Food intake elicited by central administration of orexins/hypocretins: identification of hypothalamic sites of action 1 This study was presented in part at the 28th Annual Meeting of the Society for Neuroscience, Los Angeles, CA, in November 1998. 1

@article{Dube1999FoodIE,
  title={Food intake elicited by central administration of orexins/hypocretins: identification of hypothalamic sites of action
 1
 This study was presented in part at the 28th Annual Meeting of the Society for Neuroscience, Los Angeles, CA, in November 1998.
 
 
 1
 
},
  author={Michael G. Dube and Satya P. Kalra and Pushpa S. Kalra},
  journal={Brain Research},
  year={1999},
  volume={842},
  pages={473-477}
}
Orexin-induced feeding requires NMDA receptor activation in the perifornical region of the lateral hypothalamus.
TLDR
Glutamatergic systems in the LH/PFA mediating the feeding response to orexin-A through NMDA receptors are demonstrated to initiate feeding through N-methyl-d-aspartic acid (NMDA) receptors.
Hypoglycemia activates orexin neurons and selectively increases hypothalamic orexin-B levels: responses inhibited by feeding and possibly mediated by the nucleus of the solitary tract.
TLDR
The hypothesis that orexin neurons are stimulated by falling glucose levels but are readily inhibited by signals related to nutrient ingestion is supported and it is suggested that they may functionally link with neuronal activity in the NTS.
Orexin-A does not stimulate food intake in old rats.
TLDR
Results of the present study indicate that the function of the orexin system is diminished in old rats, and the decrease in the OX1R protein level in the hypothalamus could be responsible for orexIn-A's lack of stimulation of food intake in old Rats.
Peptides that regulate food intake: appetite-inducing accumbens manipulation activates hypothalamic orexin neurons and inhibits POMC neurons.
Corticolimbic circuits involving the prefrontal cortex, amygdala, and ventral striatum determine the reward value of food and might play a role in environmentally induced obesity. Chemical
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TLDR
The galanin-induced augmentation of cumulative food intake up to 2 h after injection was due to the initial increase in food consumption during the 0 to 20-min interval, which suggests that galan in acts by activation of feeding behavior and not by suppression of satiety signals in these fasted animals, in which satiety messages are presumably not initially operative.
Independent feeding and metabolic actions of orexins in mice.
TLDR
Direct evidence is provided that OX peptides are more likely to be involved in the control of energy metabolism than of food intake in mice.
Interacting appetite-regulating pathways in the hypothalamic regulation of body weight.
TLDR
Multiple orexigenic and anorexigenic pathways in the hypothalamic ARN appear to represent redundancy, a characteristic of regulated biological systems to provide a "fail-safe" neural mechanism to meet an organism's constant energy needs for growth and maintenance.
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