@article{MTMT:34221294,
	title = {Hunger-promoting hypothalamic AgRP neurons control structure and function of the medial prefrontal cortex},
	url = {https://m2.mtmt.hu/api/publication/34221294},
	author = {Stutz, Bernardo and Waterson, Michael and Sestan-Pesa, Matija and Dietrich, Marcelo and Skarica, Mario and Sestan, Nenad and Rácz, Bence and Magyar, Aletta and Sótonyi, Péter and Liu, Zhong-Wu and Gao, Xiao-Bing and Matyas, Ferenc and Stoiljkovic, Milan and Horváth, Tamás},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {166},
	unique-id = {34221294},
	issn = {0022-3042},
	keywords = {Biochemistry & Molecular Biology},
	year = {2023},
	eissn = {1471-4159},
	pages = {138-139}
}

@book{MTMT:33880969,
	title = {Body, Brain, Behavior: Three Views and a Conversation},
	url = {https://m2.mtmt.hu/api/publication/33880969},
	isbn = {9780128180938},
	author = {Horváth, Tamás and Hirsch, J. and Molnár, Z.},
	doi = {10.1016/B978-0-12-818093-8.00032-X},
	publisher = {Elsevier B.V.},
	unique-id = {33880969},
	abstract = {Body, Brain, Behavior: Three Views and a Conversation describes brain research on the frontiers, with a particular emphasis on the relationship between the brain and its development and evolution, peripheral organs, and other brains in communication. The book expands current views of neuroscience by illustrating the integration of these disciplines. By using a novel method of conversations between 3 scientists of different disciplines, cellular, endocrine, developmental, and social processes are seamlessly woven into topics that relate to contemporary living in health and disease. This book is a critical read for anyone who wants to become familiar with the inner workings of the nervous system and its intimate connections to the universe of contemporary life issues. © 2022 Elsevier Inc. All rights reserved.},
	year = {2022},
	pages = {1-415}
}

@article{MTMT:33035643,
	title = {AgRP neurons control structure and function of the medial prefrontal cortex},
	url = {https://m2.mtmt.hu/api/publication/33035643},
	author = {Stutz, Bernardo and Waterson, Michael J. and Šestan-Peša, Matija and Dietrich, Marcelo O. and Škarica, Mario and Sestan, Nenad and Rácz, Bence and Magyar, Aletta and Sótonyi, Péter and Liu, Zhong-Wu and Gao, Xiao-Bing and Mátyás, Ferenc and Stoiljkovic, Milan and Horváth, Tamás},
	doi = {10.1038/s41380-022-01691-8},
	journal-iso = {MOL PSYCHIATR},
	journal = {MOLECULAR PSYCHIATRY},
	volume = {27},
	unique-id = {33035643},
	issn = {1359-4184},
	year = {2022},
	eissn = {1476-5578},
	pages = {3951-3960},
	orcid-numbers = {Stutz, Bernardo/0000-0001-5282-6400; Šestan-Peša, Matija/0000-0002-9873-6387; Dietrich, Marcelo O./0000-0001-9781-2221; Škarica, Mario/0000-0002-2478-014X; Sestan, Nenad/0000-0003-0966-9619; Magyar, Aletta/0000-0002-2644-4182; Gao, Xiao-Bing/0000-0002-2035-4936; Mátyás, Ferenc/0000-0002-3903-8896; Stoiljkovic, Milan/0000-0001-7354-6846}
}

