@article{MTMT:34766210, title = {microRNA-33 controls hunger signaling in hypothalamic AgRP neurons}, url = {https://m2.mtmt.hu/api/publication/34766210}, author = {Price, N.L. and Fernández-Tussy, P. and Varela, L. and Cardelo, M.P. and Shanabrough, M. and Aryal, B. and de, Cabo R. and Suárez, Y. and Horváth, Tamás and Fernández-Hernando, C.}, doi = {10.1038/s41467-024-46427-0}, journal-iso = {NAT COMMUN}, journal = {NATURE COMMUNICATIONS}, volume = {15}, unique-id = {34766210}, issn = {2041-1723}, abstract = {AgRP neurons drive hunger, and excessive nutrient intake is the primary driver of obesity and associated metabolic disorders. While many factors impacting central regulation of feeding behavior have been established, the role of microRNAs in this process is poorly understood. Utilizing unique mouse models, we demonstrate that miR-33 plays a critical role in the regulation of AgRP neurons, and that loss of miR-33 leads to increased feeding, obesity, and metabolic dysfunction in mice. These effects include the regulation of multiple miR-33 target genes involved in mitochondrial biogenesis and fatty acid metabolism. Our findings elucidate a key regulatory pathway regulated by a non-coding RNA that impacts hunger by controlling multiple bioenergetic processes associated with the activation of AgRP neurons, providing alternative therapeutic approaches to modulate feeding behavior and associated metabolic diseases. © The Author(s) 2024.}, keywords = {Animals; NEURONS; metabolism; MICE; GENETICS; MOUSE; animal; physiology; OBESITY; OBESITY; OBESITY; Feeding Behavior; nerve cell; fatty acid; neurology; microRNA; MICRORNAS; hunger; hunger; hunger; agouti related protein; agouti-related protein; hypothalamus; hypothalamus; Mirn33 microRNA, mouse}, year = {2024}, eissn = {2041-1723} } @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} } @article{MTMT:33912086, title = {Impaired Ghrelin Signaling Does Not Lead to Alterations of Anxiety-like Behaviors in Adult Mice Chronically Exposed to THC during Adolescence}, url = {https://m2.mtmt.hu/api/publication/33912086}, author = {Sestan-Pesa, Matija and Shanabrough, Marya and Horváth, Tamás and Miletta, Maria Consolata}, doi = {10.3390/biomedicines11010144}, journal-iso = {BIOMEDICINES}, journal = {BIOMEDICINES}, volume = {11}, unique-id = {33912086}, abstract = {As marijuana use during adolescence has been increasing, the need to understand the effects of its long-term use becomes crucial. Previous research suggested that marijuana consumption during adolescence increases the risk of developing mental illnesses, such as schizophrenia, depression, and anxiety. Ghrelin is a peptide produced primarily in the gut and is important for feeding behavior. Recent studies have shown that ghrelin and its receptor, the growth hormone secretagogue receptor (GHSR), play important roles in mediating stress, as well as anxiety and depression-like behaviors in animal models. Here, we investigated the effects of chronic tetrahydrocannabinol (THC) administration during late adolescence (P42-55) in GHSR (GHSR (-/-)) knockout mice and their wild-type littermates in relation to anxiety-like behaviors. We determined that continuous THC exposure during late adolescence did not lead to any significant alterations in the anxiety-like behaviors of adult mice, regardless of genotype, following a prolonged period of no exposure (1 month). These data indicate that in the presence of intact or impaired ghrelin/GHSR signaling, THC exposure during late adolescence has limited if any long-term impact on anxiety-like behaviors in mice.}, keywords = {Ghrelin; ENDOCANNABINOID SYSTEM; Late adolescence; tetrahydrocannabinol (THC); GHSR signaling}, year = {2023}, eissn = {2227-9059} } @article{MTMT:33859437, title = {Neonatal loss of FGFR2 in astroglial cells affects locomotion, sociability, working memory, and glia-neuron interactions in mice}, url = {https://m2.mtmt.hu/api/publication/33859437}, author = {Stevens, Hanna E. and Scuderi, Soraya and Collica, Sarah C. and Tomasi, Simone and Horváth, Tamás and Vaccarino, Flora M.