CD47 seems to affect the astrocytes rather than the nerve fibers. This has also been demonstrated by inhibiting the astrocytic proliferation where the drawback of non-glial-associated growth is abolished as long as the astrocytic migration is hampered. Thus, the absence of CD47 may prevent drawback of the axons that form the non-glial-associated nerve fibers. The paraventricular hypothalamus is a critical brain region for both feeding and energy expenditure regulation. Within the PVH, there are distinct subsets of peptidergic neurons including oxytocin, vasopressin, thyrotropin releasing hormone and corticotropin releasing hormone neurons, which send projections throughout the brain as well as to the median eminence or posterior pituitary. These projections form the structural basis through which the PVH in the regulates a diverse set of physiologic functions including energy homeostasis. Substantial data supports a role for oxytocin in regulating body weight. Oxytocin neurons show relatively high co-localization with the expression of FTO gene, a gene in which mutations have been shown to be significantly associated with human obesity. Reduced oxytocin neuron number and cell volume, and reduced baseline oxytocin profiles have been associated with the PraderWilli syndrome, a human obesity syndrome notable for severe hyperphagia. Oxytocin neurons appear to at least partially mediate the anorexigenic action of leucine. Administration of oxytocin decreases food intake while administration of oxytocin receptor antagonists results in hyperphagia. Current evidence supports a model in which PVH oxytocin neurons project to the nucleus of solitary tract and release oxytocin to modulate the activity of local hindbrain neurons and ‘‘fine tune’’ the response of NTS neurons to satiety signals arising in the gut and/ or periphery. In addition, diminished oxytocin has been shown to be associated with hyperphagic obesity secondary to haploinsufficiency of Single-minded 1, a transcription factor required for PVH development. Importantly, oxytocin reduces high-fat induced obesity by restricting energy intake. Consistent with this result, a recent study suggested that synaptotagmin-4 regulates oxytocin release to modulate feeding and that defects in this regulation may mediate diet-induced obesity. Taken together, these data demonstrate an important role for oxytocin in the regulation of food intake. Despite the compelling evidence for a role of oxytocin in feeding regulation, there are inconsistencies regarding the role of oxytocin in other animal studies. Mice with deficiency of oxytocin or its receptor show either normal body weight or mild obesity. Even in the case of obesity, mice show reduced energy expenditure but normal feeding. Whether these discrepancies could be attributable to developmental compensation in response to germline gene deletion is not clear. Previous studies targeting agouti-related peptide neurons revealed that disruption of these neurons in the neonatal period induced profound developmental compensation that MK-2206 2HCl almost completely masked the physiologic function of these neurons. To test the necessity of oxytocin neurons in feeding regulation and avoid any developmental compensation occurring from germline deletion of oxytocin or its receptor, we generated mice with a specific lesion of oxytocin neurons in adult mice using a temporally controlled, genetic lesioning approach. After achieving, 95% ablation of oxytocin neurons, our results demonstrate that oxytocin neurons are dispensable for feeding regulation in males and females.