Kindling induces a lasting, regionally selective increase of kynurenic acid in the nucleus accumbens.

We determined endogenous kynurenic acid in nine brain regions and plasma of amygdala-kindled rats at different intervals (24 h or 50 days) after the last fully kindled seizure. Data obtained were compared with age-matched electrode-implanted and non-implanted control groups. Kindling induced a lasting increase in kynurenate in nucleus accumbens, whereas no significant alterations were seen in hippocampus, cerebral cortex, olfactory bulb, striatum, thalamus, tectum, cerebellum, pons/medulla, or plasma. The regionally selective alteration in the nucleus accumbens is in line with previous studies indicating that this brain region functions as a modulatory interface between the limbic and motor systems and may be critically involved in seizure propagation in the kindling model of temporal lobe epilepsy. The increased levels of the endogenous glutamate antagonist kynurenate in nucleus accumbens may be interpreted as a compensatory change to reduce enhanced excitation in this brain region.