scholarly journals A novel cholinergic neural pathway and its role in the drug relapse

2021 ◽  
Author(s):  
Teng He ◽  
Wenwen Chen ◽  
Yu Fan ◽  
Xing Xu ◽  
Zilin Wang ◽  
...  
Keyword(s):  
Food Intake ◽  
Conditioned Place Preference ◽  
Choline Acetyltransferase ◽  
Aminobutyric Acid ◽  
Central Nucleus ◽  
Parabrachial Nucleus ◽  
Neural Pathway ◽  
Lateral Parabrachial Nucleus ◽  
Drug Relapse ◽  
Cholinergic Projection

The lateral parabrachial nucleus (LPB) is critical hub implicated in the control of food intake, reward and aversion. Here, we identified a novel cholinergic projection from choline acetyltransferase (ChAT)-positive neurons in external portion of the lateral parabrachial nucleus (eLPBChAT) to γ-aminobutyric acid (GABA) neurons in central nucleus of amygdala (CeAGABA), activation of which could block methamphetamine (METH)-primed conditioned place preference (CPP) in mice.

scholarly journals Lateral parabrachial nucleus and opioid mechanisms of the central nucleus of the amygdala in the control of sodium intake

2017 ◽  
Vol 316 ◽  
pp. 11-17 ◽  
Author(s):  
Gláucia M.F. Andrade-Franzé ◽  
Silvia Gasparini ◽  
Laurival A. De Luca ◽  
Patrícia M. De Paula ◽  
Débora S.A. Colombari ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Central Nucleus ◽  
Parabrachial Nucleus ◽  
Lateral Parabrachial Nucleus ◽  
Opioid Mechanisms

Interactions between central nucleus of the amygdala and lateral parabrachial nucleus in the control of sodium intake

Appetite ◽  
2009 ◽  
Vol 52 (3) ◽  
pp. 816
Author(s):  
G.M.F. Andrade ◽  
C.A.F. Andrade ◽  
L.A. De Luca ◽  
P.M. De Paula ◽  
J.V. Menani
Keyword(s):  
Sodium Intake ◽  
Central Nucleus ◽  
Parabrachial Nucleus ◽  
Lateral Parabrachial Nucleus

scholarly journals Lipopolysacharide Rapidly and Completely Suppresses AgRP Neuron-Mediated Food Intake in Male Mice

Endocrinology ◽  
2016 ◽  
Vol 157 (6) ◽  
pp. 2380-2392 ◽  
Author(s):  
Yang Liu ◽  
Ying Huang ◽  
Tiemin Liu ◽  
Hua Wu ◽  
Huxing Cui ◽  
...  
Keyword(s):  
Food Intake ◽  
Parabrachial Nucleus ◽  
Designer Drug ◽  
Male Mice ◽  
Moderate Dose ◽  
Related Peptide ◽  
Lateral Parabrachial Nucleus ◽  
Melanocortin 4 Receptor ◽  
Double Immunohistochemistry ◽  
Stimulation Of

Although Agouti-related peptide (AgRP) neurons play a key role in the regulation of food intake, their contribution to the anorexia caused by proinflammatory insults has yet to be identified. Using a combination of neuroanatomical and pharmacogenetics experiments, this study sought to investigate the importance of AgRP neurons and downstream targets in the anorexia caused by the peripheral administration of a moderate dose of lipopolysaccharide (LPS) (100 μg/kg, ip). First, in the C57/Bl6 mouse, we demonstrated that LPS induced c-fos in select AgRP-innervated brain sites involved in feeding but not in any arcuate proopiomelanocortin neurons. Double immunohistochemistry further showed that LPS selectively induced c-Fos in a large subset of melanocortin 4 receptor-expressing neurons in the lateral parabrachial nucleus. Secondly, we used pharmacogenetics to stimulate the activity of AgRP neurons during the course of LPS-induced anorexia. In AgRP-Cre mice expressing the designer receptor hM3Dq-Gq only in AgRP neurons, the administration of the designer drug clozapine-N-oxide (CNO) induced robust food intake. Strikingly, CNO-mediated food intake was rapidly and completely blunted by the coadministration of LPS. Neuroanatomical experiments further indicated that LPS did not interfere with the ability of CNO to stimulate c-Fos in AgRP neurons. In summary, our findings combined together support the view that the stimulation of select AgRP-innervated brain sites and target neurons, rather than the inhibition of AgRP neurons themselves, is likely to contribute to the rapid suppression of food intake observed during acute bacterial endotoxemia.

