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The Journal of Neuroscience, June 1, 2003, 23(11):4667-4676

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Degeneration of the Amygdala/Piriform Cortex and Enhanced Fear/Anxiety Behaviors in Sodium Pump 2 Subunit (Atp1a2)-Deficient Mice

Keiko Ikeda,¹ Tatsushi Onaka,² Makoto Yamakado,³ Junichi Nakai,⁴ Tomo-o Ishikawa,^5,6 Makoto M. Taketo,^5,6 and Kiyoshi Kawakami¹

¹ Department of Biology Jichi Medical School, Kawachi, Tochigi 329-0498, Japan, ² Department of Physiology Jichi Medical School, Kawachi, Tochigi 329-0498, Japan, ³ Department of Anatomy, Jichi Medical School, Kawachi, Tochigi 329-0498, Japan, ⁴ Department of Information Physiology, National Institute for Physiological Science, Okazaki 444-8585, Japan, ⁵ Department of Pharmacology, Graduate School of Medicine, Kyoto University, Sakyo, Kyoto 606-8501, Japan, and ⁶ Banyu Tsukuba Research Institute (Merck), Tsukuba 300-2611, Japan

The sodium pump is the enzyme responsible for the maintenance of Na⁺ and K⁺ gradients across the cell membrane. Four isoforms of the catalytic subunit have been identified, but their individual roles remain essentially unknown. To investigate the necessary functions of the 2 subunit in vivo, we generated and analyzed mice defective in the 2 subunit gene. Mice homozygous for the 2 mutation died just after birth and displayed selective neuronal apoptosis in the amygdala and piriform cortex. In these regions, high expression of c-Fos before apoptosis indicated neural hyperactivity, and re-uptake of glutamic acid and GABA into P₂ fraction containing crude synaptosome was impaired. These results indicate that the 2 subunit plays a critical role regulating neural activity in the developing amygdala and piriform cortex. Further supporting a role of the2 subunit in the function of the amygdala, heterozygous adult mice showed augmented fear/anxiety behaviors and enhanced neuronal activity in the amygdala and piriform cortex after conditioned fear stimuli.

Key words: amygdala; piriform cortex; knock-out mice; Na,K-ATPase; neurotransmitter uptake; fear-anxiety behavior

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Received Jan. 29, 2003; revised Mar. 11, 2003; accepted Mar. 17, 2003.

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