Thiamine supplementation mood and cognitive functioning.

From what I understand there appears to be an inverse relationship between glutamate and dopamine in the prefrontal cortex - sulbutiamine's ability to increase firing rates of the kainate receptors would cause a decrease in dopamine release in the PFC (and cingular cortex too, apparently!) I know large doses of kynurenic acid are neurotoxic, presumably from activation of kainate receptors everywhere they're found (they're not as common as AMPA or NMDA receptors, interestingly).

One thing I don't like about this abstract is that it doesn't specify pre- or post-synaptic kainate receptors - it could be either, or it could be both! I think distinguishing this is important, because pre-synaptic kainate receptors tend to mediate excitatory effects, and post-synaptic kainate receptors tend to mediate inhbitory effects (via the release of GABA).

Kainate receptors don't seem to be near as important as AMPA/NMDA receptors, but it's certainly too early in the research to be conclusive about anything! This section from the wiki page was particularly notable (to me at least):

Unlike AMPA receptors, kainate receptors play only a minor role in signaling at synapses.[4]

Rather, kainate receptors may have a more subtle role in synaptic plasticity, affecting the likelihood that the postsynaptic cell will fire in response to future stimulation.[5][6] Activating kainate receptors in the…