scholarly journals Ghrelin in the lateral parabrachial nucleus influences the excitability of glucosensing neurons, increases food intake and body weight

2020 ◽  
Vol 9 (12) ◽  
pp. 1168-1177
Author(s):  
Caishun Zhang ◽  
Junhua Yuan ◽  
Qian Lin ◽  
Manwen Li ◽  
Liuxin Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Firing Rate ◽  
Body Weight Gain ◽  
Parabrachial Nucleus ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Lateral Parabrachial Nucleus

Ghrelin plays a pivotal role in the regulation of food intake, body weight and energy metabolism. However, these effects of ghrelin in the lateral parabrachial nucleus (LPBN) are unexplored. C57BL/6J mice and GHSR−/− mice were implanted with cannula above the right LPBN and ghrelin was microinjected via the cannula to investigate effect of ghrelin in the LPBN. In vivo electrophysiological technique was used to record LPBN glucose-sensitive neurons to explore potential udnderlying mechanisms. Microinjection of ghrelin in LPBN significantly increased food intake in the first 3 h, while such effect was blocked by [D-Lys3]-GHRP-6 and abolished in GHSR−/− mice. LPBN ghrelin microinjection also significantly increased the firing rate of glucose-excited (GE) neurons and decreased the firing rate of glucose-inhibited (GI) neurons. Additionally, LPBN ghrelin microinjection also significantly increased c-fos expression. Chronic ghrelin administration in the LPBN resulted in significantly increased body weight gain. Meanwhile, no significant changes were observed in both mRNA and protein expression levels of UCP-1 in BAT. These results demonstrated that microinjection of ghrelin in LPBN could increase food intake through the interaction with growth hormone secretagogue receptor (GHSR) in C57BL/6J mice, and its chronic administration could also increase body weight gain. These effects might be associated with altered firing rate in the GE and GI neurons.

scholarly journals Ghrelin Receptor Stimulation of the Lateral Parabrachial Nucleus in Rats Increases Food Intake but not Food Motivation

Obesity ◽  
2020 ◽  
Vol 28 (8) ◽  
pp. 1503-1511
Author(s):  
Tina Bake ◽  
Marie V. Le May ◽  
Christian E. Edvardsson ◽  
Heike Vogel ◽  
Ulrika Bergström ◽  
...  
Keyword(s):  
Food Intake ◽  
Parabrachial Nucleus ◽  
Food Motivation ◽  
Receptor Stimulation ◽  
Ghrelin Receptor ◽  
Lateral Parabrachial Nucleus ◽  
Stimulation Of

scholarly journals Functional and Neurochemical Identification of Ghrelin Receptor (GHSR)-Expressing Cells of the Lateral Parabrachial Nucleus in Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Marie V. Le May ◽  
Fiona Peris-Sampedro ◽  
Iris Stoltenborg ◽  
Erik Schéle ◽  
Tina Bake ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Food Choice ◽  
Viral Vector ◽  
Sucrose Solution ◽  
Parabrachial Nucleus ◽  
Growth Hormone Secretagogue ◽  
Lateral Parabrachial Nucleus ◽  
Obesogenic Diet

The lateral parabrachial nucleus (lPBN), located in the pons, is a well-recognized anorexigenic center harboring, amongst others, the calcitonin gene-related peptide (CGRP)-expressing neurons that play a key role. The receptor for the orexigenic hormone ghrelin (the growth hormone secretagogue receptor, GHSR) is also abundantly expressed in the lPBN and ghrelin delivery to this site has recently been shown to increase food intake and alter food choice. Here we sought to explore whether GHSR-expressing cells in the lPBN (GHSRlPBN cells) contribute to feeding control, food choice and body weight gain in mice offered an obesogenic diet, involving studies in which GHSRlPBN cells were silenced. We also explored the neurochemical identity of GHSRlPBN cells. To silence GHSRlPBN cells, Ghsr-IRES-Cre male mice were bilaterally injected intra-lPBN with a Cre-dependent viral vector expressing tetanus toxin-light chain. Unlike control wild-type littermates that significantly increased in body weight on the obesogenic diet (i.e., high-fat high-sugar free choice diet comprising chow, lard and 9% sucrose solution), the heterozygous mice with silenced GHSRlPBN cells were resistant to diet-induced weight gain with significantly lower food intake and fat weight. The lean phenotype appeared to result from a decreased food intake compared to controls and caloric efficiency was unaltered. Additionally, silencing the GHSRlPBN cells altered food choice, significantly reducing palatable food consumption. RNAscope and immunohistochemical studies of the lPBN revealed considerable co-expression of GHSR with glutamate and pituitary adenylate cyclase-activating peptide (PACAP), and much less with neurotensin, substance P and CGRP. Thus, the GHSRlPBN cells are important for diet-induced weight gain and adiposity, as well as in the regulation of food intake and food choice. Most GHSRlPBN cells were found to be glutamatergic and the majority (76%) do not belong to the well-characterized anorexigenic CGRP cell population.

