Prenatal hypoxia produces memory deficits associated with impairment of long-term synaptic plasticity in young rats

Neurobiol Learn Mem. 2019 Oct:164:107066. doi: 10.1016/j.nlm.2019.107066. Epub 2019 Aug 7.

Abstract

Prenatal hypoxia often results in dramatic alterations in developmental profiles and behavioral characteristics, including learning and memory, in later life. Despite the accumulation of considerable amounts of experimental data, the mechanisms underlying developmental deficits caused by prenatal hypoxia remain unclear. In the present study, we investigated whether prenatal hypoxia on embryonic day 14 (E14) affected synaptic properties in the hippocampus and hippocampal-related cognitive functions in young rats. We found that 20- to 30-d-old rats subjected to prenatal hypoxia had significantly disturbed basal synaptic transmission in CA3-CA1 synapses and a two-fold decrease in hippocampal long-term synaptic potentiation. These alterations were accompanied by a significant decline in the protein level of GluN2B but not GluN2A NMDA receptor subunits. In addition, the number of synaptopodin-positive dendritic spines in the CA1 area of the hippocampus was reduced in the rats exposed to prenatal hypoxia. These changes resulted in significant learning and memory deficits in a novel object recognition test.

Keywords: LTP; Learning; NMDA receptor; Novel object recognition; Prenatal hypoxia; Synaptopodin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dendritic Spines / physiology
  • Excitatory Postsynaptic Potentials
  • Female
  • Hippocampus / physiopathology*
  • Hypoxia / physiopathology*
  • Hypoxia / psychology*
  • Long-Term Potentiation*
  • Male
  • Memory Disorders / etiology
  • Memory Disorders / physiopathology*
  • Rats, Wistar
  • Receptors, N-Methyl-D-Aspartate / physiology

Substances

  • Receptors, N-Methyl-D-Aspartate