An aberrant link between gamma oscillation and functional connectivity in Aβ1–42-mediated memory deficits in rats

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disease that gradually induces cognitive deficits in the elderly. Impairment of working memory was typically observed in AD. As amyloid-β peptide (Aβ) is a causative factor for the cognitive impairments in AD, developing a mechanistic understanding of the contribution of Aβ to cognitive impairments may yield insights into the pathophysiology of AD. Gamma oscillations as well as functional connectivity have been recognized to play important roles in various cognitive functions. Gamma oscillation is hypothesized as the results of the coordinated interaction of neural network. However, the temporal link between gamma oscillation and functional connectivity in working memory has remained largely unexplored. Moreover, whether Aβ-induced working memory deficit is due to the abnormal link between gamma oscillation and functional connectivity? Therefore, in the present study, local field potentials (LFPs) were recorded via multi-electrodes implanted in rat prefrontal cortex (PFC) for the control group and Aβ-injected group (Aβ group) when they performed a Y-maze working memory task. Gamma oscillations and functional connectivity among LFPs were respectively estimated. Compared with the control group, the Aβ group showed significantly weaker oscillations and functional connectivity among LFPs. Moreover, the time gap between gamma oscillation and functional connectivity was examined. The precise temporal link between the gamma oscillation and functional connectivity in the control group and the Aβ-induced abnormal link in the Aβ group were noticed. Our results indicate that the link between gamma oscillation and functional connectivity may provide a potential mechanism for the Aβ1–42-induced working memory deficits.