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28 results on '"Cabral, Agustina"'

2. GHSR in a Subset of GABA Neurons Controls Food Deprivation-Induced Hyperphagia in Male Mice

Author

Cornejo, María Paula, Fernandez, Gimena, Cabral, Agustina, Barrile, Franco, Heredia, Florencia, García Romero, Guadalupe, Zubimendi Sampieri, Juan Pablo, Quelas, Juan Ignacio, Cantel, Sonia, Fehrentz, Jean-Alain, Alonso, Antonia, Pla, Ramon, Ferran, José Luis, Andreoli, María Florencia, De Francesco, Pablo Nicolas, Perelló, Mario, Cornejo, María Paula, Fernandez, Gimena, Cabral, Agustina, Barrile, Franco, Heredia, Florencia, García Romero, Guadalupe, Zubimendi Sampieri, Juan Pablo, Quelas, Juan Ignacio, Cantel, Sonia, Fehrentz, Jean-Alain, Alonso, Antonia, Pla, Ramon, Ferran, José Luis, Andreoli, María Florencia, De Francesco, Pablo Nicolas, and Perelló, Mario

Abstract

The growth hormone secretagogue receptor (GHSR), primarily known as the receptor for the hunger hormone ghrelin, potently controls food intake, yet the specific Ghsr-expressing cells mediating the orexigenic effects of this receptor remain incompletely characterized. Since Ghsr is expressed in gamma-aminobutyric acid (GABA)–producing neurons, we sought to investigate whether the selective expression of Ghsr in a subset of GABA neurons is sufficient to mediate GHSR's effects on feeding. First, we crossed mice that express a tamoxifen-dependent Cre recombinase in the subset of GABA neurons that express glutamic acid decarboxylase 2 (Gad2) enzyme (Gad2-CreER mice) with reporter mice, and found that ghrelin mainly targets a subset of Gad2-expressing neurons located in the hypothalamic arcuate nucleus (ARH) and that is predominantly segregated from Agouti-related protein (AgRP)–expressing neurons. Analysis of various single-cell RNA-sequencing datasets further corroborated that the primary subset of cells coexpressing Gad2 and Ghsr in the mouse brain are non-AgRP ARH neurons. Next, we crossed Gad2-CreER mice with reactivable GHSR-deficient mice to generate mice expressing Ghsr only in Gad2-expressing neurons (Gad2-GHSR mice). We found that ghrelin treatment induced the expression of the marker of transcriptional activation c-Fos in the ARH of Gad2-GHSR mice, yet failed to induce food intake. In contrast, food deprivation–induced refeeding was higher in Gad2-GHSR mice than in GHSR-deficient mice and similar to wild-type mice, suggesting that ghrelin-independent roles of GHSR in a subset of GABA neurons is sufficient for eliciting full compensatory hyperphagia in mice.

Published
2024
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5. Ghrelin action in the PVH of male mice: accessibility, neuronal targets and CRH neurons activation

Author

Fernandez, Gimena, primary, De Francesco, Pablo N, additional, Cornejo, María P, additional, Cabral, Agustina, additional, Aguggia, Julieta P, additional, Duque, Victor J, additional, Sayar, Nilufer, additional, Cantel, Sonia, additional, Burgos, Juan I, additional, Fehrentz, Jean-Alain, additional, Rorato, Rodrigo, additional, Atasoy, Deniz, additional, Mecawi, André S, additional, and Perello, Mario, additional

Published
2023
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11. Development of a novel fluorescent ligand of growth hormone secretagogue receptor based on the N-Terminal Leap2 region

Author

Barrile, Franco, primary, M'Kadmi, Céline, additional, De Francesco, Pablo N., additional, Cabral, Agustina, additional, García Romero, Guadalupe, additional, Mustafá, Emilio R., additional, Cantel, Sonia, additional, Damian, Marjorie, additional, Mary, Sophie, additional, Denoyelle, Séverine, additional, Banères, Jean-Louis, additional, Marie, Jacky, additional, Raingo, Jesica, additional, Fehrentz, Jean-Alain, additional, and Perelló, Mario, additional

