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  1. Article ; Online: Protocol to prepare mouse spinal cord for patch-clamp and histology experiments

    Sang-Hyeon Ju / Jong-Woo Sohn

    STAR Protocols, Vol 4, Iss 2, Pp 102345- (2023)

    2023  

    Abstract: Summary: The spinal cord is a part of the central nervous system located within the spinal canal of the vertebrae. Here, we present a protocol to prepare mouse spinal cord sections for patch-clamp and histology experiments. We describe steps for ... ...

    Abstract Summary: The spinal cord is a part of the central nervous system located within the spinal canal of the vertebrae. Here, we present a protocol to prepare mouse spinal cord sections for patch-clamp and histology experiments. We describe steps for isolating spinal cord from the spinal canal and obtaining acute slices for patch-clamp experiments. For histology experiments, we detail fixing spinal cord for cryosectioning and imaging. This protocol provides procedures to assess neuronal activity and protein expression of sympathetic preganglionic neurons.For complete details on the use and execution of this protocol, please refer to Ju et al.1
    Keywords Metabolism ; Neuroscience ; Science (General) ; Q1-390
    Language English
    Publishing date 2023-06-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Protocol for sodium depletion and measurement of sodium appetite in mice

    Seahyung Park / Jong-Woo Sohn

    STAR Protocols, Vol 2, Iss 4, Pp 101026- (2021)

    2021  

    Abstract: Summary: Sodium appetite is a state that motivates animals to consume normally unappetizing concentrations of sodium. Here we describe a protocol to induce sodium appetite in mice by furosemide-induced diuresis and measure sodium intake using volumetric ... ...

    Abstract Summary: Sodium appetite is a state that motivates animals to consume normally unappetizing concentrations of sodium. Here we describe a protocol to induce sodium appetite in mice by furosemide-induced diuresis and measure sodium intake using volumetric drinking tubes. This protocol induces sodium appetite rapidly and can be used to assess the effect of various treatments on sodium appetite. This protocol does not require electronic equipment and can be implemented easily.For complete details on the use and execution of this protocol, please refer to Park et al. (2020).
    Keywords Metabolism ; Model Organisms ; Neuroscience ; Behavior ; Science (General) ; Q1-390
    Language English
    Publishing date 2021-12-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Leptin-inhibited neurons in the lateral parabrachial nucleus do not alter food intake or glucose balance

    Seahyung Park / Kevin W. Williams / Jong-Woo Sohn

    Animal Cells and Systems, Vol 26, Iss 3, Pp 92-

    2022  Volume 98

    Abstract: The lateral parabrachial nucleus (LPBN) has been shown to be involved in the suppression of appetite at the pharmacological, optogenetic and chemogenetic levels. However, the signalling that mediates activation of these neurons in physiological ... ...

    Abstract The lateral parabrachial nucleus (LPBN) has been shown to be involved in the suppression of appetite at the pharmacological, optogenetic and chemogenetic levels. However, the signalling that mediates activation of these neurons in physiological conditions has been hindered by difficulties in segregating different cell populations in this region. Using reporter mice, we identify at the electrophysiological level the effects of an anorexic hormone, leptin, on leptin receptor (ObR)-expressing neurons in the LPBN (LPBNObR neurons). Application of leptin caused inhibition in a subpopulation of LPBNObR neurons. This effect was mediated by an increased potassium conductance and was also accompanied by a decrease in excitatory synaptic input onto these neurons. However, mimicking the inhibitory effects of leptin on LPBNObR neurons through chemogenetics led to no changes in feeding or glucose levels, which suggests that leptin action on LPBNObR neurons may not be sufficient to regulate these metabolic aspects.
    Keywords Appetite ; glucose ; leptin ; parabrachial nucleus ; chemogenetics ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher Taylor & Francis Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Ion channels in the central regulation of energy and glucose homeostasis

    Jong-WooSohn

    Frontiers in Neuroscience, Vol

    2013  Volume 7

    Abstract: Ion channels are critical regulators of neuronal excitability and synaptic function in the brain. Recent evidence suggests that ion channels expressed by neurons within the brain are responsible for regulating energy and glucose homeostasis. In addition, ...

    Abstract Ion channels are critical regulators of neuronal excitability and synaptic function in the brain. Recent evidence suggests that ion channels expressed by neurons within the brain are responsible for regulating energy and glucose homeostasis. In addition, the central effects of neurotransmitters and hormones are at least in part achieved by modifications of ion channel activity. This review focuses on ion channels and their neuronal functions followed by a discussion of the identified roles for specific ion channels in the central pathways regulating food intake, energy expenditure, and glucose balance.
    Keywords Diabetes Mellitus ; Obesity ; GABA-A receptors ; Ionotropic glutamate receptors (iGluRs) ; K channels ; patch clamp electrophysiology ; TRPC channels ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; Medicine ; R
    Language English
    Publishing date 2013-05-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Gαi/o-coupled Htr2c in the paraventricular nucleus of the hypothalamus antagonizes the anorectic effect of serotonin agents

    Eun-Seon Yoo / Li Li / Lin Jia / Caleb C. Lord / Charlotte E. Lee / Shari G. Birnbaum / Claudia R. Vianna / Eric D. Berglund / Kathryn A. Cunningham / Yong Xu / Jong-Woo Sohn / Chen Liu

    Cell Reports, Vol 37, Iss 7, Pp 109997- (2021)

    2021  

    Abstract: Summary: The anorexigenic effect of serotonergic compounds has largely been attributed to activation of serotonin 2C receptors (Htr2cs). Using mouse genetic models in which Htr2c can be selectively deleted or restored (in Htr2c-null mice), we investigate ...

