We appreciate the interest of Drs Shim and Adityanjee in the mechanistic
implications of our study, which described the interactive effects of lamotrigine
and ketamine in healthy human subjects.1
They question whether reductions in N-methyl-D-aspartate
receptor (NMDAR) function produced by ketamine in fact enhance regional glutamatergic
neurotransmission via non-NMDARs. Because of this concern, they question whether
lamotrigine reduces the hyperglutamatergic effects of ketamine or whether
it attenuates ketamine's effects through other mechanisms. In response to
these queries, it is important to point out that the study in question is
quite limited in its capacity to determine how lamotrigine attenuates ketamine's
effects. The fact that lamotrigine reduced the psychotogenic and cognitive
effects of ketamine, but potentiated the euphoric effects of ketamine, may
have mechanistic significance. For example, it suggests that lamotrigine is
not simply antagonizing the effects of ketamine at the NMDAR. Preclinical
research may provide insight into the interactive effects of lamotrigine and
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