}, doi = {10.1038/s41398-023-02372-y}, journal-iso = {TRANSL PSYCHIAT}, journal = {TRANSLATIONAL PSYCHIATRY}, volume = {13}, unique-id = {33859437}, issn = {2158-3188}, abstract = {Fibroblast growth factor receptor 2 (FGFR2) is almost exclusively expressed in glial cells in postnatal mouse brain, but its impact in glia for brain behavioral functioning is poorly understood. We compared behavioral effects from FGFR2 loss in both neurons and astroglial cells and from FGFR2 loss in astroglial cells by using either the pluripotent progenitor-driven hGFAP-cre or the tamoxifen-inducible astrocyte-driven GFAP-creER(T2) in Fgfr2 floxed mice. When FGFR2 was eliminated in embryonic pluripotent precursors or in early postnatal astroglia, mice were hyperactive, and had small changes in working memory, sociability, and anxiety-like behavior. In contrast, FGFR2 loss in astrocytes starting at 8 weeks of age resulted only in reduced anxiety-like behavior. Therefore, early postnatal loss of FGFR2 in astroglia is critical for broad behavioral dysregulation. Neurobiological assessments demonstrated that astrocyte-neuron membrane contact was reduced and glial glutamine synthetase expression increased only by early postnatal FGFR2 loss. We conclude that altered astroglial cell function dependent on FGFR2 in the early postnatal period may result in impaired synaptic development and behavioral regulation, modeling childhood behavioral deficits like attention deficit hyperactivity disorder (ADHD).}, year = {2023}, eissn = {2158-3188} } @article{MTMT:34855345, title = {Plant mitochondrial FMT and its mammalian homolog CLUH controls development and behavior in Arabidopsis and locomotion in mice}, url = {https://m2.mtmt.hu/api/publication/34855345}, author = {Ralevski, Alexandra and Apelt, Federico and Olas, Justyna J. and Mueller-Roeber, Bernd and Rugarli, Elena I. and Kragler, Friedrich and Horváth, Tamás}, doi = {10.1007/s00018-022-04382-3}, journal-iso = {CELL MOL LIFE SCI}, journal = {CELLULAR AND MOLECULAR LIFE SCIENCES}, volume = {79}, unique-id = {34855345}, issn = {1420-682X}, year = {2022}, eissn = {1420-9071} } @article{MTMT:33911811, title = {Ventromedial hypothalamic OGT drives adipose tissue lipolysis and curbs obesity}, url = {https://m2.mtmt.hu/api/publication/33911811}, author = {Wang, Qi and Zhang, Bichen and Stutz, Bernardo and Liu, Zhong-Wu and Horváth, Tamás and Yang, Xiaoyong}, doi = {10.1126/sciadv.abn8092}, journal-iso = {SCI ADV}, journal = {SCIENCE ADVANCES}, volume = {8}, unique-id = {33911811}, issn = {2375-2548}, abstract = {The ventromedial hypothalamus (VMH) is known to regulate body weight and counterregulatory response. However, how VMH neurons regulate lipid metabolism and energy balance remains unknown. O-linked beta-d-N-acetylglucosamine (O-GlcNAc) modification (O-GlcNAcylation), catalyzed by O-GlcNAc transferase (OGT), is considered a cellular sensor of nutrients and hormones. Here, we report that genetic ablation of OGT in VMH neurons inhibits neuronal excitability. Mice with VMH neuron-specific OGT deletion show rapid weight gain, increased adiposity, and reduced energy expenditure, without significant changes in food intake or physical activity. The obesity phenotype is associated with adipocyte hypertrophy and reduced lipolysis of white adipose tissues. In addition, OGT deletion in VMH neurons down-regulates the sympathetic activity and impairs the sympathetic innervation of white adipose tissues. These findings identify OGT in the VMH as a homeostatic set point that controls body weight and underscore the importance of the VMH in regulating lipid metabolism through white adipose tissue-specific innervation.}, year = {2022}, eissn = {2375-2548} } @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:32881945, title = {From Molecule to Behavior: Hypocretin/orexin Revisited From a Sex-dependent Perspective}, url = {https://m2.mtmt.hu/api/publication/32881945}, author = {Gao, Xiao-Bing and Horváth, Tamás}, doi = {10.1210/endrev/bnab042}, journal-iso = {ENDOCR REV}, journal = {ENDOCRINE REVIEWS}, unique-id = {32881945}, issn = {0163-769X}, abstract = {The hypocretin/orexin (Hcrt/Orx) system in the perifornical lateral hypothalamus has been recognized as a critical node in a complex network of neuronal systems controlling both physiology and behavior in vertebrates. Our understanding of the Hcrt/Orx system and its array of functions and actions has grown exponentially in merely 2 decades. This review will examine the latest progress in discerning the roles played by the Hcrt/Orx system in regulating homeostatic functions and in executing instinctive and learned behaviors. Furthermore, the gaps that currently exist in our knowledge of sex-related differences in this field of study are discussed.}, keywords = {Homeostasis; social behavior; orexin; sex-related difference; Hypocretin; motivational behavior; lateral hypothalamic area (LHA)}, year = {2021}, eissn = {1945-7189}, orcid-numbers = {Gao, Xiao-Bing/0000-0002-2035-4936} }