@article{MTMT:34566049,
	title = {Cholinergic control of GnRH neuron physiology and luteinizing hormone secretion in male mice: involvement of ACh/GABA co-transmission},
	url = {https://m2.mtmt.hu/api/publication/34566049},
	author = {Vastagh, Csaba and Farkas, Imre and Csillag, Veronika and Watanabe, Masahiko and Kalló, Imre and Liposits, Zsolt},
	doi = {10.1523/JNEUROSCI.1780-23.2024},
	journal-iso = {J NEUROSCI},
	journal = {JOURNAL OF NEUROSCIENCE},
	volume = {44},
	unique-id = {34566049},
	issn = {0270-6474},
	abstract = {GnRH-synthesizing neurons orchestrate reproduction centrally. Early studies have proposed the contribution of acetylcholine (ACh) to hypothalamic control of reproduction, although the causal mechanisms haven't been clarified. Here, we report that in vivo pharmacogenetic activation of the cholinergic system increased the secretion of luteinizing hormone (LH) in orchidectomized mice. 3DISCO immunocytochemistry and electron microscopy revealed the innervation of GnRH neurons by cholinergic axons. Retrograde viral labeling initiated from GnRH-Cre neurons identified the medial septum and the diagonal band of Broca as exclusive sites of origin for cholinergic afferents of GnRH neurons. In acute brain slices, ACh and the ACh receptor (AChR) agonist carbachol evoked a biphasic effect on the firing rate in GnRH neurons, first increasing and then diminishing it. In the presence of tetrodotoxin, carbachol induced an inward current, followed by a decline in the frequency of mPSCs, indicating a direct influence on GnRH cells. RT-PCR and whole-cell patch-clamp studies revealed that GnRH neurons expressed both nicotinic (α4β2, α3β4, and α7) and muscarinic (M1-M5) ACh receptors. The nicotinic AChRs contributed to the nicotine-elicited inward current and the rise in firing rate. Muscarine via M1 and M3 receptors increased, while via M2 and M4 reduced the frequency of both miniature postsynaptic currents (mPSCs) and firing. Optogenetic activation of channelrhodopsin-2-tagged cholinergic axons modified GnRH neuronal activity and evoked co-transmission of ACh and GABA from a subpopulation of boutons. These findings confirm that the central cholinergic system immensely regulates GnRH neurons and activates the HPG-axis via ACh and ACh/GABA neurotransmissions in male mice.},
	year = {2024},
	eissn = {1529-2401},
	orcid-numbers = {Vastagh, Csaba/0000-0002-5008-0999; Farkas, Imre/0000-0002-0159-4408; Liposits, Zsolt/0000-0002-3508-2750}
}

@article{MTMT:32600821,
	title = {Characterization of orexin input to dopamine neurons of the ventral tegmental area projecting to the medial prefrontal cortex and shell of nucleus accumbens},
	url = {https://m2.mtmt.hu/api/publication/32600821},
	author = {Kalló, Imre and Omrani, Azar and Meye, Frank J. and de Jong, Han and Liposits, Zsolt and Adan, Roger A. H.},
	doi = {10.1007/s00429-021-02449-8},
	journal-iso = {BRAIN STRUCT FUNC},
	journal = {BRAIN STRUCTURE & FUNCTION},
	volume = {227},
	unique-id = {32600821},
	issn = {1863-2653},
	keywords = {Dopamine; prefrontal cortex; Ventral tegmental area; nucleus accumbens; orexin},
	year = {2022},
	eissn = {1863-2661},
	pages = {1083-1098},
	orcid-numbers = {Liposits, Zsolt/0000-0002-3508-2750; Adan, Roger A. H./0000-0001-8994-0661}
}

