Trigueiros-Cunha Nuno, Leão Pedro, Renard Nicole, Tavares Maria Amélia, Eybalin Michel
INSERM U. 583, Institut des Neurosciences de Montpellier, BP74103, 80 Avenue Augustin Fliche, 34091 Montpellier, France.
Brain Res. 2006 May 1;1086(1):55-64. doi: 10.1016/j.brainres.2006.02.066. Epub 2006 Apr 13.
Prenatal cocaine exposure causes alterations in auditory brainstem response in children and experimental animals and has adverse effects on auditory information processing and language skills in children. These effects may result from lesions in the cochlea since this organ is particularly sensitive to chemical insults during the development. We have thus studied here the effect of prenatal cocaine exposure on the maturation of the rat cochlea using the transient non-catecholaminergic expression of tyrosine hydroxylase in spiral ganglion neurons as an index of cochlear maturation and morphometry to evaluate the maturation of primary auditory neurons and the organ of Corti. We showed that prenatal cocaine exposure accelerated the cochlear maturation. In the basal coil of cochleas from PND8 cocaine-treated pups, the Kölliker's organ had disappeared, the tunnel of Corti was opened, and the stria vascularis no longer contained undifferentiated marginal cells. The maximum expression of tyrosine hydroxylase in type I primary auditory neurons occurred at PND8 instead of PND12 in pair-fed controls. On the other hand, the prenatal cocaine exposure had no effect on the width and height of the organ of Corti, spiral ganglion volume and number and size of primary auditory neurons. In conclusion, our data suggest that prenatal cocaine exposure, though not lethal to primary auditory neurons, accelerates aspects of the cochlear sensorineural maturation. This accelerated cochlear maturation in cocaine-treated rat pups could cause auditory dysfunctions by desynchronizing the development of the whole auditory pathway.
产前接触可卡因会导致儿童和实验动物的听觉脑干反应发生改变，并对儿童的听觉信息处理和语言技能产生不利影响。这些影响可能源于耳蜗的损伤，因为该器官在发育过程中对化学损伤特别敏感。因此，我们在此研究了产前接触可卡因对大鼠耳蜗成熟的影响，以螺旋神经节神经元中酪氨酸羟化酶的瞬时非儿茶酚胺能表达作为耳蜗成熟的指标，并通过形态计量学评估初级听觉神经元和柯蒂氏器的成熟情况。我们发现产前接触可卡因会加速耳蜗成熟。在出生后第8天接受可卡因处理的幼崽的耳蜗基底螺旋中，柯蒂氏器已经消失，柯蒂氏管开放，血管纹中不再含有未分化的边缘细胞。在出生后第8天，I型初级听觉神经元中酪氨酸羟化酶的表达达到最大值，而在配对喂养的对照组中则是在出生后第12天。另一方面，产前接触可卡因对柯蒂氏器的宽度和高度、螺旋神经节体积以及初级听觉神经元的数量和大小没有影响。总之，我们的数据表明，产前接触可卡因虽然对初级听觉神经元没有致命影响，但会加速耳蜗感觉神经成熟的某些方面。在接受可卡因处理的大鼠幼崽中，这种加速的耳蜗成熟可能会使整个听觉通路的发育不同步，从而导致听觉功能障碍。