    Abstract Summary: The anorexigenic effect of serotonergic compounds has largely been attributed to activation of serotonin 2C receptors (Htr2cs). Using mouse genetic models in which Htr2c can be selectively deleted or restored (in Htr2c-null mice), we investigate the role of Htr2c in forebrain Sim1 neurons. Unexpectedly, we find that Htr2c acts in these neurons to promote food intake and counteract the anorectic effect of serotonergic appetite suppressants. Furthermore, Htr2c marks a subset of Sim1 neurons in the paraventricular nucleus of the hypothalamus (PVH). Chemogenetic activation of these neurons in adult mice suppresses hunger, whereas their silencing promotes feeding. In support of an orexigenic role of PVH Htr2c, whole-cell patch-clamp experiments demonstrate that activation of Htr2c inhibits PVH neurons. Intriguingly, this inhibition is due to Gαi/o-dependent activation of ATP-sensitive K+ conductance, a mechanism of action not identified previously in the mammalian nervous system.
    Keywords Htr2c ; feeding ; obesity ; KATP ; lorcaserin ; hypothalamus ; Biology (General) ; QH301-705.5
    Subject code 590
    Language English
    Publishing date 2021-11-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Angiopoietin-Like Growth Factor Involved in Leptin Signaling in the Hypothalamus

    Yunseon Jang / Jun Young Heo / Min Joung Lee / Jiebo Zhu / Changjun Seo / Da Hyun Go / Sung Kyung Yoon / Date Yukari / Yuichi Oike / Jong-Woo Sohn / Minho Shong / Gi Ryang Kweon

    International Journal of Molecular Sciences, Vol 22, Iss 3443, p

    2021  Volume 3443

    Abstract: The hypothalamic regulation of appetite governs whole-body energy balance. Satiety is regulated by endocrine factors including leptin, and impaired leptin signaling is associated with obesity. Despite the anorectic effect of leptin through the regulation ...

    Abstract The hypothalamic regulation of appetite governs whole-body energy balance. Satiety is regulated by endocrine factors including leptin, and impaired leptin signaling is associated with obesity. Despite the anorectic effect of leptin through the regulation of the hypothalamic feeding circuit, a distinct downstream mediator of leptin signaling in neuron remains unclear. Angiopoietin-like growth factor (AGF) is a peripheral activator of energy expenditure and antagonizes obesity. However, the regulation of AGF expression in brain and localization to mediate anorectic signaling is unknown. Here, we demonstrated that AGF is expressed in proopiomelanocortin (POMC)-expressing neurons located in the arcuate nucleus (ARC) of the hypothalamus. Unlike other brain regions, hypothalamic AGF expression is stimulated by leptin-induced signal transducers and activators of transcription 3 (STAT3) phosphorylation. In addition, leptin treatment to hypothalamic N1 cells significantly enhanced the promoter activity of AGF. This induction was abolished by the pretreatment of ruxolitinib, a leptin signaling inhibitor. These results indicate that hypothalamic AGF expression is induced by leptin and colocalized to POMC neurons.
    Keywords hypothalamus ; AGF ; leptin ; POMC neuron ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 630
    Language English
    Publishing date 2021-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Leptin and insulin engage specific PI3K subunits in hypothalamic SF1 neurons

    Jong-Woo Sohn / Youjin Oh / Ki Woo Kim / Syann Lee / Kevin W. Williams / Joel K. Elmquist

    Molecular Metabolism, Vol 5, Iss 8, Pp 669-

    2016  Volume 679

    Abstract: Objective: The ventromedial hypothalamic nucleus (VMH) regulates energy balance and glucose homeostasis. Leptin and insulin exert metabolic effects via their cognate receptors expressed by the steroidogenic factor 1 (SF1) neurons within the VMH. However, ...

