Mechanisms by which perinatal viral infections can disrupt hippocampal deve
lopment and cause selective neuronal death may have implications for tempor
al lobe epilepsy and schizophrenia. Despite abnormalities of inhibitory int
erneurons in these diseases, the causal relationships between such neurotra
nsmitter changes and viral infections remain unclear. This relationship was
examined in a model in which rats, infected with lymphocytic choriomeningi
tis virus (LCMV) as neonates, manifest a gradual loss of hippocampal dentat
e granule cells and neuronal hyperexcitability. The current data demonstrat
e that GABAergic interneurons are dual immunostained for LCMV antigens prio
r to the loss of dentate granule cells, supporting the hypothesis that LCMV
may disrupt developing inhibitory circuits causing unbalanced excitatory n
eurotransmission and the eventual death of dentate granule cells due to exc
itotoxicity. NeuroReport 11:2433-2438 (C) 2000 Lippincott Williams & Wilkin
s.