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Melanin concentrating-hormone expressing (MCH) neurons located in the lateral hypothalamus play an important role in the regulation of metabolism homeostasis. Both an MCH knockout and ablation of MCH neurons result in reduced food intake and leanness. Previous studies have revealed differences between the effects of MCH neural ablation and MCH knockout, raising the possibility that additional transmitters besides MCH mediate the effects of these neurons.

In the present study, Schneeberger, Tan, et al. found that the great majority of MCH neurons are glutamatergic. They compared the physiologic effects of ablating glutamate signaling in these neurons to either an MCH knockout or MCH neural ablation. They found that the effects of knocking out the glutamate transporter and MCH were different, suggesting that the function of MCH neurons is a composite of the function of a classic neurotransmitter and a neuropeptide. In some cases, these functions are redundant, for example weight maintenance and food intake, and in other cases non-redundant, for example in glutamate producing MCH neurons roles in sucrose preference and glucose metabolism control. The most likely possibility to explain these differences is that the peptides and classical neurotransmitter project to and act at partially overlapping sites.

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In this section authors briefly report on their work recently published in Molecular Metabolism.

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Florian Merkle
University of Cambridge, UK
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