Intermittent Hypoxia Disrupts Synaptic Long Term Depression

Abstract

Long term potentiation (LTP), activity‐dependent synaptic strengthening, and long term depression (LTD), activity dependent synaptic attenuation, are two forms of synaptic plasticity whose underlying mechanisms permit flexibility in synaptic communication and serve as substrates for learning and memory. Intermittent hypoxia (IH), a hallmark of sleep apnea, is known to impair spatial learning and memory. The objective of this study is determine how LTP and LTD are affected by IH. We hypothesize that IH impedes efficacy of activity dependent synaptic plasticity in the hippocampus, a brain structure important to learning and memory. We examined in vitro LTP and LTD in hippocampal brain slices following IH exposure. Electrophysiological recordings showed that LTP in area CA1 could be evoked in control and IH exposed groups, yet the magnitude of LTP following IH was decreased (LTP: control 184.72±15.93% vs. IH 145.35±6.34% baseline) . While LTD could be elicited in the control group (63.31±3.03% baseline), LTD could not be evoked from the IH exposed group (104.18±3.44% baseline). Although IH impacted both forms of long term synaptic plasticity, this was not accompanied by differences in paired‐pulse facilitation, indicating that short‐term plasticity was unaffected by IH. These findings demonstrate that IH affects mechanisms of activity‐dependent regulation of synaptic efficacy, which may involve IH‐dependent changes in NMDA receptor contribution to these phenomena. Our findings further contribute to understanding potential neurophysiological changes that may decrease the threshold for cognitive decline associated with sleep apnea.Support or Funding InformationThis work was supported by NIH R01 NS10742101 (AJG).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.