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Mechanisms deciphered in these studies indicate that the interaction between serotonin and GLP-1 in the hindbrain increases proopiomelanocortin/cocaine- and amphetamine-regulated transcript (POMC/CART) neuron activity, leading to induction of satiety signals and suppression of neuropeptide Y/agouti-related peptide (NPY/AgRP) neuron activity, which in turn suppresses hunger
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In contrast, although increases in other neurotrophic factors such as neurotrophin-3 and glial cell line-derived neurotrophic factor have been reported in certain experimental settings, the precise molecular mechanisms underlying their regulation remain less clearly defined [60]