@article{MTMT:31828021,
	title = {Gonadal Cycle-Dependent Expression of Genes Encoding Peptide-, Growth Factor-, and Orphan G-Protein-Coupled Receptors in Gonadotropin- Releasing Hormone Neurons of Mice},
	url = {https://m2.mtmt.hu/api/publication/31828021},
	author = {Vastagh, Csaba and Csillag, Veronika and Solymosi, Norbert and Farkas, Imre and Liposits, Zsolt},
	doi = {10.3389/fnmol.2020.594119},
	journal-iso = {FRONT MOL NEUROSCI},
	journal = {FRONTIERS IN MOLECULAR NEUROSCIENCE},
	volume = {13},
	unique-id = {31828021},
	issn = {1662-5099},
	keywords = {neuropeptides; MOUSE; GROWTH FACTORS; Transcriptome; Proestrus; G-protein-coupled receptors; slice electrophysiology; GNR},
	year = {2021},
	eissn = {1662-5099},
	orcid-numbers = {Vastagh, Csaba/0000-0002-5008-0999; Farkas, Imre/0000-0002-0159-4408; Liposits, Zsolt/0000-0002-3508-2750}
}

@article{MTMT:31828015,
	title = {Insulin-like growth factor 1 (IGF-1) increases GABAergic neurotransmission to GnRH neurons via suppressing the retrograde tonic endocannabinoid signaling pathway in mice.},
	url = {https://m2.mtmt.hu/api/publication/31828015},
	author = {Bálint, Flóra and Csillag, Veronika and Vastagh, Csaba and Liposits, Zsolt and Farkas, Imre},
	doi = {10.1159/000514043},
	journal-iso = {NEUROENDOCRINOLOGY},
	journal = {NEUROENDOCRINOLOGY},
	volume = {111},
	unique-id = {31828015},
	issn = {0028-3835},
	abstract = {Hypophysiotropic gonadotropin releasing-hormone (GnRH) neurons orchestrate various physiological events that control the onset of puberty. Previous studies showed that insulin-like growth factor 1 (IGF-1) induces the secretion of GnRH and accelerates the onset of puberty, suggesting a regulatory role of this hormone upon GnRH neurons.To reveal responsiveness of GnRH neurons to IGF-1 and elucidate molecular pathways acting downstream to the IGF-1 receptor (IGF-1R), in vitro electrophysiological experiments were carried out on GnRH-GFP neurons in acute brain slices from prepubertal (23-29 days) and pubertal (50-day) male mice.Administration of IGF-1 (13 nM) significantly increased the firing rate and frequency of spontaneous postsynaptic currents (sPSCs), and that of excitatory GABAergic miniature postsynaptic currents (mPSCs). No GABAergic mPSCs were induced by IGF-1 in the presence of GABAA-R blocker picrotoxin. The increase in the mPSC frequency was prevented by the use of IGF-1R antagonist, JB1 (1 µM) or the intracellularly applied PI3K blocker (LY294002, 50 µM) showing involvement of IGF-1R and PI3K in the mechanism. Blockade of the transient receptor potential vanilloid 1 (TRPV1), an element of the tonic retrograde endocannabinoid machinery by AMG9810 (10 µM) or antagonizing cannabinoid receptor type-1 (CB1) by AM251 (1 µM) abolished the effect.These findings indicate that IGF-1 arrests the tonic retrograde endocannabinoid pathway in GnRH neurons and this disinhibition increases the release of GABA from presynaptic terminals that, in turn, activates GnRH neurons leading to the fine-tuning of the hypothalamo-pituitary-gonadal axis.},
	year = {2021},
	eissn = {1423-0194},
	pages = {1219-1230},
	orcid-numbers = {Vastagh, Csaba/0000-0002-5008-0999; Liposits, Zsolt/0000-0002-3508-2750; Farkas, Imre/0000-0002-0159-4408}
}

