In addition to the changes in the hippocampus, EE was able to regulate leptin sensitivity in young mice and leave metabolic and synaptic imprints to prevent obesity, the mechanism of which involves an increase in activation of STAT3 and a transfer of the excitation/inhibition balance toward the form er in α-melanocyte-stimulating hormone (α-MSH) neurons and toward the latter in agouti-related peptide (AgRP)/Neuropeptide Y (NPY) neurons. Here, LEP is linked to obesity due to melanocortin 4 receptor deficiency.