[正常和产前内源性血清素缺乏大鼠产后早期bÖtzinger复合体gaba -能神经网络的形成]。

L I Khozhai, N V Ilyichova
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引用次数: 0

摘要

研究了正常Wistar大鼠出生后早期(哺乳动物呼吸系统功能成熟期)和产前血清素含量降低时,Bötzingercomplex (BötC)中gaba能神经元和表达不同类型gaba受体(GABAAα1和GABAB1)的神经元的分布动态。在出生后第5、9和20天,研究人员对两组大鼠幼崽进行了大脑研究:对照组(n=9),由完整的雌性所生,以及实验组(n=13),由接受了副氯苯丙氨酸的母亲所生,导致内源性血清素水平下降。采用免疫细胞化学方法检测GABA的产生及GABAAα1和gabab1受体的表达情况。结果表明,抑制性gaba能网络inBötC的成熟发生在出生后早期(第9天)。gabaa α1和GABAB1受体的表达与GABA同时发生,但它们的成熟具有不同的特点。GABAAα1受体的形成较早(第9天),与GABA的表达时间一致。gabab1受体的成熟发生得较晚——仅在第三周。产前血清素缺乏导致BötC神经元GABA和GABAAα1受体的表达延迟,并破坏含有GABA、GABAAα1和GABAB1受体的终端和突触网络的形成。
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[FORMATION OF GABA-ERGIC NEURAL NETWORK IN BÖTZINGER COMPLEX IN RATS DURING EARLY POSTNATAL PERIOD IN NORM AND IN PRENATAL DEFICIENCY OF ENDOGENOUS SEROTONIN].

The dynamics of the distribution of GABAergic neurons and neurons expressing different types of GABA receptors (GABAAα1 and GABAB1) was studied in Bötzingercomplex (BötC) in the early postnatal period (the period of functional maturation of the respiratory system in mammals) in norm and prenatal reduction of serotonin content in Wistar rats. The brain was studied on postnatal Days 5, 9 and 20 in two groups of rat pups: control (n=9), born by intact females, and experimental (n=13), born from mothers that received parachlorophenylalanine, causing the depression of endogenous serotonin level. Imunocytochemical methods were used to detect the neurons producing GABA and expressing GABAAα1 and GABAB1 receptors. It was shown that the maturation of the inhibitory GABAergic network in BötC occurred in the early postnatal period (by Day 9). Simultaneously with GABA, the expression of GABAAα1 and GABAB1 receptors took place, however their maturation has the distinctive features. The formation of GABAAα1 receptors occurred earlier (by Day 9) and coincided in time with the expression of GABA. The maturation of GABAB1 receptors happened later — only by the third week. Prenatal serotonin deficiency caused a delay in the expression of GABA and GABAAα1 receptors by the neurons of BötC, as well as the disruption of the formation of a network of terminals and synapses containing GABA, GABAAα1 and GABAB1 receptors.

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