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10.3390/ijms22020832

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63 demonstrated that recombinant MSTN proteins produced in bacteria and eukaryotes behave differently in the regulation of C2C12 myoblast proliferation

The glutamate hypothesis proposes that symptoms of schizophrenia and cognitive impairments are the result of the hypofunction of N-methyl-D-aspartate receptors (NMDARs) on -aminobutyric acid (GABA) interneurons in the cerebral cortex, resulting in overactivation of downstream glutamate signaling to the VTA and, possibly, consequent dopamine release in the mesolimbic system [4,21,22]