@article{MTMT:32909442,
	title = {AgRP neurons control feeding behaviour at cortical synapses via peripherally derived lysophospholipids},
	url = {https://m2.mtmt.hu/api/publication/32909442},
	author = {Endle, Heiko and Horta, Guilherme and Stutz, Bernardo and Muthuraman, Muthuraman and Tegeder, Irmgard and Schreiber, Yannick and Snodgrass, Isabel Faria and Gurke, Robert and Liu, Zhong-Wu and Sestan-Pesa, Matija and Radyushkin, Konstantin and Streu, Nora and Fan, Wei and Baumgart, Jan and Li, Yan and Kloss, Florian and Groppa, Sergiu and Opel, Nils and Dannlowski, Udo and Grabe, Hans J. and Zipp, Frauke and Rácz, Bence and Horváth, Tamás and Nitsch, Robert and Vogt, Johannes},
	doi = {10.1038/s42255-022-00589-7},
	journal-iso = {NAT METAB},
	journal = {NATURE METABOLISM},
	volume = {4},
	unique-id = {32909442},
	abstract = {Phospholipid levels are influenced by peripheral metabolism. Within the central nervous system, synaptic phospholipids regulate glutamatergic transmission and cortical excitability. Whether changes in peripheral metabolism affect brain lipid levels and cortical excitability remains unknown. Here, we show that levels of lysophosphatidic acid (LPA) species in the blood and cerebrospinal fluid are elevated after overnight fasting and lead to higher cortical excitability. LPA-related cortical excitability increases fasting-induced hyperphagia, and is decreased following inhibition of LPA synthesis. Mice expressing a human mutation (Prg-1R346T) leading to higher synaptic lipid-mediated cortical excitability display increased fasting-induced hyperphagia. Accordingly, human subjects with this mutation have higher body mass index and prevalence of type 2 diabetes. We further show that the effects of LPA following fasting are under the control of hypothalamic agouti-related peptide (AgRP) neurons. Depletion of AgRP-expressing cells in adult mice decreases fasting-induced elevation of circulating LPAs, as well as cortical excitability, while blunting hyperphagia. These findings reveal a direct influence of circulating LPAs under the control of hypothalamic AgRP neurons on cortical excitability, unmasking an alternative non-neuronal route by which the hypothalamus can exert a robust impact on the cortex and thereby affect food intake.},
	keywords = {neurophysiology; Homeostasis; hypothalamus},
	year = {2022},
	eissn = {2522-5812},
	pages = {683-692}
}

@article{MTMT:32185509,
	title = {Mitochondrial cristae-remodeling protein OPA1 in POMC neurons couples Ca2+ homeostasis with adipose tissue lipolysis},
	url = {https://m2.mtmt.hu/api/publication/32185509},
	author = {Gómez-Valadés, Alicia G. and Pozo, Macarena and Varela, Luis and Boudjadja, Mehdi Boutagouga and Ramírez, Sara and Chivite, Iñigo and Eyre, Elena and Haddad-Tóvolli, Roberta and Obri, Arnaud and Milà-Guasch, Maria and Altirriba, Jordi and Schneeberger, Marc and Imbernón, Mónica and Garcia-Rendueles, Angela R. and Gama-Perez, Pau and Rojo-Ruiz, Jonathan and Rácz, Bence and Alonso, Maria Teresa and Gomis, Ramon and Zorzano, Antonio and D’Agostino, Giuseppe and Alvarez, Clara V. and Nogueiras, Rubén and Garcia-Roves, Pablo M. and Horváth, Tamás and Claret, Marc},
	doi = {10.1016/j.cmet.2021.07.008},
	journal-iso = {CELL METAB},
	journal = {CELL METABOLISM},
	volume = {33},
	unique-id = {32185509},
	issn = {1550-4131},
	year = {2021},
	eissn = {1932-7420},
	pages = {1820-1835}
}

@article{MTMT:31519149,
	title = {GLP-1 Receptor Signaling in Astrocytes Regulates Fatty Acid Oxidation, Mitochondrial Integrity, and Function},
	url = {https://m2.mtmt.hu/api/publication/31519149},
	author = {Timper, Katharina and del Rio-Martin, Almudena and Cremer, Anna Lena and Bremser, Stephan and Alber, Jens and Giavalisco, Patrick and Varela, Luis and Heilinger, Christian and Nolte, Hendrik and Trifunovic, Aleksandra and Horváth, Tamás and Kloppenburg, Peter and Backes, Heiko and Bruening, Jens C.},
	doi = {10.1016/j.cmet.2020.05.001},
	journal-iso = {CELL METAB},
	journal = {CELL METABOLISM},
	volume = {31},
	unique-id = {31519149},
	issn = {1550-4131},
	abstract = {Astrocytes represent central regulators of brain glucose metabolism and neuronal function. They have recently been shown to adapt their function in response to alterations in nutritional state through responding to the energy state-sensing hormones leptin and insulin. Here, we demonstrate that glucagon-like peptide (GLP)-1 inhibits glucose uptake and promotes beta-oxidation in cultured astrocytes. Conversely, postnatal GLP-1 receptor (GLP-1R) deletion in glial fibrillary acidic protein (GFAP)-expressing astrocytes impairs astrocyte mitochondrial integrity and activates an integrated stress response with enhanced fibroblast growth factor (FGF)21 production and increased brain glucose uptake. Accordingly, central neutralization of FGF21 or astrocyte-specific FGF21 inactivation abrogates the improvements in glucose tolerance and learning in mice lacking GLP-1R expression in astrocytes. Collectively, these experiments reveal a role for astrocyte GLP-1R signaling in maintaining mitochondrial integrity, and lack of GLP-1R signaling mounts an adaptive stress response resulting in an improvement of systemic glucose homeostasis and memory formation.},
	year = {2020},
	eissn = {1932-7420},
	pages = {1189-1205}
}

