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We began analyzing https://www.nature.com/articles/ncomms11905, but it redirected us to https://www.nature.com/articles/ncomms11905. The analysis below is for the second page.

Title[redir]:
Genetically and functionally defined NTS to PBN brain circuits mediating anorexia | Nature Communications
Description:
The central nervous system controls food consumption to maintain metabolic homoeostasis. In response to a meal, visceral signals from the gut activate neurons in the nucleus of the solitary tract (NTS) via the vagus nerve. These NTS neurons then excite brain regions known to mediate feeding behaviour, such as the lateral parabrachial nucleus (PBN). We previously described a neural circuit for appetite suppression involving calcitonin gene-related protein (CGRP)-expressing PBN (CGRPPBN) neurons; however, the molecular identity of the inputs to these neurons was not established. Here we identify cholecystokinin (CCK) and noradrenergic, dopamine Ξ²-hydroxylase (DBH)-expressing NTS neurons as two separate populations that directly excite CGRPPBN neurons. When these NTS neurons are activated using optogenetic or chemogenetic methods, food intake decreases and with chronic stimulation mice lose body weight. Our optogenetic results reveal that CCK and DBH neurons in the NTS directly engage CGRPPBN neurons to promote anorexia. Neurons in the nucleus of the solitary tract (NTS) are known to receive visceral signals from the gut during feeding. Here, the authors identify two populations of CCK- and DBH-expressing NTS neurons that work to suppress food intake when activated via opto- or chemogenetic stimulation.

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Keywords {πŸ”}

neurons, nts, article, food, dbhnts, google, scholar, mice, ccknts, cas, intake, pbn, cno, activation, cgrppbn, feeding, cck, nucleus, animals, brain, fig, fos, expressing, nature, lateral, data, expression, observed, injection, activated, cells, hmdq, injected, group, mcherry, cgrp, mouse, min, tract, stimulation, sections, rat, receptor, measured, light, solitary, parabrachial, inputs, control, projections,

Topics {βœ’οΈ}

nature portfolio cre-dependent paav-hsyn-dio-hm3dq privacy policy research diets advertising circular open-field arena preserve g-protein signal-transduction chemogenetic tools knight nature donkey anti-goat igg social media cre-dependent aav1-dio-chr2 open-field arena 45 min nature 483 nature 503 nature 0/ reprints high-resolution single-cell imaging paav-ef1Ξ±-dio-synaptophysin cre recombinase-dependent adeno paav1-ef1Ξ±-dio-synaptophysin paav-ef1Ξ±-dio-chr2 hypothalamic agouti-related peptide paav-ef1Ξ±-dio-mcherry author information authors low-fos-expressing group based light-emitting diode illumination open-field test ice-cold cutting solution beta3-adrenoceptor polymorphisms relate system patch-clamp amplifier bio-serve dustless pellets injecting aav1-dio-synaptophysin control aav-dio-mcherry virus serotonin agonist-induced hypophagia brain cytokine-independent switch maintain metabolic homoeostasis ad libitum access long-term signals responding promote feeding-related disorders beta2-adrenoceptor polymorphisms relate tyrosine hydroxylase-positive cells pre-restriction body weight fibre optic cannulae allowed unrestricted access prolactin-releasing peptide-immunoreactivity open field maladaptive eating patterns high mg2+/ca2+ ratio protein-coupled receptors

Schema {πŸ—ΊοΈ}

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         headline:Genetically and functionally defined NTS to PBN brain circuits mediating anorexia
         description:The central nervous system controls food consumption to maintain metabolic homoeostasis. In response to a meal, visceral signals from the gut activate neurons in the nucleus of the solitary tract (NTS) via the vagus nerve. These NTS neurons then excite brain regions known to mediate feeding behaviour, such as the lateral parabrachial nucleus (PBN). We previously described a neural circuit for appetite suppression involving calcitonin gene-related protein (CGRP)-expressing PBN (CGRPPBN) neurons; however, the molecular identity of the inputs to these neurons was not established. Here we identify cholecystokinin (CCK) and noradrenergic, dopamine β-hydroxylase (DBH)-expressing NTS neurons as two separate populations that directly excite CGRPPBN neurons. When these NTS neurons are activated using optogenetic or chemogenetic methods, food intake decreases and with chronic stimulation mice lose body weight. Our optogenetic results reveal that CCK and DBH neurons in the NTS directly engage CGRPPBN neurons to promote anorexia. Neurons in the nucleus of the solitary tract (NTS) are known to receive visceral signals from the gut during feeding. Here, the authors identify two populations of CCK- and DBH-expressing NTS neurons that work to suppress food intake when activated via opto- or chemogenetic stimulation.
         datePublished:2016-06-15T00:00:00Z
         dateModified:2016-06-15T00:00:00Z
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      headline:Genetically and functionally defined NTS to PBN brain circuits mediating anorexia
      description:The central nervous system controls food consumption to maintain metabolic homoeostasis. In response to a meal, visceral signals from the gut activate neurons in the nucleus of the solitary tract (NTS) via the vagus nerve. These NTS neurons then excite brain regions known to mediate feeding behaviour, such as the lateral parabrachial nucleus (PBN). We previously described a neural circuit for appetite suppression involving calcitonin gene-related protein (CGRP)-expressing PBN (CGRPPBN) neurons; however, the molecular identity of the inputs to these neurons was not established. Here we identify cholecystokinin (CCK) and noradrenergic, dopamine β-hydroxylase (DBH)-expressing NTS neurons as two separate populations that directly excite CGRPPBN neurons. When these NTS neurons are activated using optogenetic or chemogenetic methods, food intake decreases and with chronic stimulation mice lose body weight. Our optogenetic results reveal that CCK and DBH neurons in the NTS directly engage CGRPPBN neurons to promote anorexia. Neurons in the nucleus of the solitary tract (NTS) are known to receive visceral signals from the gut during feeding. Here, the authors identify two populations of CCK- and DBH-expressing NTS neurons that work to suppress food intake when activated via opto- or chemogenetic stimulation.
      datePublished:2016-06-15T00:00:00Z
      dateModified:2016-06-15T00:00:00Z
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