Retroviruses have been proposed as one of the infectious agents involved in the pathogenesis of schizophrenia. They can cause neuronal death by endogenous toxin(s), such as quinolinic acid (QUIN), released by virus‐activated brain macrophages/microglia. QUIN is an endogenous excitotoxin, with an affinity at specific NMDA‐R heteromers. We have administered QUIN to 12‐day‐old rat males by infusions of 250 nmol QUIN into each lateral ventricle. On day 50 the rats exhibited a tendency to higher basal acoustic startle responses (120 dB), but their prepulse inhibition (PPI) was deficient at 73, 75 and 80 dB. The deficit in PPI correlated with the neuronal losses and with the decreased receptor binding of [3H]glutamate in lesioned brains. The data provide further evidence that the toxin‐induced neuronal deficit and glutamate‐receptor loss in supra‐pontine brain regions may impair sensorimotor gating in the animal model of schizophrenia.Acknowledgement:  Supported by IGA MH CR No. NF6031‐3.