Riluzole prevents soluble Aβ1-42 oligomers-induced perturbation of spontaneous discharge in the hippocampal CA1 region of rats

Abnormal accumulation of soluble amyloid beta (A beta) is believed to cause malfunction of neurons in Alzheimer's disease (AD). The hippocampus is one of the earliest affected brain regions in AD. However, little effort has been made to investigate the effects of soluble A beta(1-42) oligomers on discharge properties of hippocampal neurons in vivo. This study was designed to examine the effects of soluble A beta(1-42) oligomers on the discharge properties of hippocampal CA1 neurons using extracellular single-unit recordings in vivo. The protective effects of riluzole (RLZ) were also investigated for the prevention of soluble oligomers of A beta(1-42)-induced alterations in the spontaneous discharge of hippocampal neurons. The results showed that (1) the mean frequency of spontaneous discharge was increased by the local application of 100 mu M A beta(1-42) oligomers; (2) A beta(1-42) oligomers also induced alterations of the neuronal firing patterns in the hippocampal CA1 region; and (3) pretreatment with 20 mu M RLZ effectively inhibited the A beta(1-42)-induced enhancement of spontaneous discharge and alterations of neuronal firing patterns in CA1 neurons. Our study suggested that A beta(1-42) oligomers induced hyperactivity and perturbed the firing patterns in hippocampal neurons. RLZ may provide neuroprotective effects on the A beta(1-42)-induced perturbation of neuronal activities in the hippocampal region of rats.