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This first-in-class drug candidate is believed to help regulate excitatory neurotransmission in two ways: through pre-synaptic inhibition of glutamate release via sigma-1 receptor agonist activity and through postsynaptic glutamate response modulation via uncompetitive, low-affinity NMDA antagonist activity.
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Interesting. I was unaware that DXM also inhibited glutamate release. Glutamate activates the NMDA receptor (along with co-agonist glycine). Glutamate (the principal excitatory neurotransmitter) also serves as the precursor for the synthesis of GABA (the principal inhibitory neurotransmitter). So I'm guessing that DXM may lower concentrations of GABA as well.
Fascinating.
