Morphological analysis of the GABA function using knockout mice lacking of molecules involved in GABAergic signaling

1.作为敲除小鼠的正常对照，我们研究了GABA能神经元、GABA能突触和GABA去除系统在发育小鼠脊髓中的个体发生。我们研究了舌下神经和面神经变性和再生过程中gaba能信号的变化。我们发现GABA能信号在再生过程中转变为未成熟形式，提示GABA可能作为一种兴奋性递质参与轴突再生。我们从形态学上研究了缺乏谷氨酸脱羧酶（GAD）、水泡GABA转运蛋白（VGAT）和氯化钾共转运蛋白（KCC2）三种GABA能信号相关分子的敲除小鼠。我们发现三种基因敲除小鼠脊髓背角calbinin阳性或calretinin阳性中间神经元的数量和定位，提示GABA可能参与了发育过程中脊髓中间神经元的迁移和增殖。

1.We investigated the ontogeny of GABAergic neurons, GABAergic synapses, and GABA removal system in the developing mouse spinal cord as the normal control of knockout mice.2.We investigated the changes in GABAergic signaling during degeneration and regeneration of hypoglossal and facial nerves. We found that GABAergic signaling changed to the immatute form during regeneration, suggesting that GABA may act as an excitatory transmitter and be involved in regeneration of axons.3.We morphologically investigated the knockout mice lacking three molecules involved in GABAergic signaling, glutamic acid decarboxylase (GAD), vesicular GABA transporter (VGAT), and potassium chloride cotransporter (KCC2). We found that the number and localization of calbindin-positive or calretinin-positive interneurons in the dorsal horn of spinal cord of three types of knockout mice, suggesting that GABA might be involved in migration and proliferation of interneurons in the spinal cord during development.