽  
Different Types ◽  
Hypothalamic Arcuate Nucleus

AbstractObesity is primarily a consequence of consuming calories beyond energetic requirements, but underpinning drivers have not been fully defined. 5-Hydroxytryptamine (5-HT) neurons in the dorsal Raphe nucleus (5-HTDRN) regulate different types of feeding behavior, such as eating to cope with hunger or for pleasure. Here, we observed that activation of 5-HTDRN to hypothalamic arcuate nucleus (5-HTDRN → ARH) projections inhibits food intake driven by hunger via actions at ARH 5-HT2C and 5-HT1B receptors, whereas activation of 5-HTDRN to ventral tegmental area (5-HTDRN → VTA) projections inhibits non-hunger-driven feeding via actions at 5-HT2C receptors. Further, hunger-driven feeding gradually activates ARH-projecting 5-HTDRN neurons via inhibiting their responsiveness to inhibitory GABAergic inputs; non-hunger-driven feeding activates VTA-projecting 5-HTDRN neurons through reducing a potassium outward current. Thus, our results support a model whereby parallel circuits modulate feeding behavior either in response to hunger or to hunger-independent cues.

Interleukin-1 beta-induced anorexia and pyrexia in rat: relationship to hypothalamic neuropeptide Y

1995 ◽  
Vol 269 (5) ◽  
pp. E852-E857 ◽  
Author(s):  
H. D. McCarthy ◽  
S. Dryden ◽  
G. Williams
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Core Temperature ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Interleukin 1 ◽  
Medial Preoptic Area ◽  
Interleukin 1 Beta

We investigated the effect of recombinant human interleukin-1 beta (rhIL-1 beta)-induced anorexia and pyrexia on the hypothalamic neuropeptide Y (NPY)-ergic system, which stimulates feeding and reduces thermogenesis. In meal-fed rats, food intake decreased by 83%, 90 min after IL-1 beta treatment (1.3 micrograms/100 g ip; n - 8) vs. controls. NPY concentrations were significantly higher in the medial preoptic area (MPO), paraventricular (PVN), ventromedial (VMN), and dorsomedial (DMN) nuclei but unchanged in the arcuate nucleus (ARC) in both IL-1 beta-treated and pair-fed groups. Indomethacin (0.25 mg/100 g ip) reduced IL-1 beta-induced anorexia and tended to normalize NPY concentrations. In study 2, IL-1 beta increased core temperature by 1.1 degrees C above preinjection values (P < 0.001) and significantly raised NPY concentrations in the MPO, PVN, VMN, and DMN compared with controls, 60 min postinjection. Indomethacin prevented the pyrexia and normalized hypothalamic NPY levels. As NPY concentrations were not increased in the ARC (the hypothalamic site of synthesis), we suggest that the increased NPY levels may result from blocked release, which would be in accord with the known experimental effects of NPY.

scholarly journals Central infusions of leptin and GLP-1-(7-36) amide differentially stimulate c-FLI in the rat brain

1996 ◽  
Vol 271 (4) ◽  
pp. R1096-R1100 ◽  
Author(s):  
G. Van Dijk ◽  
T. E. Thiele ◽  
J. C. Donahey ◽  
L. A. Campfield ◽  
F. J. Smith ◽  
...  
Keyword(s):  
Food Intake ◽  
Area Postrema ◽  
Hypothalamic Nucleus ◽  
Dark Phase ◽  
Short Term ◽  
Dorsomedial Hypothalamus ◽  
Lateral Parabrachial Nucleus ◽  
The Central Nervous System ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Recently, glucagon-like peptide-1-(7-36) amide (GLP-1) and leptin have been implicated in the regulation of food intake. In the present study, we compared the effects of third ventricular administration (i3vt) of leptin (3.5 micrograms) and GLP-1 (10.0 micrograms) on short-term food intake and c-Fos-like immunoreactivity (c-FLI) in hypothalamic, limbic, and hindbrain areas in the rat. Relative to controls, infusion of leptin or GLP-1 (3 h before lights off) significantly reduced food intake over the first 2 h in the dark phase (53 and 63%, respectively). In different rats, infusion of leptin or GLP-1 elevated c-FLI in the paraventricular hypothalamus and central amygdala. Furthermore, leptin selectively elevated c-FLI in the dorsomedial hypothalamus, whereas GLP-1 selectively elevated c-FLI in the nucleus of the solitary tract, area postrema, lateral parabrachial nucleus, and arcuate hypothalamic nucleus. The fact that most of the c-FLI after leptin or GLP-1 administration was observed in separate regions within the central nervous system (CNS) suggests different roles for leptin and GLP-1 in the CNS regulation of food intake and body weight.

scholarly journals Direct modulation of GFAP-expressing glia in the arcuate nucleus bi-directionally regulates feeding

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Naiyan Chen ◽  
Hiroki Sugihara ◽  
Jinah Kim ◽  
Zhanyan Fu ◽  
Boaz Barak ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Glial Activation ◽  
Inhibitory Input ◽  
Neuronal Populations ◽  
Structural Connections ◽  
Neuronal Subtype ◽  
Agouti Related Protein

Multiple hypothalamic neuronal populations that regulate energy balance have been identified. Although hypothalamic glia exist in abundance and form intimate structural connections with neurons, their roles in energy homeostasis are less known. Here we show that selective Ca2+ activation of glia in the mouse arcuate nucleus (ARC) reversibly induces increased food intake while disruption of Ca2+ signaling pathway in ARC glia reduces food intake. The specific activation of ARC glia enhances the activity of agouti-related protein/neuropeptide Y (AgRP/NPY)-expressing neurons but induces no net response in pro-opiomelanocortin (POMC)-expressing neurons. ARC glial activation non-specifically depolarizes both AgRP/NPY and POMC neurons but a strong inhibitory input to POMC neurons balances the excitation. When AgRP/NPY neurons are inactivated, ARC glial activation fails to evoke any significant changes in food intake. Collectively, these results reveal an important role of ARC glia in the regulation of energy homeostasis through its interaction with distinct neuronal subtype-specific pathways.

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