Light Kim E, Brown Donna P, Newton Bruce W, Belcher Scott M, Kane Cynthia J M
Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences, 4301 W. Markham, Little Rock, AR 72205, USA.
Brain Res. 2002 Jan 4;924(1):71-81. doi: 10.1016/s0006-8993(01)03224-3.
Ethanol causes loss of Purkinje cells in the cerebellum during the early stages of differentiation and maturation by a presently unknown mechanism. Neuronal vulnerability in the cerebellum parallels the prominent temporal and anatomical gradients of development (i.e. early to late interlobular and posterior to anterior, respectively). Development of Purkinje cells is known to require binding of the neurotrophins, including brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3), to the tyrosine-kinase (Trk) receptors TrkB and TrkC, respectively. In addition, Purkinje cells are reported to experience a critical switch between BDNF dependence and NT3 dependence during the period of highest ethanol sensitivity between postnatal days (PN) 4-6. To test the hypothesis that ethanol alters neurotrophin signaling leading to Purkinje neuronal death, the immunohistochemical expression of TrkB and TrkC receptors on Purkinje cells of rat pups following a moderate dose of ethanol was determined at various times surrounding the period of postnatal ethanol vulnerability. Ethanol selectively decreased Purkinje cell expression of TrkB and TrkC receptors following exposures within the vulnerable period (PN4-6). These results suggest that ethanol may induce loss of Purkinje cells by alteration of neurotrophic regulation at this critical stage.
乙醇通过目前未知的机制,在分化和成熟的早期阶段导致小脑浦肯野细胞丢失。小脑中神经元的易损性与发育过程中显著的时间和解剖学梯度平行(即分别从早期到晚期小叶间,以及从后到前)。已知浦肯野细胞的发育需要神经营养因子,包括脑源性神经营养因子(BDNF)和神经营养因子-3(NT3),分别与酪氨酸激酶(Trk)受体TrkB和TrkC结合。此外,据报道,在出生后第4 - 6天(PN)乙醇敏感性最高的时期,浦肯野细胞在BDNF依赖性和NT3依赖性之间经历关键转变。为了验证乙醇改变神经营养因子信号传导导致浦肯野神经元死亡的假说,在出生后乙醇易损期周围的不同时间,测定了中度剂量乙醇处理后大鼠幼崽浦肯野细胞上TrkB和TrkC受体的免疫组化表达。在易损期(PN4 - 6)暴露后,乙醇选择性降低了浦肯野细胞TrkB和TrkC受体的表达。这些结果表明,乙醇可能通过在这个关键阶段改变神经营养调节来诱导浦肯野细胞丢失。