Abstract
Obesity has become a global issue, and the overconsumption of food is thought to be a major contributor. However, the regulatory neural circuits that regulate palatable food consumption remain unclear. Here, we report that somatostatin (SOM) neurons and GABAergic (VGAT) neurons in the basal forebrain (BF) play specific roles in regulating feeding. Optogenetic stimulation of BF SOM neurons increased fat and sucrose intake within minutes and promoted anxiety-like behaviors. Furthermore, optogenetic stimulation of projections from BF SOM neurons tothe lateral hypothalamic area (LHA) selectively resulted in fat intake. In addition, activation of BF VGAT neurons rapidly induced general food intake and gnawing behaviors. Whole-brain mapping of inputs and outputs showed that BF SOM neurons form bidirectional connections with several brain areas important in feeding and regulation of emotion. Collectively, these results suggest that BF SOM neurons play a selective role in hedonic feeding.
Highlights
Obesity is a serious global public health concern (Finucane et al, 2011; Swinburn et al, 2009)
Our fluorescence in situ hybridization (FISH) data demonstrated that Vesicular GABA transporter (VGAT) and PV neurons were distributed in all basal forebrain (BF) sub-regions
Most of SOM neurons were concentrated within the ventral region of BF, including the horizontal limb of the diagonal band (HDB), magnocellular preoptic nucleus (MCPO), and substantia innominata (SI), and only a small subset was found in ventral pallidum (VP) (Figure S1)
Summary
Obesity is a serious global public health concern (Finucane et al, 2011; Swinburn et al, 2009). A key environmental factor that has contributed to the rising prevalence of obesity is the easy availability of relatively inexpensive, highly palatable, energy-dense foods with little anticipated risk of food scarcity. In such environments, overconsumption is thought to be driven mainly by hedonic eating (Zheng and Berthoud, 2008). Overconsumption is thought to be driven mainly by hedonic eating (Zheng and Berthoud, 2008) In this form of eating, the intake is not driven by metabolic need but by the reward experienced when consuming the food and is relevant to highly palatable energy-dense food (Lowe and Butryn, 2007). Ablation or inhibition of AGRP neurons suppresses feeding (Krashes et al, 2011; Luquet et al, 2005), and activation of AGRP neurons elicits food seeking and food consumption within minutes, even in well-fed mice (Aponte et al, 2011; Atasoy et al, 2012; Betley et al, 2015; Krashes et al, 2011)
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