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The Journal of Neuroscience, March 22, 2006, 26(12):3309-3318; doi:10.1523/JNEUROSCI.3850-05.2006

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Development/Plasticity/Repair
Maternal Stress Produces Learning Deficits Associated with Impairment of NMDA Receptor-Mediated Synaptic Plasticity

Gi Hoon Son,^1 * Dongho Geum,^2 * Sooyoung Chung,¹ Eun Joo Kim,³ Ji-Hoon Jo,⁵ Chang-Mee Kim,⁴ Kun Ho Lee,¹ Hyun Kim,⁴ Sukwoo Choi,¹ Hyun Taek Kim,³ Chang-Joong Lee,⁵ and Kyungjin Kim¹

¹School of Biological Sciences, Seoul National University, Seoul 151-742, Korea, ²Graduate School of Medicine, ³Department of Psychology, and ⁴College of Medicine, Korea University, Seoul 136-705, Korea, and ⁵Department of Biology, Inha University, Inchon 402-752, Korea

Correspondence should be addressed to Dr. Kyungjin Kim, School of Biological Sciences, Seoul National University, Seoul 151-742, Seoul, Korea. Email: kyungjin{at}snu.ac.kr

Stress in adulthood can have a profound effect on physiology and behavior, but the extent to which prolonged maternal stress affects the brain function of offspring when they are adult remains primarily unknown. In the present work, chronic immobilization stress to pregnant mice affected fetal growth and development. When pups born from stressed mice were reared to adulthood in an environment identical to that of nonstressed controls, several physiological parameters were essentially unaltered. However, spatial learning and memory was significantly impaired in the maternally stressed offspring in adulthood. Furthermore, electrophysiological examination revealed a significant reduction in NMDA receptor-mediated long-term potentiation in the CA1 area of hippocampal slices. Subsequent biochemical analysis demonstrated a substantial decrease in NR1 and NR2B subunits of the NMDA receptor in synapses of the hippocampus, and the interaction between these two subunits appeared to be reduced. These results suggest that prolonged maternal stress leads to long-lasting malfunction of the hippocampus, which extends to and is manifested in adulthood.

Key words: maternal stress; hippocampus; learning and memory; synaptic plasticity; long-term potentiation; LTP; NMDA receptor

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Received March 9, 2004; revised Jan. 6, 2006; accepted Feb. 12, 2006.

Correspondence should be addressed to Dr. Kyungjin Kim, School of Biological Sciences, Seoul National University, Seoul 151-742, Seoul, Korea. Email: kyungjin{at}snu.ac.kr

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