Published
2019
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12. N-terminal LEAP2 region exhibits inverse agonist activity toward the ghrelin receptor

Author

M'Kadmi, Celine, Cabral, Agustina, Barrile, Franco, Julien Giribaldi , Julien, Sonia, Cantel, Marjorie, Damian, Sophie, Mary, Séverine, Denoyelle, Sébastien, Dutertre, Sylvie, Péraldi-Roux, Jérémie, Neasta, Catherine, Oiry, Jean-Louis, Banères, Jacky Marie and Mario Perello and Jean-Alain, Fehrentz, Institut des Biomolécules Max Mousseron [Pôle Chimie Balard] (IBMM), and Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM)-Institut de Chimie du CNRS (INC)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV]Life Sciences [q-bio], ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2019

14. N-Terminal Liver-Expressed Antimicrobial Peptide 2 (LEAP2) Region Exhibits Inverse Agonist Activity toward the Ghrelin Receptor

Author

M’Kadmi, Céline, primary, Cabral, Agustina, additional, Barrile, Franco, additional, Giribaldi, Julien, additional, Cantel, Sonia, additional, Damian, Marjorie, additional, Mary, Sophie, additional, Denoyelle, Séverine, additional, Dutertre, Sébastien, additional, Péraldi-Roux, Sylvie, additional, Neasta, Jérémie, additional, Oiry, Catherine, additional, Banères, Jean-Louis, additional, Marie, Jacky, additional, Perello, Mario, additional, and Fehrentz, Jean-Alain, additional

Published
2018
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16. Evidence Supporting a Role for Constitutive Ghrelin Receptor Signaling in Fasting-Induced Hyperphagia in Male Mice

Author

Fernandez, Gimena, primary, Cabral, Agustina, additional, Andreoli, María F, additional, Labarthe, Alexandra, additional, M'Kadmi, Céline, additional, Ramos, Jorge G, additional, Marie, Jacky, additional, Fehrentz, Jean-Alain, additional, Epelbaum, Jacques, additional, Tolle, Virginie, additional, and Perello, Mario, additional

Published
2017
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19. Neuroanatomical and functional characterization of CRF neurons of the amygdala using a novel transgenic mouse model

Author

De Francesco, Pablo, Valdivia Torres, Lesly Spring, Cabral, Agustina, Reynaldo, Mirta Beatriz, Raingo, Jesica, Sakata, I., Osborne-Lawrence, S., Zigman, J.M., and Perelló, Mario

Subjects
endocrine system, stress, food intake, nervous system, Biología Celular, Microbiología, digestive, oral, and skin physiology, amygdala, hormones, hormone substitutes, and hormone antagonists
Abstract

The corticotropin-releasing factor (CRF)-producing neurons of the amygdala have been implicated in behavioral and physiological responses associated with fear, anxiety, stress, food intake and reward. To overcome the difficulties in identifying CRF neurons within the amygdala, a novel transgenic mouse line, in which the humanized recombinant Renilla reniformis green fluorescent protein (hrGFP) is under the control of the CRF promoter (CRF-hrGFP mice), was developed. First, the CRF-hrGFP mouse model was validated and the localization of CRF neurons within the amygdala was systematically mapped. Amygdalar hrGFP-expressing neurons were located primarily in the interstitial nucleus of the posterior limb of the anterior commissure, but also present in the central amygdala. Secondly, the marker of neuronal activation c-Fos was used to explore the response of amygdalar CRF neurons in CRF-hrGFP mice under different experimental paradigms. C-Fos induction was observed in CRF neurons of CRF-hrGFP mice exposed to an acute social defeat stress event, a fasting/refeeding paradigm or lipopolysaccharide (LPS) administration. In contrast, no c-Fos induction was detected in CRF neurons of CRF-hrGFP mice exposed to restraint stress, forced swimming test, 48-h fasting, acute high-fat diet (HFD) consumption, intermittent HFD consumption, ad libitum HFD consumption, HFD withdrawal, conditioned HFD aversion, ghrelin administration or melanocortin 4 receptor agonist administration. Thus, this study fully characterizes the distribution of amygdala CRF neurons in mice and suggests that they are involved in some, but not all, stress or food intake-related behaviors recruiting the amygdala.