@article{MTMT:31657980,
	title = {Networking of glucagon-like peptide-1 axons with GnRH neurons in the basal forebrain of male mice revealed by 3DISCO-based immunocytochemistry and optogenetics.},
	url = {https://m2.mtmt.hu/api/publication/31657980},
	author = {Vastagh, Csaba and Farkas, Imre and Scott, Michael M and Liposits, Zsolt},
	doi = {10.1007/s00429-020-02167-7},
	journal-iso = {BRAIN STRUCT FUNC},
	journal = {BRAIN STRUCTURE & FUNCTION},
	volume = {226},
	unique-id = {31657980},
	issn = {1863-2653},
	abstract = {Glucagon-like peptide-1 (GLP-1) regulates reproduction centrally, although, the neuroanatomical basis of the process is unknown. Therefore, the putative networking of the central GLP-1 and gonadotropin-releasing hormone (GnRH) systems was addressed in male mice using whole mount immunocytochemistry and optogenetics. Enhanced antibody penetration and optical clearing procedures applied to 500-1000 µm thick basal forebrain slices allowed the simultaneous visualization of the two distinct systems in the basal forebrain. Beaded GLP-1-IR axons innervated about a quarter of GnRH neurons (23.2 ± 1.4%) forming either single or multiple contacts. GnRH dendrites received a more intense GLP-1 innervation (64.6 ± 0.03%) than perikarya (35.4 ± 0.03%). The physiological significance of the innervation was examined by optogenetic activation of channelrhodopsin-2 (ChR2)-expressing axons of preproglucagon (GCG) neurons upon the firing of GnRH neurons by patch clamp electrophysiology in acute brain slices of triple transgenic mice (Gcg-cre/ChR2/GFP-GnRH). High-frequency laser beam stimulation (20 Hz, 10 ms pulse width, 3 mW laser power) of ChR2-expressing GCG axons in the mPOA increased the firing rate of GnRH neurons (by 75 ± 17.3%, p = 0.0007). Application of the GLP-1 receptor antagonist, Exendin-3-(9-39) (1 μM), prior to the photo-stimulation, abolished the facilitatory effect. In contrast, low-frequency trains of laser pulses (0.2 Hz, 60 pulses) had no effect on the spontaneous postsynaptic currents of GnRH neurons. The findings indicate a direct wiring of GLP-1 neurons with GnRH cells which route is excitatory for the GnRH system. The pathway may relay metabolic signals to GnRH neurons and synchronize metabolism with reproduction.},
	keywords = {TRANSGENIC MICE; GLUCAGON-LIKE PEPTIDE-1; patch clamp; optogenetics; GnRH neuron; slice electrophysiology; 3DISCO; Neuronal networking},
	year = {2021},
	eissn = {1863-2661},
	pages = {105-120},
	orcid-numbers = {Vastagh, Csaba/0000-0002-5008-0999; Farkas, Imre/0000-0002-0159-4408; Liposits, Zsolt/0000-0002-3508-2750}
}

@article{MTMT:31371873,
	title = {Ghrelin Receptor Stimulation of the Lateral Parabrachial Nucleus in Rats Increases Food Intake but not Food Motivation},
	url = {https://m2.mtmt.hu/api/publication/31371873},
	author = {Bake, Tina and Le May, Marie V. and Edvardsson, Christian E. and Vogel, Heike and Bergström, Ulrika and Albers, Marjorie Nicholson and Skibicka, Karolina P. and Farkas, Imre and Liposits, Zsolt and Dickson, Suzanne L.},
	doi = {10.1002/oby.22875},
	journal-iso = {OBESITY},
	journal = {OBESITY},
	volume = {28},
	unique-id = {31371873},
	issn = {1930-7381},
	keywords = {Ghrelin; protein fos; ghrelin receptor},
	year = {2020},
	eissn = {1930-739X},
	pages = {1503-1511},
	orcid-numbers = {Bake, Tina/0000-0003-0500-5129; Farkas, Imre/0000-0002-0159-4408; Liposits, Zsolt/0000-0002-3508-2750; Dickson, Suzanne L./0000-0002-3822-5294}
}

@article{MTMT:31286495,
	title = {Az ösztrogének lehetséges szerepe a vastagbéldaganatok kialakulásában},
	url = {https://m2.mtmt.hu/api/publication/31286495},
	author = {Leiszter, Katalin and Udvardyné Galamb, Orsolya and Kalmár, Alexandra and Zsigrai, Sára and Valcz, Gábor and Szigeti, Krisztina Andrea and Barták, Barbara Kinga and Nagy, Zsófia Brigitta and Dank, Magdolna and Liposits, Zsolt and Igaz, Péter and Tulassay, Zsolt and Molnár, Béla},
	doi = {10.1556/650.2020.31674},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {161},
	unique-id = {31286495},
	issn = {0030-6002},
	keywords = {ESTRADIOL; colorectal cancer; ÖSZTRADIOL; Estrogen receptor pathway; vastagbélrák; ösztrogénreceptor-jelútrendszer},
	year = {2020},
	eissn = {1788-6120},
	pages = {532-543},
	orcid-numbers = {Udvardyné Galamb, Orsolya/0000-0002-7042-5667; Zsigrai, Sára/0000-0002-6161-5637; Valcz, Gábor/0000-0002-7109-3529; Dank, Magdolna/0000-0002-4442-8733; Liposits, Zsolt/0000-0002-3508-2750; Igaz, Péter/0000-0003-2192-554X; Tulassay, Zsolt/0000-0003-2452-6640; Molnár, Béla/0000-0001-6655-7942}
}

