Glucose-responsive neurons of the paraventricular thalamus control sucrose-seeking behavior

Labouèbe, Gwenaël; Boutrel, Benjamin; Tarussio, David; Thorens, Bernard

doi:10.1038/nn.4331

Cited by 113 publications

(145 citation statements)

References 21 publications

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“…This discrepancy could be due to differences in the species used in these experiments. Also, in our experiments, the reduction in GLUT2 expression was limited to ependymal cells and tanycytes, while in the transgenic line, expression was also affected in neurons sensitive to hypoglycemia located in the brainstem (Tarussio et al, 2014) or neurons in the thalamus involved in carbohydrate preference (Labouebe et al, 2016). We also showed that suppression of GLUT2 expression in tanycytes leads to the loss in response to increased icv glucose, supporting a role for indirect control of glucose over the expression of neuropeptides that control hunger and satiety.…”

Section: Discussionmentioning

confidence: 47%

“…However, those that exist have been corroborated by the use of mice expressing a fluorescent reporter gene (eYFP) under the control of the GLUT2 promoter, GLUT2‐eYFP mice (Mounien et al, 2010). GLUT2 was found in neurons and astrocytes dispersed in many structures, including the hypothalamus, the brain stem, the thalamic area (Arluison, Quignon, Thorens, Leloup, & Penicaud, 2004; Labouebe, Boutrel, Tarussio, & Thorens, 2016) and in tanycytes (Garcia et al, 2003). Tanycytes are radial glial‐like cells surrounding the lateral walls of the infundibular recess (Recabal, Caprile, & Garcia‐Robles, 2017).…”

Section: Introductionmentioning

confidence: 99%

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Glial hypothalamic inhibition of GLUT2 expression alters satiety, impacting eating behavior

Barahona

Llanos

Recabal

et al. 2017

Glia

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Glucose is a key modulator of feeding behavior. By acting in peripheral tissues and in the central nervous system, it directly controls the secretion of hormones and neuropeptides and modulates the activity of the autonomic nervous system. GLUT2 is required for several glucoregulatory responses in the brain, including feeding behavior, and is localized in the hypothalamus and brainstem, which are the main centers that control this behavior. In the hypothalamus, GLUT2 has been detected in glial cells, known as tanycytes, which line the basal walls of the third ventricle (3V). This study aimed to clarify the role of GLUT2 expression in tanycytes in feeding behavior using 3V injections of an adenovirus encoding a shRNA against GLUT2 and the reporter EGFP (Ad‐shGLUT2). Efficient in vivo GLUT2 knockdown in rat hypothalamic tissue was demonstrated by qPCR and Western blot analyses. Specificity of cell transduction in the hypothalamus and brainstem was evaluated by EGFP‐fluorescence and immunohistochemistry, which showed EGFP expression specifically in ependymal cells, including tanycytes. The altered mRNA levels of both orexigenic and anorexigenic neuropeptides suggested a loss of response to increased glucose in the 3V. Feeding behavior analysis in the fasting‐feeding transition revealed that GLUT2‐knockdown rats had increased food intake and body weight, suggesting an inhibitory effect on satiety. Taken together, suppression of GLUT2 expression in tanycytes disrupted the hypothalamic glucosensing mechanism, which altered the feeding behavior.

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Section: Discussionmentioning

confidence: 47%

Section: Introductionmentioning

confidence: 99%

Glial hypothalamic inhibition of GLUT2 expression alters satiety, impacting eating behavior

Barahona

Llanos

Recabal

et al. 2017

Glia

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“…4c). PVT is involved in motivated behaviours 36 including feeding 37,38 , and AgRP →PVT stimulation induces feeding 35 . Using CRACM, we found that BLA →InsCtx neurons and BLA inhibitory interneurons received synaptic input from PVT (Extended Data Fig.…”

Section: A Pathway From Agrp Neurons To Insctxmentioning

confidence: 99%

Homeostatic circuits selectively gate food cue responses in insular cortex

Livneh

Ramesh

Burgess

et al. 2017

Nature

282

293

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Physiological needs bias perception and attention to relevant sensory cues. This process is ‘hijacked’ by drug addiction, causing cue-induced cravings and relapse. Similarly, its dysregulation contributes to failed diets, obesity, and eating disorders. Neuroimaging studies in humans have implicated insular cortex in these phenomena. However, it remains unclear how ‘cognitive’ cortical representations of motivationally relevant cues are biased by subcortical circuits that drive specific motivational states. Here we develop a microprism-based cellular imaging approach to monitor visual cue responses in the insular cortex of behaving mice across hunger states. Insular cortex neurons demonstrate food- cue-biased responses that are abolished during satiety. Unexpectedly, while multiple satiety-related visceral signals converge in insular cortex, chemogenetic activation of hypothalamic ‘hunger neurons’ (expressing agouti-related peptide (AgRP)) bypasses these signals to restore hunger-like response patterns in insular cortex. Circuit mapping and pathway-specific manipulations uncover a pathway from AgRP neurons to insular cortex via the paraventricular thalamus and basolateral amygdala. These results reveal a neural basis for state-specific biased processing of motivationally relevant cues.

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“…Feeding is likely regulated by these neurons because they are a source of inhibitory drive onto downstream, possibly orexigenic, hypothalamus neurons (Castro et al, 2015;Zheng et al, 2007). Much less is known about how inputs to the NAc influence consummatory behavior, although there is increasing interest in this topic (Do-Monte et al, 2017;Labouè be et al, 2016;Parker et al, 2015;Tellez et al, 2016).…”

Section: Nac Involvement In Feeding Behaviormentioning

confidence: 99%

Coordinated Reductions in Excitatory Input to the Nucleus Accumbens Underlie Food Consumption

Reed

Lafferty

Mendoza

et al. 2018

Neuron

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Reward-seeking behavior is regulated by a diverse collection of inputs to the nucleus accumbens (NAc). The information encoded in each excitatory afferent to the NAc is unknown, in part because it is unclear when these pathways are active in relation to behavior. Here we compare the activity profiles of amygdala, hippocampal, and thalamic inputs to the NAc shell in mice performing a cued reward-seeking task using GCaMP-based fiber photometry. We find that the rostral and caudal ends of the NAc shell are innervated by distinct but intermingled populations of forebrain neurons that exhibit divergent feeding-related activity. In the rostral NAc shell, a coordinated network-wide reduction in excitatory drive correlates with feeding, and reduced input from individual pathways is sufficient to promote it. Overall, the data suggest that pathway-specific input activity at a population level may vary more across the NAc than between pathways.

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Glucose-responsive neurons of the paraventricular thalamus control sucrose-seeking behavior

Cited by 113 publications

References 21 publications

Glial hypothalamic inhibition of GLUT2 expression alters satiety, impacting eating behavior

Glial hypothalamic inhibition of GLUT2 expression alters satiety, impacting eating behavior

Homeostatic circuits selectively gate food cue responses in insular cortex

Coordinated Reductions in Excitatory Input to the Nucleus Accumbens Underlie Food Consumption

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