@article{MTMT:31319253,
	title = {Nesfatin-1 decreases the motivational and rewarding value of food},
	url = {https://m2.mtmt.hu/api/publication/31319253},
	author = {Dore, Riccardo and Krotenko, Regina and Reising, Jan Philipp and Murru, Luca and Sundaram, Sivaraj Mohana and Di, Spiezio Alessandro and Mueller-Fielitz, Helge and Schwaninger, Markus and Joehren, Olaf and Mittag, Jens and Passafaro, Maria and Shanabrough, Marya and Horváth, Tamás and Schulz, Carla and Lehnert, Hendrik},
	doi = {10.1038/s41386-020-0682-3},
	journal-iso = {NEUROPSYCHOPHARMACOL},
	journal = {NEUROPSYCHOPHARMACOLOGY},
	volume = {45},
	unique-id = {31319253},
	issn = {0893-133X},
	abstract = {Homeostatic and hedonic pathways distinctly interact to control food intake. Dysregulations of circuitries controlling hedonic feeding may disrupt homeostatic mechanisms and lead to eating disorders. The anorexigenic peptides nucleobindin-2 (NUCB2)/nesfatin-1 may be involved in the interaction of these pathways. The endogenous levels of this peptide are regulated by the feeding state, with reduced levels following fasting and normalized by refeeding. The fasting state is associated with biochemical and behavioral adaptations ultimately leading to enhanced sensitization of reward circuitries towards food reward. Although NUCB2/nesfatin-1 is expressed in reward-related brain areas, its role in regulating motivation and preference for nutrients has not yet been investigated. We here report that both dopamine and GABA neurons express NUCB2/nesfatin-1 in the VTA. Ex vivo electrophysiological recordings show that nesfatin-1 hyperpolarizes dopamine, but not GABA, neurons of the VTA by inducing an outward potassium current. In vivo, central administration of nesfatin-1 reduces motivation for food reward in a high-effort condition, sucrose intake and preference. We next adopted a 2-bottle choice procedure, whereby the reward value of sucrose was compared with that of a reference stimulus (sucralose + optogenetic stimulation of VTA dopamine neurons) and found that nesfatin-1 fully abolishes the fasting-induced increase in the reward value of sucrose. These findings indicate that nesfatin-1 reduces energy intake by negatively modulating dopaminergic neuron activity and, in turn, hedonic aspects of food intake. Since nesfatin-1 ' s actions are preserved in conditions of leptin resistance, the present findings render the NUCB2/nesfatin-1 system an appealing target for the development of novel therapeutical treatments towards obesity.},
	keywords = {RAT-BRAIN; RECEPTOR; NEUROPEPTIDE; IMMUNOREACTIVITY; OXYTOCIN; DOPAMINERGIC-NEURONS; BLOOD-BRAIN-BARRIER; absence; Appetite; Neurosciences; Pharmacology & Pharmacy},
	year = {2020},
	eissn = {1470-634X},
	pages = {1645-1655},
	orcid-numbers = {Schwaninger, Markus/0000-0002-4510-9718}
}

@article{MTMT:31260011,
	title = {Metabolic Lateralization in the Hypothalamus of Male Rats Related to Reproductive and Satiety States},
	url = {https://m2.mtmt.hu/api/publication/31260011},
	author = {Kiss, Dávid Sándor and Tóth, István and Jócsák, Gergely and Bartha, Tibor and Frenyó V., László and Bárány, Zoltán Balázs and Horváth, Tamás and Zsarnovszky, Attila},
	doi = {10.1007/s43032-019-00131-3},
	journal-iso = {REPROD SCI},
	journal = {REPRODUCTIVE SCIENCES},
	volume = {27},
	unique-id = {31260011},
	issn = {1933-7191},
	year = {2020},
	eissn = {1933-7205},
	pages = {1197-1205},
	orcid-numbers = {Tóth, István/0000-0002-0168-4753}
}