@article{MTMT:30744376,
	title = {Blunted leptin sensitivity during hedonic overeating can be reinstated by activating galanin 2 receptors (Gal2R) in the lateral hypothalamus.},
	url = {https://m2.mtmt.hu/api/publication/30744376},
	author = {Leidmaa, Este and Gazea, Mary and Patchev, Alexandre V and Pissioti, Anna and Gassen, Nils Christian and Kimura, Mayumi and Liposits, Zsolt and Kalló, Imre and Almeida, Osborne F X},
	doi = {10.1111/apha.13345},
	journal-iso = {ACTA PHYSIOL},
	journal = {ACTA PHYSIOLOGICA},
	volume = {228},
	unique-id = {30744376},
	issn = {1748-1708},
	abstract = {Since foods with high hedonic value are often consumed in excess of energetic needs, this study was designed to identify the mechanisms that may counter anorexigenic signalling in the presence of hedonic foods in lean animals.Mice, in different states of satiety (fed/fasted, or fed/fasted and treated with ghrelin or leptin, respectively), were allowed to choose between high-fat/high-sucrose and standard foods. Intake of each food type and the activity of hypothalamic neuropetidergic neurons that regulate appetite were monitored. In some cases, food choice was monitored in leptin-injected fasted mice that received microinjections of galanin receptor agonists into the lateral hypothalamus.Appetite-stimulating orexin neurons in the lateral hypothalamus are rapidly activated when lean, satiated mice consume a highly palatable food (PF); such activation (upregulated c-Fos expression) occurred even after administration of the anorexigenic hormone leptin and despite intact leptin signalling in the hypothalamus. The ability of leptin to restrain PF eating is restored when a galanin receptor 2 (Gal2R) agonist is injected into the lateral hypothalamus.Hedonically-loaded foods interrupt the inhibitory actions of leptin on orexin neurons and interfere with the homeostatic control of feeding. Overeating of palatable foods can be curtailed in lean animals by activating Gal2R in the lateral hypothalamus. This article is protected by copyright. All rights reserved.},
	keywords = {GALANIN; Ghrelin; leptin; LATERAL HYPOTHALAMUS; orexin; hedonia; overeating},
	year = {2020},
	eissn = {1748-1716},
	orcid-numbers = {Liposits, Zsolt/0000-0002-3508-2750}
}

