Food consumption and body weight regulations are done in the hypothalamus. Indeed, hypothalamus is the brain\\\'s main area in controlling food intake. Hypothalamus controls food intake via special nuclei such as: ARC, PVN, DMH, VMH and LHA. PVN are second order neurons. This nucleus received multiple inputs from different areas of the brain via specific and non-specific receptors. NPYR and α2-adrenoceptors are orexigenic receptors, but Melanocortin receptors are anorexigenic receptors. PVN integrated inputs from multiple areas, and then transmitted various outputs for central regulation of food intake. To identify neural pathways and the role of neurotransmitters on central control of food intake in PVN, multiple researches have been done via injection of various neurotransmitters on the laboratory animals. Leptin applies its effect on regulation of feeding behaviours through arcuate nucleus-paraventricular nucleus axis and MC4R receptor. Also, Insulin is a hypophagic neurotransmitter, and its hypophagic effect applied in PVN via NPY1 and MC4R receptors. Ghrelin has a biphasic effect on food intake in birds and mammals. In birds, ghrelin inhibits food intake, but in mammals stimulated food intake. In birds, ghrelin via 5HT2A receptor on CRF neurons located on PVN reduced food intake. In mammals via GHSR (ghrelin receptor) and NPY1 receptors increased food intake. Somatostatin acts in the brain as an inhibitory and hyperphagic neurotransmitter. Hyperphagic effect of Somatostatin on PVN exert via SST2, OX1 and NPY1 receptors respectively. Therefore, PVN has an important effect on central regulation of food intake via different neurotransmitters and pathway.

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