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.

scholarly journals Forebrain neurons that project to the gustatory parabrachial nucleus in rat lack glutamic acid decarboxylase

2008 ◽  
Vol 294 (1) ◽  
pp. R52-R57 ◽  
Author(s):  
Shalini Saggu ◽  
Robert F. Lundy
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Input Resistance ◽  
Central Nucleus ◽  
Parabrachial Nucleus ◽  
Acid Decarboxylase ◽  
Inhibitory Influence ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Forebrain Neurons

Evidence suggests that GABA might mediate the inhibitory influence of centrifugal inputs on taste-evoked responses in the parabrachial nucleus (PBN). Previous studies show that activation of the gustatory cortex (GC), bed nucleus of the stria terminalis (BNST), central nucleus of the amygdala (CeA), and lateral hypothalamus (LH) inhibits PBN taste responses, GABAergic neurons are present in these forebrain regions, and GABA reduces the input resistance of PBN neurons. The present study investigated the expression of glutamic acid decarboxylase immunoreactivity (GAD_67 ir) in GC, BNST, CeA, and LH neurons that project to the PBN in rats. After anesthesia (50 mg/kg ip Nembutal), injections of the retrograde tracer Fluorogold (FG) were made in the physiologically defined gustatory PBN. Brain tissue containing the above forebrain structures was processed and examined for FG and GAD_67 ir. Similar to previous studies, each forebrain site contained retrogradely labeled neurons. Our results suggest further that the major source of input to the PBN taste region is the CeA (608 total cells) followed by GC (257 cells), LH (106 cells), and BNST (92 cells). This suggests a differential contribution to centrifugal control of PBN taste processing. We further show that despite the presence of GAD_67 neurons in each forebrain area, colocalization was extremely rare, occurring only in 3 out of 1,063 FG-labeled cells. If we assume that the influence of centrifugal input is mediated by direct projections to the gustatory region of the PBN, then GABAergic forebrain neurons apparently are not part of this descending pathway.

Anxiety Reduction and Maternal Aggression in Postpartum Nonhuman Mammals

2020 ◽  
pp. 164-193
Author(s):  
Michael Numan
Keyword(s):  
Neural Circuitry ◽  
Corticotropin Releasing Factor ◽  
Anxiety Reduction ◽  
Central Nucleus ◽  
Ventromedial Nucleus ◽  
Stria Terminalis ◽  
Maternal Aggression ◽  
Postpartum Anxiety ◽  
Bed Nucleus ◽  
Crf Neurons

Chapter 6 explores the neural mechanisms that regulate the decrease in anxiety and increase in maternal aggression that co-occur in postpartum mammals. Too much anxiety antagonizes maternal aggression. Therefore, postpartum anxiety reduction promotes maternal aggression. The neural circuitry of maternal aggression includes projections from the ventromedial nucleus of the hypothalamus to the periaqueductal gray and to other brainstem sites. Anxiety-related behaviors are mediated by corticotropin-releasing factor (CRF) neurons, and the projection of central nucleus of amygdala (CeA) CRF neurons to the dorsal bed nucleus of the stria terminalis is involved. Neural circuits are described to show how enhanced CRF release can depress maternal aggression. These circuits are typically downregulated in postpartum females, and oxytocin (OT) is involved. OT exerts anxiolytic effects and one mechanism of OT action is to depress the output of CeA.

Naltrexone administered to central nucleus of amygdala or PVN: neural dissociation of diet and energy

2000 ◽  
Vol 279 (1) ◽  
pp. R86-R92 ◽  
Author(s):  
Michael J. Glass ◽  
Charles J. Billington ◽  
Allen S. Levine
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Neural Circuitry ◽  
Brain Regions ◽  
Wide Distribution ◽  
Central Nucleus ◽  
Total Energy Consumption ◽  
Direct Stimulation ◽  
The Central Nervous System ◽  
Diet Intake

There is evidence that opioids may affect food consumption through mechanisms as diverse as reward or energy metabolism. However, these hypotheses are derived from studies employing peripheral or, more rarely, intracerebroventricular administration of drugs. Opioid receptors have a wide distribution in the central nervous system and include a number of regions implicated in food intake such as the hypothalamic paraventricular nucleus (PVN) and the central nucleus of the amygdala (ACe). It is not known whether local opioid receptor blockade in either of these regions will produce similar effects on food intake. To examine this issue, a chronic cannula was aimed at either the PVN or ACe of rats that were fed a choice of a high-fat and high-carbohydrate diet, which allows for the measurement of both preference and total energy consumption. Naltrexone influenced preferred and nonpreferred food consumption, depending on the site of administration. Consumption of both preferred and nonpreferred diets was suppressed after PVN naltrexone administration, whereas only preferred diet intake was reduced after ACe injection of naltrexone. The present evidence indicates that direct stimulation of different brain regions with naltrexone may be associated with diverse effects on diet selection, which may be accounted for by manipulation of specific functional neural circuitry.

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