@article{MTMT:30830798,
	title = {Hypothalamic dopamine signaling regulates brown fat thermogenesis.},
	url = {https://m2.mtmt.hu/api/publication/30830798},
	author = {Folgueira, Cintia and Beiroa, Daniel and Porteiro, Begoña and Duquenne, Manon and Puighermanal, Emma and Fondevila, Marcos F and Barja-Fernández, Silvia and Gallego, Rosalia and Hernández-Bautista, René and Castelao, Cecilia and Senra, Ana and Seoane, Patricia and Gómez, Noemi and Aguiar, Pablo and Guallar, Diana and Fidalgo, Miguel and Romero-Pico, Amparo and Adan, Roger and Blouet, Clemence and Labandeira-García, Jose Luís and Jeanrenaud, Françoise and Kalló, Imre and Liposits, Zsolt and Salvador, Javier and Prevot, Vincent and Dieguez, Carlos and Lopez, Miguel and Valjent, Emmanuel and Frühbeck, Gema and Seoane, Luisa M and Nogueiras, Ruben},
	doi = {10.1038/s42255-019-0099-7},
	journal-iso = {NAT METAB},
	journal = {NATURE METABOLISM},
	volume = {1},
	unique-id = {30830798},
	abstract = {Dopamine signaling is a crucial part of the brain reward system and can affect feeding behavior. Dopamine receptors are also expressed in the hypothalamus, which is known to control energy metabolism in peripheral tissues. Here we show that pharmacological or chemogenetic stimulation of dopamine receptor 2 (D2R) expressing cells in the lateral hypothalamic area (LHA) and the zona incerta (ZI) decreases body weight and stimulates brown fat activity in rodents in a feeding-independent manner. LHA/ZI D2R stimulation requires an intact sympathetic nervous system and orexin system to exert its action and involves inhibition of PI3K in the LHA/ZI. We further demonstrate that, as early as 3 months after onset of treatment, patients treated with the D2R agonist cabergoline experience an increase in energy expenditure that persists for one year, leading to total body weight and fat loss through a prolactin-independent mechanism. Our results may provide a mechanistic explanation for how clinically used D2R agonists act in the CNS to regulate energy balance.},
	keywords = {Dopamine; DOPAMINE-RECEPTOR; PROLACTIN; cholesterol; sex hormone binding globulin; triacylglycerol; stress activated protein kinase; protein kinase B; Fibroblast growth factor 21; orexin receptor; high-density lipoprotein cholesterol; orexin receptors; low density lipoprotein-cholesterol},
	year = {2019},
	eissn = {2522-5812},
	pages = {811-829},
	orcid-numbers = {Liposits, Zsolt/0000-0002-3508-2750}
}

@article{MTMT:30814315,
	title = {Secretin Regulates Excitatory GABAergic Neurotransmission to GnRH Neurons via Retrograde NO Signaling Pathway in Mice.},
	url = {https://m2.mtmt.hu/api/publication/30814315},
	author = {Csillag, Veronika and Vastagh, Csaba and Liposits, Zsolt and Farkas, Imre},
	doi = {10.3389/fncel.2019.00371},
	journal-iso = {FRONT CELL NEUROSCI},
	journal = {FRONTIERS IN CELLULAR NEUROSCIENCE},
	volume = {13},
	unique-id = {30814315},
	issn = {1662-5102},
	abstract = {In mammals, reproduction is regulated by a wide range of metabolic hormones that maintain the proper energy balance. In addition to regulating feeding and energy expenditure, these metabolic messengers also modulate the functional performance of the hypothalamic-pituitary-gonadal (HPG) axis. Secretin, a member of the secretin-glucagon-vasoactive intestinal peptide hormone family, has been shown to alter reproduction centrally, although the underlying mechanisms have not been explored yet. In order to elucidate its central action in the neuroendocrine regulation of reproduction, in vitro electrophysiological slice experiments were carried out on GnRH-GFP neurons in male mice. Bath application of secretin (100 nM) significantly increased the frequency of the spontaneous postsynaptic currents (sPSCs) to 118.0 ± 2.64% compared to the control, and that of the GABAergic miniature postsynaptic currents (mPSCs) to 147.6 ± 19.19%. Resting membrane potential became depolarized by 12.74 ± 4.539 mV after secretin treatment. Frequency of evoked action potentials (APs) also increased to 144.3 ± 10.8%. The secretin-triggered elevation of the frequency of mPSCs was prevented by using either a secretin receptor antagonist (3 μM) or intracellularly applied G-protein-coupled receptor blocker (GDP-β-S; 2 mM) supporting the involvement of secretin receptor in the process. Regarding the actions downstream to secretin receptor, intracellular blockade of protein kinase A (PKA) with KT-5720 (2 μM) or intracellular inhibition of the neuronal nitric oxide synthase (nNOS) by NPLA (1 μM) abolished the stimulatory effect of secretin on mPSCs. These data suggest that secretin acts on GnRH neurons via secretin receptors whose activation triggers the cAMP/PKA/nNOS signaling pathway resulting in nitric oxide release and in the presynaptic terminals this retrograde NO machinery regulates the GABAergic input to GnRH neurons.},
	keywords = {metabolism; reproduction; GABA; nitric oxide; secretin; GnRH neuron; Retrograde signaling},
	year = {2019},
	eissn = {1662-5102},
	orcid-numbers = {Vastagh, Csaba/0000-0002-5008-0999; Liposits, Zsolt/0000-0002-3508-2750; Farkas, Imre/0000-0002-0159-4408}
}