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By targeting GS-mediated neurotransmitter homeostasis, pharmacological doses of VE could restore GS levels through scavenging the ROS generated during seizures and suppressing protein kinase C (PKC), a negative regulator of GS expression [3]

And so that's what they were coming to a conclusion

Receptor downregulation is the most likely cause

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Acetyl-L-carnitine has a neuromodulatory influence on neuronal phenotypes during early [PMID: 1477960] Laboratory literature summary: Acetyl-L-carnitine has a neuromodulatory influence on neuronal phenotypes during early embryogenesis in the chick embryo

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