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

Abstract

Abnormal accumulation of soluble amyloid beta (Aβ) 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 Aβ1–42 oligomers on discharge properties of hippocampal neurons in vivo. This study was designed to examine the effects of soluble Aβ1–42 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 Aβ1–42-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 μM Aβ1–42 oligomers; (2) Aβ1–42 oligomers also induced alterations of the neuronal firing patterns in the hippocampal CA1 region; and (3) pretreatment with 20 μM RLZ effectively inhibited the Aβ1–42-induced enhancement of spontaneous discharge and alterations of neuronal firing patterns in CA1 neurons. Our study suggested that Aβ1–42 oligomers induced hyperactivity and perturbed the firing patterns in hippocampal neurons. RLZ may provide neuroprotective effects on the Aβ1–42-induced perturbation of neuronal activities in the hippocampal region of rats.