scholarly journals Activation of catecholamine neurons in the ventral medulla reduces CCK-induced hypophagia and c-Fos activation in dorsal medullary catecholamine neurons

2018 ◽  
Vol 315 (3) ◽  
pp. R442-R452
Author(s):  
Ai-Jun Li ◽  
Qing Wang ◽  
Sue Ritter
Keyword(s):  
Food Intake ◽  
Ventrolateral Medulla ◽  
Designer Drug ◽  
Cell Group ◽  
Cell Groups ◽  
Increase Food Intake ◽  
Threatening Condition ◽  
Metabolic Conditions ◽  
Fos Expression ◽  
Catecholamine Neurons

Catecholamine (CA) neurons within the A1 and C1 cell groups in the ventrolateral medulla (VLM) potently increase food intake when activated by glucose deficit. In contrast, CA neurons in the A2 cell group of the dorsomedial medulla are required for reduction of food intake by cholecystokinin (CCK), a peptide that promotes satiation. Thus dorsal and ventral medullary CA neurons are activated by divergent metabolic conditions and mediate opposing behavioral responses. Acute glucose deficit is a life-threatening condition, and increased feeding is a key response that facilitates survival of this emergency. Thus, during glucose deficit, responses to satiation signals, like CCK, must be suppressed to ensure glucorestoration. Here we test the hypothesis that activation of VLM CA neurons inhibits dorsomedial CA neurons that participate in satiation. We found that glucose deficit produced by the antiglycolytic glucose analog, 2-deoxy-d-glucose, attenuated reduction of food intake by CCK. Moreover, glucose deficit increased c-Fos expression by A1 and C1 neurons while reducing CCK-induced c-Fos expression in A2 neurons. We also selectively activated A1/C1 neurons in TH-Cre+ transgenic rats in which A1/C1 neurons were transfected with a Cre-dependent designer receptor exclusively activated by a designer drug (DREADD). Selective activation of A1/C1 neurons using the DREADD agonist, clozapine- N-oxide, attenuated reduction of food intake by CCK and prevented CCK-induced c-Fos expression in A2 CA neurons, even under normoglycemic conditions. Results support the hypothesis that activation of ventral CA neurons attenuates satiety by inhibiting dorsal medullary A2 CA neurons. This mechanism may ensure that satiation does not terminate feeding before restoration of normoglycemia.

scholarly journals Orexin-A enhances feeding in male rats by activating hindbrain catecholamine neurons

2015 ◽  
Vol 309 (4) ◽  
pp. R358-R367 ◽  
Author(s):  
Ai-Jun Li ◽  
Qing Wang ◽  
Hana Davis ◽  
Rong Wang ◽  
Sue Ritter
Keyword(s):  
Food Intake ◽  
Male Rats ◽  
Ventrolateral Medulla ◽  
Orexin A ◽  
Catecholaminergic Neurons ◽  
Close Proximity ◽  
Cell Groups ◽  
Increase Food Intake ◽  
Catecholamine Neurons ◽  
Positive Direct

Both lateral hypothalamic orexinergic neurons and hindbrain catecholaminergic neurons contribute to control of feeding behavior. Orexin fibers and terminals are present in close proximity to hindbrain catecholaminergic neurons, and fourth ventricular (4V) orexin injections that increase food intake also increase c-Fos expression in hindbrain catecholamine neurons, suggesting that orexin neurons may stimulate feeding by activating catecholamine neurons. Here we examine that hypothesis in more detail. We found that 4V injection of orexin-A (0.5 nmol/rat) produced widespread activation of c-Fos in hindbrain catecholamine cell groups. In the A1 and C1 cell groups in the ventrolateral medulla, where most c-Fos-positive neurons were also dopamine β hydroxylase (DBH) positive, direct injections of a lower dose (67 pmol/200 nl) of orexin-A also increased food intake in intact rats. Then, with the use of the retrogradely transported immunotoxin, anti-DBH conjugated to saporin (DSAP), which targets and destroys DBH-expressing catecholamine neurons, we examined the hypothesis that catecholamine neurons are required for orexin-induced feeding. Rats given paraventricular hypothalamic injections of DSAP, or unconjugated saporin (SAP) as control, were implanted with 4V or lateral ventricular (LV) cannulas and tested for feeding in response to ventricular injection of orexin-A (0.5 nmol/rat). Both LV and 4V orexin-A stimulated feeding in SAP controls, but DSAP abolished these responses. These results reveal for the first time that catecholamine neurons are required for feeding induced by injection of orexin-A into either LV or 4V.