@article{MTMT:31205043,
	title = {Prefrontal Cortical and Behavioral Adaptations to Surgical Delivery Mediated by Metabolic Principles},
	url = {https://m2.mtmt.hu/api/publication/31205043},
	author = {Taylor-Giorlando, Melissa and Scheinost, Dustin and Ment, Laura and Rothman, Dough and Horváth, Tamás},
	doi = {10.1093/cercor/bhz046},
	journal-iso = {CEREB CORTEX},
	journal = {CEREBRAL CORTEX},
	volume = {29},
	unique-id = {31205043},
	issn = {1047-3211},
	abstract = {We previously observed an association between mode of delivery and brain mitochondrial mechanisms in pups. We also showed that mitochondrial processes impact adult behavior. However, no experimental data is available to causally connect mode of delivery with cellular processes of neurons in the cerebral cortex and adult behavior. Here we show that surgical delivery of pups alters mitochondrial dynamics and spine synapses of layer 3 pyramidal neurons of the prefrontal cortex compared to the values of mice delivered vaginally. These alterations in ultrastructure seen in adult mice delivered surgically were associated with the development of behavioral phenotypes resembling those characteristic of animal models of psychiatric illness. This included impaired performance in prepulse inhibition as well as hyperlocomotion in the open field and elevated plus maze tests. Knocking out a mitochondria-related gene, UCP-2, blocked cellular and behavioral adaptations induced by surgical delivery. These results highlight a crucial role for brain mitochondrial adaptations in the process of birth to affect neuronal circuitry in support of normal and altered adult behaviors. Further, these findings were supported with neuroimaging data from human neonates delivered vaginally and surgically, suggesting that the murine findings have human clinical relevance.},
	keywords = {SCHIZOPHRENIA; MEMORY; CORTEX; prefrontal cortex; hippocampus; Connectivity; UNIT-ACTIVITY; Cesarean Section; NEUROGENESIS; neurodevelopment; Neuronal density; CESAREAN-SECTION; adult behavior},
	year = {2019},
	eissn = {1460-2199},
	pages = {5061-5071}
}

@article{MTMT:30707414,
	title = {Dopamine neuronal protection in the mouse Substantia nigra by GHSR is independent of electric activity},
	url = {https://m2.mtmt.hu/api/publication/30707414},
	author = {Stutz, Bernardo and Nasrallah, Carole and Nigro, Mariana and Curry, Daniel and Liu, Zhong-Wu and Gao, Xiao-Bing and Elsworth, John D. and Mintz, Liat and Horváth, Tamás},
	doi = {10.1016/j.molmet.2019.02.005},
	journal-iso = {MOL METAB},
	journal = {MOLECULAR METABOLISM},
	volume = {24},
	unique-id = {30707414},
	issn = {2212-8778},
	abstract = {Objective: Dopamine neurons in the Substantia nigra (SN) play crucial roles in control of voluntary movement. Extensive degeneration of this neuronal population is the cause of Parkinson's disease (PD). Many factors have been linked to SN DA neuronal survival, including neuronal pacemaker activity (responsible for maintaining basal firing and DA tone) and mitochondrial function. DIn-101, a naturally occurring splice variant of the human ghrelin gene, targets the ghrelin receptor (GHSR) present in the SN DA cells. Ghrelin activation of GHSR has been shown to protect SN DA neurons against 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine (MPTP) treatment. We decided to compare the actions of DIn-101 with ghrelin and identify the mechanisms associated with neuronal survival. Methods: Histologial, biochemical, and behavioral parameters were used to evaluate neuroprotection. Inflammation and redox balance of SN DA cells were evaluated using histologial and real-time PCR analysis. Designer Receptors Exclusively Activated by Designer Drugs (DREADD) technology was used to modulate SN DA neuron electrical activity and associated survival. Mitochondria! dynamics in SN DA cells was evaluated using electron microscopy data. Results: Here, we report that the human isoform displays an equivalent neuroprotective factor. However, while exogenous administration of mouse ghrelin electrically activates SN DA neurons increasing dopamine output, as well as locomotion, the human isoform significantly suppressed dopamine output, with an associated decrease in animal motor behavior. Investigating the mechanisms by which GHSR mediates neuroprotection, we found that dopamine cell-selective control of electrical activity is neither sufficient nor necessary to promote SN DA neuron survival, including that associated with GHSR activation. We found that DIn101 pre-treatment diminished MPTP-induced mitochondria! aberrations in SN DA neurons and that the effect of DIn101 to protect dopamine cells was dependent on mitofusin 2, a protein involved in the process of mitochondria! fusion and tethering of the mitochondria to the endoplasmic reticulum. Conclusions: Taken together, these observations unmasked a complex role of GHSR in dopamine neuronal protection independent on electric activity of these cells and revealed a crucial role for mitochondrial dynamics in some aspects of this process. (C) 2019 Published by Elsevier GmbH.},
	keywords = {PARKINSONS-DISEASE; MESSENGER-RNA; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; mitochondrial dynamics; Parkinson’s; COMPLEX-I DEFICIENCY; mitofusin 2; Dopamine neuron; unacylated ghrelin; MITOCHONDRIAL-DNA DELETIONS; GHRELIN INHIBITS APOPTOSIS; O-ACYLTRANSFERASE GOAT; DESACYL-GHRELIN},
	year = {2019},
	eissn = {2212-8778},
	pages = {120-138}
}