Published
2015

21. Des-Acyl Ghrelin and Ghrelin O-Acyltransferase Regulate Hypothalamic-Pituitary-Adrenal Axis Activation and Anxiety in Response to Acute Stress

Author

Stark, Romana, primary, Santos, Vanessa V., additional, Geenen, Bram, additional, Cabral, Agustina, additional, Dinan, Tara, additional, Bayliss, Jacqueline A., additional, Lockie, Sarah H., additional, Reichenbach, Alex, additional, Lemus, Moyra B., additional, Perello, Mario, additional, Spencer, Sarah J., additional, Kozicz, Tamas, additional, and Andrews, Zane B., additional

Published
2016
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22. Constitutive and ghrelin-dependent GHSR1a activation impairs CaV2.1 and CaV2.2 currents in hypothalamic neurons

Author

López Soto, Eduardo Javier, primary, Agosti, Francina, additional, Cabral, Agustina, additional, Mustafa, Emilio Roman, additional, Damonte, Valentina Martínez, additional, Gandini, Maria Alejandra, additional, Rodríguez, Silvia, additional, Castrogiovanni, Daniel, additional, Felix, Ricardo, additional, Perelló, Mario, additional, and Raingo, Jesica, additional

Published
2015
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26. Constitutive and ghrelin-dependent GHSR1a activation impairs CaV2.1 and CaV2.2 currents in hypothalamic neurons.

Author

Soto, Eduardo Javier López, Agosti, Francina, Cabral, Agustina, Mustafa, Emilio Roman, Damonte, Valentina Martínez, Gandini, Maria Alejandra, Rodríguez, Silvia, Castrogiovanni, Daniel, Felix, Ricardo, Perelló, Mario, and Raingo, Jesica

Subjects
*GHRELIN receptors, *GABA, *CALCIUM channels, *CELL membranes, *VOLTAGE-gated ion channels, *NEURAL physiology, *NEUROTRANSMITTER receptors
Abstract

The growth hormone secretagogue receptor type 1a (GHSR1a) has the highest known constitutive activity of any G protein-coupled receptor (GPCR). GHSR1a mediates the action of the hormone ghrelin, and its activation increases transcriptional and electrical activity in hypothalamic neurons. Although GHSR1a is present at GABAergic presynaptic terminals, its effect on neurotransmitter release remains unclear. The activities of the voltage-gated calcium channels, CaV2.1 and CaV2.2, which mediate neurotransmitter release at presynaptic terminals, are modulated by many GPCRs. Here, we show that both constitutive and agonist-dependent GHSR1a activity elicit a strong impairment of CaV2.1 and CaV2.2 currents in rat and mouse hypothalamic neurons and in a heterologous expression system. Constitutive GHSR1a activity reduces CaV2 currents by a Gi/o-dependent mechanism that involves persistent reduction in channel density at the plasma membrane, whereas ghrelin-dependent GHSR1a inhibition is reversible and involves altered CaV2 gating via a Gq-dependent pathway. Thus, GHSR1a differentially inhibits CaV2 channels by Gi/o or Gq protein pathways depending on its mode of activation. Moreover, we present evidence suggesting that GHSR1a-mediated inhibition of CaV2 attenuates GABA release in hypothalamic neurons, a mechanism that could contribute to neuronal activation through the disinhibition of postsynaptic neurons. [ABSTRACT FROM AUTHOR]

Published
2015
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27. Estudio del rol modulador de Ghrelina y su receptor sobre los circuitos hipotalámicos que controlan el balance energético

Author

Gimena Fernandez, Perello, Mario, Cabral, Agustina Soledad, and Perelló, Mario

Subjects
CIENCIAS MÉDICAS Y DE LA SALUD, Philosophy, Energía, Neurociencias, ghrelina, GHSR, hiperfagia, eje hipotálamo-hipofiso-adrenal, desacil-ghrelina, purl.org/becyt/ford/3.1 [https], Medicina Básica, Homeostasis, purl.org/becyt/ford/3 [https], Ghrelina, Ghsr, Humanities, Ciencias Exactas
Abstract

