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

1.以正常基因敲除小鼠为对照，研究了发育过程中小鼠脊髓内GABA能神经元、GABA能突触和GABA清除系统的个体发育。2.研究了舌下神经和面神经退行性变和再生过程中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的形式，提示GABA可能作为兴奋性递质参与轴突的再生。3.对GABA能信号缺失三个分子谷氨酸脱羧酶(GAD)、囊泡GABA转运体(VGAT)和氯化钾共转运体(KCC2)的基因敲除小鼠进行了形态学研究。我们发现在三种类型的基因敲除小鼠的脊髓背角内，Calbindin阳性或Calretinin阳性的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.