Prenatal alcohol exposure alters synaptic activity of adult hippocampal dentate granule cells under conditions of enriched environment. Issue 8 (7th April 2016)

• Record Type: Journal Article
• Authors: Kajimoto, Kenta; Valenzuela, C. Fernando; Allan, Andrea M.; Ge, Shaoyu; Gu, Yan; Cunningham, Lee Anna
• Is Part Of: Hippocampus. Volume 26:Issue 8(2016)
• Page Start: 1078
• Page End: 1087
• Publication Date: 2016-04-07
• Subjects: neurogenesis -- electrophysiology -- fetal alcohol spectrum disorder -- environmental enrichment; Hippocampus (Brain) -- Periodicals; 612.825
• DOI: 10.1002/hipo.22588
• Languages: English
• ISSNs: 1050-9631

Abstract

ABSTRACT: Prenatal alcohol exposure (PAE) results in fetal alcohol spectrum disorder (FASD), which is characterized by a wide range of cognitive and behavioral deficits that may be linked to impaired hippocampal function and adult neurogenesis. Preclinical studies in mouse models of FASD indicate that PAE markedly attenuates enrichment‐mediated increases in the number of adult‐generated hippocampal dentate granule cells (aDGCs), but whether synaptic activity is also affected has not been studied. Here, we utilized retroviral birth‐dating coupled with whole cell patch electrophysiological recordings to assess the effects of PAE on enrichment‐mediated changes in excitatory and inhibitory synaptic activity as a function of DGC age. We found that exposure to an enriched environment (EE) had no effect on baseline synaptic activity of 4‐ or 8‐week‐old aDGCs from control mice, but significantly enhanced the excitatory/inhibitory ratio of synaptic activity in 8‐week‐old aDGCs from PAE mice. In contrast, exposure to EE significantly enhanced the excitatory/inhibitory ratio of synaptic activity in older pre‐existing DGCs situated in the outer dentate granule cell layer (i.e., those generated during embryonic development; dDGCs) in control mice, an effect that was blunted in PAE mice. These findings indicate distinct electrophysiological responses of hippocampal DGCs to behavioral challenge based on cellular ontogenetic age, and suggest that PAE disrupts EE‐mediated changes in overall hippocampal network activity. These findings may have implications for future therapeutic targeting of hippocampal dentate circuitry in clinical FASD. © 2016 Wiley Periodicals, Inc.