scholarly journals Ventral tegmental area orexin 1 receptors promote palatable food intake and oppose postingestive negative feedback

2016 ◽  
Vol 311 (3) ◽  
pp. R592-R599 ◽  
Author(s):  
Sarah J. Terrill ◽  
Kellie M. Hyde ◽  
Kristen E. Kay ◽  
Hayden E. Greene ◽  
Calyn B. Maske ◽  
...  

Hypothalamic orexin neurons project to numerous brain areas, including the ventral tegmental area (VTA), which is involved in motivation and food-seeking behavior. Here we address how exogenously administered orexin-A and endogenous orexin 1 receptor (OX1R) activation in the VTA affects feeding behavior. We hypothesized that orexin-A and OX1R antagonist SB334867 delivered to the VTA, at doses that were subthreshold for effect when injected into the ventricle, would affect intake of palatable foods in multiple test situations. We first used a hedonic feeding model in which satiated rats selectively consume a high-fat diet (HFD). Intra-VTA orexin-A stimulated additional consumption of chow and increased HFD intake in this model. In ad libitum-fed rats given daily 30-min test sessions, intra-VTA orexin-A also increased intake of HFD and 0.1 M sucrose. Further analysis of licking patterns revealed that that VTA orexin-A increased meal size and licking burst size only toward the end of the meal. Consistent with this finding, a subthreshold dose of VTA orexin-A prevented intake suppression induced by gastrointestinal nutrient infusion. Surprisingly, intra-VTA orexin-A had no effect on operant responding for sucrose pellets on a progressive ratio schedule of reinforcement. A role for endogenous VTA OX1R stimulation is supported by our finding that bilateral VTA injection of the selective OX1R antagonist SB334867 suppressed 0.1 M sucrose intake. Together, our data suggest that OX1R activity in the VTA facilitates food intake, potentially by counteracting postingestive negative feedback that would normally suppress feeding later in a meal.

2019 ◽  
Vol 31 (7) ◽  
Author(s):  
Sarah H. Lockie ◽  
Romana Stark ◽  
David C. Spanswick ◽  
Zane B. Andrews

2013 ◽  
Vol 38 (9) ◽  
pp. 1685-1697 ◽  
Author(s):  
Elizabeth G Mietlicki-Baase ◽  
Laura E Rupprecht ◽  
Diana R Olivos ◽  
Derek J Zimmer ◽  
Mark D Alter ◽  
...  

2010 ◽  
Vol 210 (2) ◽  
pp. 179-188 ◽  
Author(s):  
WenLin Sun ◽  
YueQiang Xue ◽  
ZaiFang Huang ◽  
Jeffery D. Steketee

2020 ◽  
Author(s):  
Daniel C. Lowes ◽  
Linda A. Chamberlin ◽  
Lisa N. Kretsge ◽  
Emma S. Holt ◽  
Atheir I. Abbas ◽  
...  

AbstractStressful experiences frequently precede depressive episodes1. Depression results in anhedonia, or disrupted reward-seeking, in most patients2. In humans3,4 and rodents5,6, stress can disrupt reward-seeking, providing a potential mechanism by which stress can precipitate depression7-9. Yet despite decades investigating how stress modulates dopamine neuron transmission between the ventral tegmental area (VTA) and nucleus accumbens (NAc), the underpinnings of the stress-anhedonia transition remain elusive10-13. Here we show that during restraint stress, VTA GABA neurons drive low frequency NAc LFP oscillations, rhythmically modulating NAc firing rates. The strength of these stress-induced NAc oscillations predict the degree of impaired reward-seeking upon release from restraint. Inhibiting VTA GABA neurons disrupts stress-induced NAc oscillations and reverses the effect of stress on reward-seeking. By contrast, mimicking these oscillations with rhythmic VTA GABA stimulation in the absence of stress blunts subsequent reward-seeking. These experiments demonstrate that VTA GABA inputs to the NAc are both necessary and sufficient for stress-induced decreases in reward seeking behavior, elucidating a key circuit-level mechanism underlying stress-induced anhedonia.


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