Aβ1-42-induced dysfunction in synchronized gamma oscillation during working memory

• Aβ1-42-induced working memory deficits in rats.
• Multi-channel recording in freely moving rats during a working memory task.
• Gamma oscillation between spikes and LFPs was quantified via phase-locking value.
• Aβ1-42-induced dysfunction in synchronized gamma oscillation during working memory.
• Abnormal gamma oscillation may provide a mechanism for working memory deficits.

Amyloid-β peptide (Aβ) is recognized as a causative factor for the cognitive impairments in Alzheimer’s disease (AD). The studies on the effects of Aβ to cognitive impairments are beneficial for lifting the veil of the pathophysiology in AD. Neuronal oscillations are proposed to play an important role in cognition and its ensuing behavior. Specially, the synchronized gamma oscillations are essential for the successful execution of working memory. However, whether the Aβ will induce the abnormal neuronal oscillations and working memory deficits has remained largely unexplored. In the present study, rats (control and Aβ-injected groups) were trained to perform a delay-alternation task on Y-maze while spikes and local field potentials (LFPs) were recorded from multi-electrodes implanted in the medial prefrontal cortex (mPFC), an area that is strongly modulated by working memory. Synchronized neuronal oscillations were assessed by phase locking between spike trains and LFPs. We found the significant working memory impairment in the Aβ-injected group. Moreover, in the control group, during the memory retention period, a transient burst of gamma synchronization preceded an animal’s correct choice, but not an animal’s error choice. In the Aβ-injected group, however, gamma synchronization experience no change in neither correct nor error trials. Our results indicate that the Aβ1-42-induced dysfunction in gamma synchronization may provide a potential mechanism for working memory deficits.