Deskin R, Seidler F J, Whitmore W L, Slotkin T A
J Neurochem. 1981 May;36(5):1683-90. doi: 10.1111/j.1471-4159.1981.tb00419.x.
To study the relationship between ontogeny of rat brain catecholamine nerve terminals and the receptor systems for the catecholamine transmitters, the developmental patterns of synaptosomal uptake mechanisms were compared with those of alpha-noradrenergic and dopaminergic receptor-mediated effects. Uptakes of [(3)H]dopamine or [(3)H]norepinephrine into dopaminergic and noradrenergic nerve terminals were low during the 1st week postpartum and increased rapidly during the 2nd week. A similar pattern was obtained for ontogeny of dopaminergic receptor binding sites, as evaluated by [(3)H]domperidone binding. Stimulation of incorporation of (33)P(i) into brain phospholipids (elicited by intracisternal injection of dopamine), which is mediated by dopaminergic receptors, was shown to be highly correlated with the maturation of both receptor binding sites and presynaptic nerve terminal uptake. A similar result was seen with norepinephrine, in that the synaptosomal uptake mechanism and norepinephrine-induced stimulation (33)P(i) incorporation into phospholipids, an alpha-noradrenergic effect, developed in a parallel fashion. To test the hypothesis that development of the receptor systems is linked to nerve terminal ontogeny, presynaptic nerve terminals were destroyed in neonates by intracisternal administration of 6-hydroxydopamine. The lesions prevented the maturational increase in the number of dopamine receptor binding sites and produced a defect in development of the dopamine- and norepinephrine-induced stimulation of (33)P(i) incorporation. The results suggest that ontogeny of both dopaminergic and alpha-noradrenergic receptor systems depend upon development of the presynaptic nerve terminals containing the transmitters.
为了研究大鼠脑儿茶酚胺神经末梢的个体发生与儿茶酚胺递质受体系统之间的关系，将突触体摄取机制的发育模式与α-去甲肾上腺素能和多巴胺能受体介导的效应的发育模式进行了比较。产后第1周，多巴胺能和去甲肾上腺素能神经末梢对[³H]多巴胺或[³H]去甲肾上腺素的摄取较低，而在第2周迅速增加。通过[³H]多潘立酮结合评估的多巴胺能受体结合位点的个体发生也获得了类似的模式。由多巴胺能受体介导的脑磷脂中³³P(i)掺入的刺激（通过脑池内注射多巴胺引发）与受体结合位点和突触前神经末梢摄取的成熟高度相关。去甲肾上腺素也得到了类似的结果，即突触体摄取机制和去甲肾上腺素诱导的³³P(i)掺入磷脂的刺激（一种α-去甲肾上腺素能效应）以平行方式发展。为了检验受体系统的发育与神经末梢个体发生相关的假设，通过脑池内给予6-羟基多巴胺破坏新生大鼠的突触前神经末梢。这些损伤阻止了多巴胺受体结合位点数量的成熟增加，并导致多巴胺和去甲肾上腺素诱导的³³P(i)掺入发育缺陷。结果表明，多巴胺能和α-去甲肾上腺素能受体系统的个体发生均依赖于含有递质的突触前神经末梢的发育。