scholarly journals Hindbrain Catecholamine Neurons Modulate the Growth Hormone But Not the Feeding Response to Ghrelin

Endocrinology ◽  
2010 ◽  
Vol 151 (7) ◽  
pp. 3237-3246 ◽  
Author(s):  
Alan J. Emanuel ◽  
Sue Ritter
Keyword(s):  
Feeding Response ◽  
Gh Treatment ◽  
Anatomical Distribution ◽  
Adrenergic Neurons ◽  
Gh Secretion ◽  
Cell Groups ◽  
Baseline Levels ◽  
Fos Expression ◽  
Catecholamine Neurons

The gastrointestinal peptide, ghrelin, elicits feeding and secretion when administered systemically or centrally. Previous studies have suggested that hypothalamic projections of hindbrain catecholamine neurons are involved in both of these actions of ghrelin. The purpose of this study was to further assess the role of hindbrain catecholamine neurons in ghrelin-induced feeding and GH secretion and to determine the anatomical distribution of the catecholamine neurons involved. We lesioned noradrenergic and adrenergic neurons that innervate the medial hypothalamus by microinjecting the retrogradely transported immunotoxin, saporin (SAP) conjugated to antidopamine-β-hydroxylase (DSAP) into the paraventricular nucleus of the hypothalamus. Controls were injected with unconjugated SAP. We found that the DSAP lesion did not impair the feeding response to central or peripheral ghrelin administration, indicating that these neurons are not required for ghrelin’s orexigenic effect. However, the GH response to ghrelin was prolonged significantly in DSAP-lesioned rats. We also found that expression of Fos, an indicator of neuronal activation, was significantly enhanced over baseline levels in A1, A1/C1, C1, and A5 cell groups after ghrelin treatment and in A1, A1/C1, and A5 cell groups after GH treatment. The similar pattern of Fos expression in catecholamine cell groups after GH and ghrelin and the prolonged GH secretion in response to ghrelin in DSAP rats together suggest that activation of hindbrain catecholamine neurons by ghrelin or GH could be a component of a negative feedback response controlling GH levels.

Injections of the of the α 1 -adrenoceptor antagonist prazosin into the median raphe nucleus increase food intake and Fos expression in orexin neurons of free-feeding rats

2017 ◽  
Vol 324 ◽  
pp. 87-95 ◽  
Author(s):  
Eduardo Simão da Silva ◽  
Rafael Appel Flores ◽  
Anderson Savaris Ribas ◽  
Ana Paula Taschetto ◽  
Moacir Serralvo Faria ◽  
...  
Keyword(s):  
Food Intake ◽  
Raphe Nucleus ◽  
Median Raphe ◽  
Median Raphe Nucleus ◽  
Adrenoceptor Antagonist ◽  
Increase Food Intake ◽  
Nucleus Increase ◽  
Fos Expression ◽  
Free Feeding ◽  
Median Raphé

scholarly journals Central administration of sodium-glucose cotransporter-2 inhibitors increases food intake involving adenosine monophosphate-activated protein kinase phosphorylation in the lateral hypothalamus in healthy rats

2021 ◽  
Vol 9 (1) ◽  
pp. e002104
Author(s):  
Kenji Takeda ◽  
Hiraku Ono ◽  
Ko Ishikawa ◽  
Tomohiro Ohno ◽  
Jin Kumagai ◽  
...  
Keyword(s):  
Food Intake ◽  
Lateral Hypothalamus ◽  
Molecular Mechanisms ◽  
Intraperitoneal Administration ◽  
Adenosine Monophosphate ◽  
Sglt2 Inhibitors ◽  
Central Administration ◽  
Hypothalamic Area ◽  
Sodium Glucose Cotransporter ◽  
Increase Food Intake

