Background and Purpose
Glutamate receptor mediated enhanced excitatory neurotransmission is
typically associated with mesial temporal lobe epilepsy with hippocampal
sclerosis (MTLE-HS). Kynurenic acid (KYNA) and quinolinic acid (QUIN)
are two important tryptophan-kynurenine pathway (KP) metabolites that
modulate glutamate receptor activity. This study was designed to test
the hypothesis that alteration in metabolism of KP metabolites in the
hippocampus of patients with MTLE-HS contributes to abnormal
glutamatergic transmission.