Bozzi Y, Pizzorusso T, Cremisi F, Rossi F M, Barsacchi G, Maffei L
Scuola Normale Superiore, Pisa, Italy.
Neuroscience. 1995 Dec;69(4):1133-44. doi: 10.1016/0306-4522(95)00321-9.
We found that deprivation of pattern vision in one eye, that leaves luminance detection performance unaffected, is sufficient to reduce brain-derived neurotrophic factor (but not trkB) messenger RNA in the visual cortex of young and adult rats. Monocular deprivation by means of eyelids' suture was performed during or after the critical period and the cortical amount of brain-derived neurotrophic factor messenger RNA was analysed by in situ hybridization and RNAase protection after 15-30 days of deprivation. A reduction of brain-derived neurotrophic factor messenger RNA was observed in the visual cortex contralateral to the deprived eye in rats monocularly deprived during the critical period. The same reduction was also found in rats monocularly deprived after the end of the critical period, when anatomical or physiological signs of monocular deprivation are absent. The pharmacological blockade of retinal activity equally affected the expression of brain-derived neurotrophic factor messenger RNA in young and adults. Quantitative RNAase protection assays revealed that the cortical level of brain-derived neurotrophic factor messenger RNA was reduced to the same extent when intraocular injections of tetrodotoxin were performed within or after the critical period. A developmental study of brain-derived neurotrophic factor messenger RNA expression in rat visual cortex showed a marked increase around the time of natural eye-opening followed by a plateau from postnatal day 20 until adult age. Messenger RNA for the kinasic domain of brain-derived neurotrophic factor receptor (trkB) was found in the dorsal lateral geniculate nucleus and the visual cortex during development and in adults. Our results suggest that the reduction of brain-derived neurotrophic factor messenger RNA induced by monocular deprivation is related to the absence of pattern vision rather than to the competitive interactions that underlie the effects of monocular deprivation during the critical period.
我们发现，单眼模式视觉剥夺在不影响亮度检测性能的情况下，足以降低幼年和成年大鼠视觉皮层中脑源性神经营养因子（而非trkB）的信使核糖核酸水平。在关键期内或关键期后通过眼睑缝合进行单眼剥夺，并在剥夺15 - 30天后通过原位杂交和核糖核酸酶保护分析脑源性神经营养因子信使核糖核酸的皮质含量。在关键期内单眼剥夺的大鼠中，观察到剥夺眼对侧视觉皮层中脑源性神经营养因子信使核糖核酸减少。在关键期结束后单眼剥夺的大鼠中也发现了同样的减少，此时不存在单眼剥夺的解剖学或生理学迹象。视网膜活动的药理学阻断同样影响幼年和成年大鼠脑源性神经营养因子信使核糖核酸的表达。定量核糖核酸酶保护分析显示，在关键期内或关键期后进行眼内注射河豚毒素时，脑源性神经营养因子信使核糖核酸的皮质水平降低程度相同。对大鼠视觉皮层中脑源性神经营养因子信使核糖核酸表达的发育研究表明，在自然睁眼前后其表达显著增加，随后从出生后第20天到成年期保持稳定。在发育过程中和成年期，在背外侧膝状核和视觉皮层中发现了脑源性神经营养因子受体（trkB）激酶结构域的信使核糖核酸。我们的结果表明，单眼剥夺诱导的脑源性神经营养因子信使核糖核酸减少与模式视觉缺失有关而非与关键期内单眼剥夺效应所基于的竞争性相互作用有关。
