UNILATERAL, NEONATAL OLFACTORY DEPRIVATION ALTERS TYROSINE-HYDROXYLASE EXPRESSION BUT NOT AROMATIC AMINO-ACID DECARBOXYLASE OR GABA IMMUNOREACTIVITY
UNILATERAL, NEONATAL OLFACTORY DEPRIVATION ALTERS TYROSINE-HYDROXYLASE EXPRESSION BUT NOT AROMATIC AMINO-ACID DECARBOXYLASE OR GABA IMMUNOREACTIVITY
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DOI：
10.1016/0306-4522(90)90018-y
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发表时间：
1990-01-01
期刊：
影响因子：
3.3
通讯作者：
BAKER, H
中科院分区：
文献类型：
--
作者：
BAKER, H
最近的出版物已经证明了一个重要的作用，嗅觉传入神经支配在维持多巴胺表型的嗅球靶神经元。该系统中控制表型表达的机制尚不清楚。这些研究采用单侧新生儿嗅觉剥夺模型来研究缺乏气味刺激对大鼠多巴胺表达的影响。酪氨酸羟化酶，多巴胺生物合成的第一个和限速酶，作为多巴胺系统的标记物，免疫反应性表现出一个大的下降40和70天后嗅觉剥夺。这些损失是区域性的，表明这种剥夺并不完全。免疫反应性GABA能神经元的数量没有减少。含有芳香族氨基酸脱羧酶（多巴胺生物合成途径中的第二种酶）的神经元数量也没有减少。嗅觉标记蛋白的免疫反应性在肾小球，传入神经支配的标记，没有显着改变，表明嗅球是不是denervated.These数据表明，新生儿剥夺，并由此产生的缺乏气味刺激，产生transneuronal的多巴胺表达的变化，而没有神经元的损失。研究还表明，神经元活性或活性依赖性释放的营养因子是必要的多巴胺表型的表达。
Recent publications have demonstrated an important role for olfactory afferent innervation in maintenance of the dopamine phenotype of olfactory bulb target neurons. The mechanisms underlying the control of phenotypic expression in this system are not known. These studies employed the model of unilateral neonatal olfactory deprivation to investigate the effects of lack of odorant stimulation on dopamine expression in the rat. Immunoreactivity of tyrosine hydroxylase, the first and rate-limiting enzyme in dopamine biosynthesis, used as a marker of the dopamine system, exhibited a large decrease both 40 and 70 days following olfactory deprivation. The losses were region specific suggesting that the deprivation was not complete. The number of immunoreactive GABAergic neurons was not reduced. The number of neurons containing aromaticl-amino acid decarboxylase (the second enzyme in the dopamine biosynthetic pathway) was also not decreased. Olfactory marker protein immunoreactivity in the glomeruli, a marker for afferent innervation, was not significantly altered indicating that the olfactory bulb was not denervated.These data demonstrate that neonatal deprivation, and the resulting lack of odorant stimulation, produces a transneuronal alteration in dopamine expression without neuronal loss. The studies also suggest that neuronal activity or the activity-dependent release of a trophic factor is necessary for the expression of the dopamine phenotype.