Lateral Hypothalamus

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Patrick M Fuller - One of the best experts on this subject based on the ideXlab platform.

  • a novel population of wake promoting gabaergic neurons in the ventral Lateral Hypothalamus
    Current Biology, 2016
    Co-Authors: Anne Venner, Christelle Anaclet, Rebecca Y Broadhurst, Clifford B Saper, Patrick M Fuller
    Abstract:

    The largest synaptic input to the sleep-promoting ventroLateral preoptic area (VLPO) [1] arises from the Lateral Hypothalamus [2], a brain area associated with arousal [3-5]. However, the neurochemical identity of the majority of these VLPO-projecting neurons within the Lateral Hypothalamus (LH), as well as their function in the arousal network, remains unknown. Herein we describe a population of VLPO-projecting neurons in the LH that express the vesicular GABA transporter (VGAT; a marker for GABA-releasing neurons). In addition to the VLPO, these neurons also project to several other established sleep and arousal nodes, including the tuberomammillary nucleus, ventral periaqueductal gray, and locus coeruleus. Selective and acute chemogenetic activation of LH VGAT(+) neurons was profoundly wake promoting, whereas acute inhibition increased sleep. Because of its direct and massive inputs to the VLPO, this population may play a particularly important role in sleep-wake switching.

Dominique Fellmann - One of the best experts on this subject based on the ideXlab platform.

Qingchun Tong - One of the best experts on this subject based on the ideXlab platform.

  • gabaergic projections from Lateral Hypothalamus to paraventricular hypothalamic nucleus promote feeding
    The Journal of Neuroscience, 2015
    Co-Authors: Zhaofei Wu, Yong Xu, Leandra R Mangieri, De Pei Li, Benjamin R Arenkiel, Qingchun Tong
    Abstract:

    Lesions of the Lateral Hypothalamus (LH) cause hypophagia. However, activation of glutamatergic neurons in LH inhibits feeding. These results suggest a potential importance for other LH neurons in stimulating feeding. Our current study in mice showed that disruption of GABA release from adult LH GABAergic neurons reduced feeding. LH GABAergic neurons project extensively to the paraventricular hypothalamic nucleus (PVH), and optogenetic stimulation of GABAergic LH → PVH fibers induced monosynaptic IPSCs in PVH neurons, and potently increased feeding, which depended on GABA release. In addition, disruption of GABA-A receptors in the PVH reduced feeding. Thus, we have identified a new feeding pathway in which GABAergic projections from the LH to the PVH promote feeding.

Anne Venner - One of the best experts on this subject based on the ideXlab platform.

  • a novel population of wake promoting gabaergic neurons in the ventral Lateral Hypothalamus
    Current Biology, 2016
    Co-Authors: Anne Venner, Christelle Anaclet, Rebecca Y Broadhurst, Clifford B Saper, Patrick M Fuller
    Abstract:

    The largest synaptic input to the sleep-promoting ventroLateral preoptic area (VLPO) [1] arises from the Lateral Hypothalamus [2], a brain area associated with arousal [3-5]. However, the neurochemical identity of the majority of these VLPO-projecting neurons within the Lateral Hypothalamus (LH), as well as their function in the arousal network, remains unknown. Herein we describe a population of VLPO-projecting neurons in the LH that express the vesicular GABA transporter (VGAT; a marker for GABA-releasing neurons). In addition to the VLPO, these neurons also project to several other established sleep and arousal nodes, including the tuberomammillary nucleus, ventral periaqueductal gray, and locus coeruleus. Selective and acute chemogenetic activation of LH VGAT(+) neurons was profoundly wake promoting, whereas acute inhibition increased sleep. Because of its direct and massive inputs to the VLPO, this population may play a particularly important role in sleep-wake switching.

Christian Luscher - One of the best experts on this subject based on the ideXlab platform.

  • accumbal d1r neurons projecting to Lateral Hypothalamus authorize feeding
    Neuron, 2015
    Co-Authors: Eoin C Oconnor, Yves Kremer, Sandrine Lefort, Masaya Harada, Vincent Pascoli, Clement Rohner, Christian Luscher
    Abstract:

    Feeding satisfies metabolic need but is also controlled by external stimuli, like palatability or predator threat. Nucleus accumbens shell (NAcSh) projections to the Lateral Hypothalamus (LH) are implicated in mediating such feeding control, but the neurons involved and their mechanism of action remain elusive. We show that dopamine D1R-expressing NAcSh neurons (D1R-MSNs) provide the dominant source of accumbal inhibition to LH and provide rapid control over feeding via LH GABA neurons. In freely feeding mice, D1R-MSN activity reduced during consumption, while their optogenetic inhibition prolonged feeding, even in the face of distracting stimuli. Conversely, activation of D1R-MSN terminals in LH was sufficient to abruptly stop ongoing consumption, even during hunger. Direct inhibition of LH GABA neurons, which received input from D1R-MSNs, fully recapitulated these findings. Together, our study resolves a feeding circuit that overrides immediate metabolic need to allow rapid consumption control in response to changing external stimuli. VIDEO ABSTRACT.

  • accumbal d1r neurons projecting to Lateral Hypothalamus authorize feeding
    Neuron, 2015
    Co-Authors: Eoin C Oconnor, Yves Kremer, Sandrine Lefort, Masaya Harada, Vincent Pascoli, Clement Rohner, Christian Luscher
    Abstract:

    Summary Feeding satisfies metabolic need but is also controlled by external stimuli, like palatability or predator threat. Nucleus accumbens shell (NAcSh) projections to the Lateral Hypothalamus (LH) are implicated in mediating such feeding control, but the neurons involved and their mechanism of action remain elusive. We show that dopamine D1R-expressing NAcSh neurons (D1R-MSNs) provide the dominant source of accumbal inhibition to LH and provide rapid control over feeding via LH GABA neurons. In freely feeding mice, D1R-MSN activity reduced during consumption, while their optogenetic inhibition prolonged feeding, even in the face of distracting stimuli. Conversely, activation of D1R-MSN terminals in LH was sufficient to abruptly stop ongoing consumption, even during hunger. Direct inhibition of LH GABA neurons, which received input from D1R-MSNs, fully recapitulated these findings. Together, our study resolves a feeding circuit that overrides immediate metabolic need to allow rapid consumption control in response to changing external stimuli. Video Abstract