IntroductionSodium glucose cotransporter-2 (SGLT2) inhibitors are widely used for diabetes treatment. Although SGLT2 inhibitors have been clinically observed to increase food intake, roles or even the presence of SGLT2 in the central nervous system (CNS) has not been established. We aimed to elucidate potential functions of SGLT2 in the CNS, and the effects of CNS-targeted SGLT2 inhibitors on food intake.Research design and methodsWe administered three kinds of SGLT2 inhibitors, tofogliflozin, dapagliflozin, and empagliflozin, into the lateral ventricle (LV) in rats and evaluated their effects on food intake. We also evaluated the effects of tofogliflozin administration in the third (3V) and fourth ventricle (4V). Intraperitoneal administration of liraglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist known to suppress food intake, was combined with central tofogliflozin to elucidate whether GLP-1 signaling antagonizes the effect of central SGLT2 inhibitors on food intake. To elucidate potential molecular mechanisms mediating changes in feeding, hypothalamic areas associated with food intake regulation were harvested and analyzed after intracerebroventricular administration (ICV) of tofogliflozin.ResultsBolus ICV injection of tofogliflozin induced a robust increase in food intake starting at 1.5 hours postinjection, and lasting for 5 days. No effect was observed when the same dose of tofogliflozin was administered intraperitoneally. ICV dapagliflozin and empagliflozin significantly enhanced food intake, although the strength of these effects varied among drugs. Food intake was most markedly enhanced when tofogliflozin was infused into the LV. Fewer or no effects were observed with infusion into the 3V or 4V, respectively. Systemic administration of liraglutide suppressed the effect of ICV tofogliflozin on food intake. ICV tofogliflozin increased phosphorylation of AMPK and c-fos expression in the lateral hypothalamus.ConclusionsSGLT2 inhibitors in the CNS increase food intake. SGLT2 activity in the CNS may regulate food intake through AMPK phosphorylation in the lateral hypothalamic area.

Negative Reinforcement–Based Treatment to Increase Food Intake

2000 ◽  
Vol 24 (4) ◽  
pp. 600-608 ◽  
Author(s):  
Edward B. Kitfield ◽  
Christopher J. Masalsky
Keyword(s):  
Food Intake ◽  
Negative Reinforcement ◽  
Increase Food Intake

Identification of Basolateral Amygdala Projection Cells and Interneurons Using Extracellular Recordings

2006 ◽  
Vol 96 (6) ◽  
pp. 3257-3265 ◽  
Author(s):  
Ekaterina Likhtik ◽  
Joe Guillaume Pelletier ◽  
Andrei T. Popescu ◽  
Denis Paré
Keyword(s):  
Firing Rate ◽  
Basolateral Amygdala ◽  
Cell Group ◽  
Small Subset ◽  
Cortical Projection ◽  
Antidromic Activation ◽  
Extracellular Recordings ◽  
Firing Rates ◽  
Cell Groups ◽  
Exact Position

This study tested whether firing rate and spike shape could be used to distinguish projection cells from interneurons in extracellular recordings of basolateral amygdala (BLA) neurons. To this end, we recorded BLA neurons in isoflurane-anesthetized animals with tungsten microelectrodes. Projection cells were identified by antidromic activation from cortical projection sites of the BLA. Although most projection cells fired spontaneously at low rates (<1 Hz), an important subset fired at higher rates (up to 6.8 Hz). In fact, the distribution of firing rates in projection cells and unidentified BLA neurons overlapped extensively, even though the latter cell group presumably contains a higher proportion of interneurons. The only difference between the two distributions was a small subset (5.1%) of unidentified neurons with unusually high firing rates (9–16 Hz). Similarly, distributions of spike durations in both cell groups were indistinguishable, although most of the fast-firing neurons had spike durations at the low end of the distribution. However, we observed that spike durations depended on the exact position of the electrode with respect to the recorded cell, varying by as much as 0.7 ms. Thus neither firing rate nor spike waveform allowed for unequivocal separation of projection cells from interneurons. Nevertheless, we propose the use of two firing rate cutoffs to obtain relatively pure samples of projection cells and interneurons: ≤1 Hz for projection cells and ≥7 Hz for fast-spiking interneurons. Supplemented with spike-duration cutoffs of ≥0.7 ms for projection cells and ≤0.5 ms for interneurons, this approach should keep instances of misclassifications to a minimum.

2: Do intense sweeteners increase food intake?

