Developmental interactions between sweat glands and the sympathetic neurons which innervate them: effects of delayed innervation on neurotransmitter plasticity and gland maturation.
Developmental interactions between sweat glands and the sympathetic neurons which innervate them: effects of delayed innervation on neurotransmitter plasticity and gland maturation.
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DOI：
10.1016/0012-1606(88)90362-4
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发表时间：
1988-12
影响因子：
2.7
通讯作者：
L. Stevens;S. Landis;S. Landis
中科院分区：
文献类型：
--
作者：
L. Stevens;S. Landis;S. Landis
以前已经证明，大鼠足垫汗腺的交感神经支配的神经递质特性在发育过程中经历了显着的变化。当轴突第一次到达发育中的腺体时，它们含有儿茶酚胺组织荧光和儿茶酚胺合成酶的免疫反应。随着腺体及其神经的成熟，儿茶酚胺消失，胆碱能和多肽能特性出现。汗腺的最终成熟由分泌能力来衡量，与神经中胆碱能功能的发展在时间上是相关的。为了确定在活体中发育的交感神经元的神经递质表型是否可塑性，交感靶点是否在决定支配它们的神经元的神经递质特性中发挥作用，以及如果腺体的成熟依赖于其神经支配，汗腺与其神经之间的正常发育相互作用被破坏。这是通过在出生后第2天一次注射6-羟基多巴胺(6-OHDA)来完成的。在这种治疗之后，去甲肾上腺素能交感神经轴突到达发育中的腺体的时间推迟了7-10天。与正常大鼠的腺体神经支配一样，6-OHDA处理的动物汗腺的轴突获得胆碱能功能，内源性儿茶酚胺的表达下降。然而，神经递质特性的变化发生在发育后期，比未治疗的动物更晚，而且并不总是完全的。甚至在成年动物中，高锰酸盐固定后，一些神经纤维继续表达内源性儿茶酚胺，许多神经末梢含有少量的小颗粒小泡。6-OHDA处理的动物的腺体神经支配也与正常大鼠不同，大多数腺体不表达VIP免疫反应。似乎在用6-OHDA治疗之后，汗腺既被正常情况下会这样做的神经元所支配，也被通常会支配足垫中其他去甲肾上腺素能靶点的神经元所支配，比如血管。因此，接触汗腺似乎不仅在正常支配汗腺的神经元中抑制去甲肾上腺素能功能并诱导胆碱能功能，而且在通常支配其他目标的神经元中也是如此。延迟性神经支配对靶点发育的影响也被观察到。汗腺对胆碱能激动剂的敏感性与胆碱能传递的开始有关。我们的结果为汗腺和它们的神经之间的相互发育相互作用提供了证据，从而允许建立功能传递。
The neurotransmitter properties of the sympathetic innervation of sweat glands in rat footpads have previously been shown to undergo a striking change during development. When axons first reach the developing glands, they contain catecholamine histofluorescence and immunoreactivity for catecholamine synthetic enzymes. As the glands and their innervation mature, catecholamines disappear and cholinergic and peptidergic properties appear. Final maturation of the sweat glands, assayed by secretory competence, is correlated temporally with the development of cholinergic function in the innervation. To determine if the neurotransmitter phenotype of sympathetic neurons developingin vivois plastic, if sympathetic targets can play a role in determining neurotransmitter properties of the neurons which innervate them, and if gland maturation is dependent upon its innervation, the normal developmental interaction between sweat glands and their innervation was disrupted. This was accomplished by a single injection of 6-hydroxy-dopamine (6-OHDA) on Postnatal Day 2. Following this treatment, the arrival of noradrenergic sympathetic axons at the developing glands was delayed 7 to 10 days. Like the gland innervation of normal rats, the axons which innervated the sweat glands of 6-OHDA-treated animals acquired cholinergic function and their expression of endogenous catecholamines declined. The change in neurotransmitter properties, however, occurred later in development than in untreated animals and was not always complete. Even in adult animals, some fibers continued to express endogenous catecholamines and many nerve terminals contained a small proportion of small granular vesicles after permanganate fixation. The gland innervation in the 6-OHDA-treated animals also differed from that of normal rats in that immunoreactivity for VIP was not expressed in the majority of glands. It seems likely that following treatment with 6-OHDA sweat glands were innervated both by neurons that would normally have done so and by neurons that would normally have innervated other, noradrenergic targets in the footpads, such as blood vessels. Contact with sweat glands, therefore, appears to suppress noradrenergic function and induce cholinergic function not only in the neurons which normally innervate the glands but also in neurons which ordinarily innervate other targets. Effects of delayed innervation were also observed on target development. The appearance of sensitivity to cholinergic agonists by the sweat glands was coupled with the onset of cholinergic transmission. Our results provide evidence for reciprocal developmental interactions between the sweat glands and their innervation which permit the establishment of functional transmission.