scholarly journals Leptin receptor signaling in the lateral parabrachial nucleus contributes to the control of food intake

2014 ◽  
Vol 307 (11) ◽  
pp. R1338-R1344 ◽  
Author(s):  
Amber L. Alhadeff ◽  
Matthew R. Hayes ◽  
Harvey J. Grill
Keyword(s):  
Food Intake ◽  
Neural Control ◽  
Leptin Receptor ◽  
Sensory Information ◽  
Progressive Ratio ◽  
Meal Size ◽  
Parabrachial Nucleus ◽  
Lateral Parabrachial Nucleus ◽  
Site Of Action ◽  
Integral Role

Pontine parabrachial nucleus (PBN) neurons integrate visceral, oral, and other sensory information, playing an integral role in the neural control of feeding. Current experiments probed whether lateral PBN (lPBN) leptin receptor (LepRb) signaling contributes to this function. Intra-lPBN leptin microinjection significantly reduced cumulative chow intake, average meal size, and body weight in rats, independent of effects on locomotor activity or gastric emptying. In contrast to the effects observed following LepRb activation in other nuclei, lPBN LepRb stimulation did not affect progressive ratio responding for sucrose reward or conditioned place preference for a palatable food. Collectively, results suggest that lPBN LepRb activation reduces food intake by modulating the neural processing of meal size/satiation signaling, and highlight the lPBN as a novel site of action for leptin-mediated food intake control.

The anorectic hormone amylin contributes to feeding-related changes of neuronal activity in key structures of the gut-brain axis

2004 ◽  
Vol 286 (1) ◽  
pp. R114-R122 ◽  
Author(s):  
T. Riediger ◽  
D. Zuend ◽  
C. Becskei ◽  
T. A. Lutz
Keyword(s):  
Food Intake ◽  
Area Postrema ◽  
Peptide Hormone ◽  
Central Nucleus ◽  
Circumventricular Organ ◽  
Hypothalamic Area ◽  
Physiological Concentration ◽  
Lateral Parabrachial Nucleus ◽  
Neuronal Mechanisms ◽  
Fos Expression

Amylin is a peptide hormone that is cosecreted with insulin from the pancreas during and after food intake. Peripherally injected amylin potently inhibits feeding by acting on the area postrema (AP), a circumventricular organ lacking a functional blood-brain barrier. We recently demonstrated that AP neurons are excited by a near physiological concentration of amylin. However, the subsequent neuronal mechanisms and the relevance of endogenously released amylin for the regulation of food intake are poorly understood. Therefore, we investigated 1) amylin's contribution to feeding-induced c-Fos expression in the rat AP and its ascending projection sites, and 2) amylin's ability to reverse fasting-induced c-Fos expression in the lateral hypothalamic area (LHA). Similar to amylin (20 μg/kg sc), refeeding of 24-h food-deprived rats induced c-Fos expression in the AP, the nucleus of the solitary tract, the lateral parabrachial nucleus, and the central nucleus of the amygdala. In AP-lesioned rats, the amylin-induced c-Fos expression in each of these sites was blunted, indicating an AP-mediated activation of these structures. Pretreatment with the amylin antagonist AC-187 (1 mg/kg sc) inhibited feeding-induced c-Fos expression in the AP. Food deprivation activated LHA neurons, a response known to be associated with hunger. This effect was reversed within 2 h after refeeding and also in nonrefed animals that received amylin. In summary, our data provide the first evidence that feeding-induced amylin release activates AP neurons projecting to subsequent relay stations known to transmit meal-related signals to the forebrain. Activation of this pathway seems to coincide with an inhibition of LHA neurons.

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