1987 ◽  
Vol 12 (3) ◽  
pp. 132-133
Author(s):  
I. Macdonald
Keyword(s):  
Food Intake ◽  
Increase Food Intake

scholarly journals Specifically Binding of D-Amino Neuraminic Acid to Ganglioside Studied in Prostate Cancer Cells

2021 ◽  
Author(s):  
Kenan Demir ◽  
Huseyin Aktug ◽  
Gurkan Yigitturk ◽  
Eda Acikgoz ◽  
Gunnur Guler ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Enzyme Inhibitor ◽  
Cancer Cell Line ◽  
Prostate Cancer Cell Line ◽  
Cell Group ◽  
Synthesis Inhibitor ◽  
Cell Groups ◽  
Negative Effect ◽  
Synthase Inhibitor

Abstract Aims: The aim of this study was to investigate the cellular binding site of human KDN (2-keto-3-deoxy-D-glycero-D-galacto-nononic acid). The KDN molecule is a member of the sialic acid family, and its expression increases in cancer cells. Although KDN has been shown to bind to GM3 (Monosialodihexosyl Ganglioside) in trout sperm.Methods and Results: Prostate cancer cell line (DU145) was used in this study. Each experimental group was divided into 3 groups: control, GCS (Glucosylceramide synthase) enzyme inhibitor Genz-123346 treated, and GM3 synthesis inhibitor Triptolide treated. Each group was stained using the immunocytochemical method for GM3, GD3 (Disialosyllactosylceramide) and KDN. The FTIR (Fourier Transform Infrared Spectroscopy) analysis was performed to elucidate the cellular changes upon treatment. The non-treated number 1 cell group stained positive with all of GM3, GD3 and KDN, the GCS enzyme blocked with Genz-123346 number 2 cell groups stained positive with only KDN. Furthermore, GD3 Synthase inhibitor Triptolide treated number 3 cell group stained positive with GM3 and KDN. Measurements with FTIR showed apoptotic features with Triptolide while Genz-123346 had no negative effect on the cell viability. The decrease in sugar constructions was revealed and the results that we obtained with staining were reinforced.Conclusions: Determining the location of bounded KDN is important in selecting new targets for cancer treatment researches. It has been shown that KDN is not inhibited by both GM3 inhibition and GD3 inhibition, and thus, KDN might also bind to different places, be specific, and not only attached to any of gangliosides of the GM or GD series.

Hypoxia-induced Fos expression in neurons projecting to the pressor region in the rostral ventrolateral medulla

Neuroscience ◽  
1997 ◽  
Vol 80 (4) ◽  
pp. 1209-1224 ◽  
Author(s):  
Y Hirooka ◽  
J.W Polson ◽  
P.D Potts ◽  
R.A.L Dampney
Keyword(s):  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Fos Expression

Fos expression in brain stem nuclei of pregnant rats after hydralazine-induced hypotension

1999 ◽  
Vol 277 (2) ◽  
pp. R532-R540 ◽  
Author(s):  
Kathleen S. Curtis ◽  
J. Thomas Cunningham ◽  
Cheryl M. Heesch
Keyword(s):  
Area Postrema ◽  
Virgin Female ◽  
Female Rats ◽  
Ventrolateral Medulla ◽  
Pregnant Rats ◽  
Induced Hypotension ◽  
Central Response ◽  
Vehicle Treatment ◽  
Fos Expression ◽  
The Brain

Fos and dopamine β-hydroxylase immunoreactivity were evaluated in the brain stems of 21-day pregnant and virgin female rats injected with either hydralazine (HDZ; 10 mg/kg iv) or vehicle. HDZ produced significant hypotension in both groups, although baseline blood pressure was lower in pregnant rats (96 ± 2.5 mmHg) than in virgin female rats (121 ± 2.8 mmHg). There were no differences in Fos immunoreactivity in the brain stems of pregnant and virgin female rats after vehicle treatment. HDZ-induced hypotension significantly increased Fos expression in both groups; however, the magnitude of the increases differed in the caudal ventrolateral medulla (CVL), the area postrema (AP), and the rostral ventrolateral medulla (RVL). Fos expression after HDZ in pregnant rats was augmented in noncatecholaminergic neurons of the CVL but was attenuated in the AP and in noncatecholaminergic neurons in the RVL. These results are consistent with differences in the sympathetic response to hypotension between pregnant and virgin female rats and indicate that the central response to hypotension may be different in pregnant rats.

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