    Abstract Objective: The ventromedial hypothalamic nucleus (VMH) regulates energy balance and glucose homeostasis. Leptin and insulin exert metabolic effects via their cognate receptors expressed by the steroidogenic factor 1 (SF1) neurons within the VMH. However, detailed cellular mechanisms involved in the regulation of these neurons by leptin and insulin remain to be identified. Methods: We utilized genetically-modified mouse models and performed patch-clamp electrophysiology experiments to resolve this issue. Results: We identified distinct populations of leptin-activated and leptin-inhibited SF1 neurons. In contrast, insulin uniformly inhibited SF1 neurons. Notably, we found that leptin-activated, leptin-inhibited, and insulin-inhibited SF1 neurons are distinct subpopulations within the VMH. Leptin depolarization of SF1 neuron also required the PI3K p110β catalytic subunit. This effect was mediated by the putative transient receptor potential C (TRPC) channel. On the other hand, hyperpolarizing responses of SF1 neurons by leptin and insulin required either of the p110α or p110β catalytic subunits, and were mediated by the putative ATP-sensitive K+ (KATP) channel. Conclusions: Our results demonstrate that specific PI3K catalytic subunits are responsible for the acute effects of leptin and insulin on VMH SF1 neurons, and provide insights into the cellular mechanisms of leptin and insulin action on VMH SF1 neurons that regulate energy balance and glucose homeostasis. Author Video: Author Video Watch what authors say about their articles Keywords: Cellular mechanism, Conditional knockout mouse, Patch clamp technique, Functional heterogeneity, Homeostasis
    Keywords Internal medicine ; RC31-1245
    Subject code 571
    Language English
    Publishing date 2016-08-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Primary cilia mediate early life programming of adiposity through lysosomal regulation in the developing mouse hypothalamus

    Chan Hee Lee / Do Kyeong Song / Chae Beom Park / Jeewon Choi / Gil Myoung Kang / Sung Hoon Shin / Ijoo Kwon / Soyoung Park / Seongjun Kim / Ji Ye Kim / Hong Dugu / Jae Woo Park / Jong Han Choi / Se Hee Min / Jong-Woo Sohn / Min-Seon Kim

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Volume 19

    Abstract: Ciliary defects and obesity has been associated, but the underlying mechanism is unclear. Here, the authors show that inhibition of ciliogenesis in POMC neurons during development results in lysosomal protein degradation-dependent axonal disruption and ... ...

    Abstract Ciliary defects and obesity has been associated, but the underlying mechanism is unclear. Here, the authors show that inhibition of ciliogenesis in POMC neurons during development results in lysosomal protein degradation-dependent axonal disruption and adult obesity in mice.
    Keywords Science ; Q
    Language English
    Publishing date 2020-11-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Primary cilia mediate early life programming of adiposity through lysosomal regulation in the developing mouse hypothalamus

    Chan Hee Lee / Do Kyeong Song / Chae Beom Park / Jeewon Choi / Gil Myoung Kang / Sung Hoon Shin / Ijoo Kwon / Soyoung Park / Seongjun Kim / Ji Ye Kim / Hong Dugu / Jae Woo Park / Jong Han Choi / Se Hee Min / Jong-Woo Sohn / Min-Seon Kim

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Volume 19

    Abstract: Ciliary defects and obesity has been associated, but the underlying mechanism is unclear. Here, the authors show that inhibition of ciliogenesis in POMC neurons during development results in lysosomal protein degradation-dependent axonal disruption and ... ...

    Abstract Ciliary defects and obesity has been associated, but the underlying mechanism is unclear. Here, the authors show that inhibition of ciliogenesis in POMC neurons during development results in lysosomal protein degradation-dependent axonal disruption and adult obesity in mice.
    Keywords Science ; Q
    Language English
    Publishing date 2020-11-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: TrpC5 Mediates Acute Leptin and Serotonin Effects via Pomc Neurons

    Yong Gao / Ting Yao / Zhuo Deng / Jong-Woo Sohn / Jia Sun / Yiru Huang / Xingxing Kong / Kai-jiang Yu / Rui-tao Wang / Hong Chen / Hongbo Guo / Jianqun Yan / Kathryn A. Cunningham / Yongsheng Chang / Tiemin Liu / Kevin W. Williams

    Cell Reports, Vol 18, Iss 3, Pp 583-

    2017  Volume 592

    Abstract: The molecular mechanisms underlying acute leptin and serotonin 2C receptor-induced hypophagia remain unclear. Here, we show that neuronal and pro-opiomelanocortin (Pomc)-specific loss of transient receptor potential cation 5 (TrpC5) subunits is ... ...

    Abstract The molecular mechanisms underlying acute leptin and serotonin 2C receptor-induced hypophagia remain unclear. Here, we show that neuronal and pro-opiomelanocortin (Pomc)-specific loss of transient receptor potential cation 5 (TrpC5) subunits is sufficient to decrease energy expenditure and increase food intake resulting in elevated body weight. Deficiency of Trpc5 subunits in Pomc neurons is also sufficient to block the anorexigenic effects of leptin and serotonin 2C receptor (Ht2Cr) agonists. The loss of acute anorexigenic effects of these receptors is concomitant with a blunted electrophysiological response to both leptin and Ht2Cr agonists in arcuate Pomc neurons. We also demonstrate that the Ht2Cr agonist lorcaserin-induced improvements in glucose and insulin tolerance are blocked by TrpC5 deficiency in Pomc neurons. Together, our results link TrpC5 subunits in the brain with leptin- and serotonin 2C receptor-dependent changes in neuronal activity, as well as energy balance, feeding behavior, and glucose metabolism.
    Keywords melanocortin ; obesity ; diabetes ; transient receptor potential cation channels ; thermogenesis ; glycemia ; patch-clamp ; electrophysiology ; leptin ; serotonin ; lorcaserin ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2017-01-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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