Some of these neurons also coproduce anorexigenic peptides such asMSH. These anorexigenic and orexigenic producing neurons extend to all the other nuclei mentioned above, to influence feeding patterns and behaviour. It is thought that NPY neurons that coexpress GABA interact with Galanin and-endorphin neurons to control the daily patterning of food intake.
Lesions of the VMN produce hyperphagia and weight gain. Although debated, the VMN is thought to be thesatiety centre? to exert restraint over feeding patterns, and thus it can be seen in lesions that the daily patterning of food intake is abolished and replaced by constant, low level feeding. However, there is a possibility that this could be simply because lesions of the VMN may disturb the flow of orexigenic signals from the ARC to the PVN/DMN. The LH is considered to be the hunger centre, and lesions produce aphagia, again confirming it as part of the appetite-regulating network. The DMN has efferents to the VMN and PVN and receives afferents from the ARC, which contain NPY, therefore it is likely that this nucleus participates in the stimulation of feeding. Along with the ARC, it has the second largest NPY neuron population, that innervate all the nuclei implied in appetite control. The paraventricular nucleus is thought also to participate in ingestive behaviour as microinjection of most orexigenic signals stimulates feeding. Suprachiasmatic nucleus lesions result in loss of regulated feeding. Its efferents terminate in the VMN, DMN and the ARC, where they terminate on the NPY and galanin producing neurons.
The observation that orexigenic and anorexigenic signal producing neurons overlap and are connected strongly supports the localisation of the appetite-regulating centre in the hypothalamus. As such, how might leptin be considered an appetite suppressant? It must be demonstrated that it acts upon the neurons in the hypothalamus that are considered to be part of this appetite-regulating network.
