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The tryptophan metabolite, kynurenic acid (KYNA), is classically known to bean antagonist of ionotropic glutamate receptors. Within the last decade severalreports have been published suggesting that KYNA also blocks nicotinicacetylcholine receptors (nAChRs) containing the \alpha7 subunit (\alpha7*).Most of these reports involve either indirect measurements of KYNA effects on\alpha7 nAChR function, or are reports of KYNA effects in complicated in vivosystems. However, a recent report investigating KYNA interactions with \alpha7nAChRs failed to detect an interaction using direct measurements of \alpha7nAChRs function. Further, it showed that a KYNA blockade of \alpha7 nAChRstimulated GABA release (an indirect measure of \alpha7 nAChR function) was notdue to KYNA blockade of the \alpha7 nAChRs. The current study measured thedirect effects of KYNA on \alpha7-containing nAChRs expressed on interneuronsin the hilar and CA1 stratum radiatum regions of the mouse hippocampus and oninterneurons in the CA1 region of the rat hippocampus. Here we show that KYNAdoes not block \alpha7* nACHRs using direct patch-clamprecording of \alpha7currents in adult brain slices.

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Nicotinic {\alpha}7 acetylcholine receptor-mediated currents are not  modulated by the tryptophan metabolite kynurenic acid in adult hippocampal  interneurons