La ghrelina es una hormona peptídica producida principalmente en el estómago que desempeña un papel fundamental en el control de la liberación de hormona de crecimiento, la homeostasis de glucosa, la actividad de ejes neuroendócrinos, el peso corporal, entre otros. La concentración plasmática de ghrelina aumenta en condiciones de balance energético negativo como el ayuno o la restricción calórica. El receptor de ghrelina (GHSR) está presente en varios sitios del hipotálamo importantes en el control del apetito o de los ejes neuroendocrinos. Una de las particularidades de GHSR es que posee una elevada actividad basal, la cual causa una elevada señalización intracelular constitutiva aún en ausencia de ghrelina. El hecho que el receptor de ghrelina esté presente en áreas del hipotálamo sin acceso inmediato a la hormona circulante y que su nivel de expresión génica aumente en condiciones de balance energético negativo, han llevado a sugerir que la actividad constitutiva del receptor poseería un rol fisiológico. Sin embargo, la regulación de la expresión de GHSR en el hipotálamo y sus implicancias fisiológicas no han sido sistemáticamente estudiadas hasta ahora. Por este motivo, el objetivo general del presente plan de Tesis Doctoral es investigar la regulación de la expresión del receptor de ghrelina a nivel hipotalámico en condiciones de balance energético negativo y sus implicancias en la regulación del apetito y del eje neuroendocrino hipotálamo-hipófiso-adrenal., Facultad de Ciencias Exactas

Published
2019

28. GHSR in a Subset of GABA Neurons Controls Food Deprivation-Induced Hyperphagia in Male Mice.

Author

Cornejo MP, Fernandez G, Cabral A, Barrile F, Heredia F, García Romero G, Zubimendi Sampieri JP, Quelas JI, Cantel S, Fehrentz JA, Alonso A, Pla R, Ferran JL, Andreoli MF, De Francesco PN, and Perelló M

Subjects
Animals, Male, Mice, Mice, Transgenic, Agouti-Related Protein metabolism, Agouti-Related Protein genetics, Mice, Inbred C57BL, GABAergic Neurons metabolism, Receptors, Ghrelin genetics, Receptors, Ghrelin metabolism, Hyperphagia metabolism, Ghrelin metabolism, Ghrelin pharmacology, Arcuate Nucleus of Hypothalamus metabolism, Food Deprivation physiology, Glutamate Decarboxylase metabolism, Glutamate Decarboxylase genetics
Abstract

The growth hormone secretagogue receptor (GHSR), primarily known as the receptor for the hunger hormone ghrelin, potently controls food intake, yet the specific Ghsr-expressing cells mediating the orexigenic effects of this receptor remain incompletely characterized. Since Ghsr is expressed in gamma-aminobutyric acid (GABA)-producing neurons, we sought to investigate whether the selective expression of Ghsr in a subset of GABA neurons is sufficient to mediate GHSR's effects on feeding. First, we crossed mice that express a tamoxifen-dependent Cre recombinase in the subset of GABA neurons that express glutamic acid decarboxylase 2 (Gad2) enzyme (Gad2-CreER mice) with reporter mice, and found that ghrelin mainly targets a subset of Gad2-expressing neurons located in the hypothalamic arcuate nucleus (ARH) and that is predominantly segregated from Agouti-related protein (AgRP)-expressing neurons. Analysis of various single-cell RNA-sequencing datasets further corroborated that the primary subset of cells coexpressing Gad2 and Ghsr in the mouse brain are non-AgRP ARH neurons. Next, we crossed Gad2-CreER mice with reactivable GHSR-deficient mice to generate mice expressing Ghsr only in Gad2-expressing neurons (Gad2-GHSR mice). We found that ghrelin treatment induced the expression of the marker of transcriptional activation c-Fos in the ARH of Gad2-GHSR mice, yet failed to induce food intake. In contrast, food deprivation-induced refeeding was higher in Gad2-GHSR mice than in GHSR-deficient mice and similar to wild-type mice, suggesting that ghrelin-independent roles of GHSR in a subset of GABA neurons is sufficient for eliciting full compensatory hyperphagia in mice., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com. See the journal About page for additional terms.)

Published
2024
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