Stevens L M, Landis S C
Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115.
Dev Biol. 1988 Dec;130(2):703-20. doi: 10.1016/0012-1606(88)90362-4.
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 developing in vivo is 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.(ABSTRACT TRUNCATED AT 400 WORDS)
先前已表明，大鼠脚垫汗腺的交感神经支配的神经递质特性在发育过程中会发生显著变化。当轴突首次到达发育中的腺体时，它们含有儿茶酚胺组织荧光以及儿茶酚胺合成酶的免疫反应性。随着腺体及其神经支配的成熟，儿茶酚胺消失，胆碱能和肽能特性出现。通过分泌能力测定的汗腺最终成熟与神经支配中胆碱能功能的发育在时间上相关。为了确定在体内发育的交感神经元的神经递质表型是否具有可塑性，交感神经靶标是否能在决定支配它们的神经元的神经递质特性中发挥作用，以及腺体成熟是否依赖于其神经支配，汗腺与其神经支配之间正常的发育相互作用被破坏。这是通过在出生后第2天单次注射6-羟基多巴胺（6-OHDA）来实现的。经过这种处理后，去甲肾上腺素能交感轴突到达发育中腺体的时间延迟了7至10天。与正常大鼠的腺体神经支配一样，支配6-OHDA处理动物汗腺的轴突获得了胆碱能功能，并且它们内源性儿茶酚胺的表达下降。然而，神经递质特性的变化在发育过程中比未处理的动物发生得更晚，并且并不总是完全的。即使在成年动物中，一些纤维仍继续表达内源性儿茶酚胺，并且在高锰酸钾固定后，许多神经末梢含有一小部分小颗粒囊泡。6-OHDA处理动物的腺体神经支配也与正常大鼠不同，因为大多数腺体中不表达血管活性肠肽（VIP）的免疫反应性。似乎在用6-OHDA处理后，汗腺既由正常情况下会支配它的神经元支配，也由正常情况下会支配脚垫中其他去甲肾上腺素能靶标（如血管）的神经元支配。因此，与汗腺的接触似乎不仅会抑制正常支配腺体的神经元中的去甲肾上腺素能功能并诱导胆碱能功能，还会在通常支配其他靶标的神经元中产生这种作用。延迟神经支配对靶标发育的影响也被观察到。汗腺对胆碱能激动剂敏感性的出现与胆碱能传递的开始相关。（摘要截取自400字）
