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氟西汀诱导的啮齿动物视觉系统可塑性。

Fluoxetine-induced plasticity in the rodent visual system.

作者信息

Bastos E F, Marcelino J L, Amaral A R, Serfaty C A

机构信息

Departamento de Neurobiologia, Universidade Federal Fluminense, Caixa Postal 100180, Niteroi, CEP 24001-970, RJ, Brazil.

出版信息

Brain Res. 1999 Apr 3;824(1):28-35. doi: 10.1016/s0006-8993(99)01184-1.

DOI:10.1016/s0006-8993(99)01184-1
PMID:10095039
Abstract

We studied the effect of fluoxetine, a selective serotonin reuptake inhibitor, in the development and lesion-induced plasticity of retinotectal axons in pigmented rats. Neonatal rats received a daily injection of either fluoxetine or vehicle from postnatal day 1 (PND 1) to PND 10 or from PND 14 to PND 28 (fluoxetine, 7.5 and 10.0 mg/kg, respectively). In the latter group, some animals received a single lesion at the temporal periphery of the left retina at PND 21. Unoperated animals were use as the control. At the end of the treatment, the animals received an intraocular injection of horseradish peroxidase (HRP) in the right (intact) eye to trace the uncrossed retinotectal pathway. Chronic fluoxetine treatment, induced, in unoperated rats, an expansion of the retinal terminal fields along the rostro-caudal axis of the tectum both in the PND 10 and PND 28 groups. Following a retinal lesion in the left eye at PND 21, the vehicle-treated group showed a small reorganization of the intact uncrossed projection. In this group only a few terminals were labeled invading the denervated tectal surface one-week after the lesion. Fluoxetine-treated animals on the other hand, showed a great amplification of plasticity with a conspicuous sprouting of the uncrossed retinal axons into denervated areas. The data suggest that fluoxetine induces extensive axonal rearrangements in neonatal and juvenile central nervous system and amplifies neuroplasticity following retinal lesions late in development.

摘要

我们研究了选择性5-羟色胺再摄取抑制剂氟西汀对有色大鼠视网膜-脑顶盖轴突发育及损伤诱导可塑性的影响。新生大鼠从出生后第1天(PND 1)至PND 10或从PND 14至PND 28每天注射氟西汀或赋形剂(氟西汀分别为7.5和10.0 mg/kg)。在后一组中,一些动物在PND 21时在左视网膜颞侧周边接受单次损伤。未手术的动物用作对照。在治疗结束时,给动物右眼(未受损眼)眼内注射辣根过氧化物酶(HRP)以追踪未交叉的视网膜-脑顶盖通路。在未手术的大鼠中,慢性氟西汀治疗在PND 10和PND 28组中均诱导视网膜终末场沿脑顶盖的前后轴扩展。在PND 21时左眼视网膜损伤后,赋形剂治疗组显示完整未交叉投射有小的重组。在该组中,损伤后一周只有少数终末被标记侵入去神经支配的脑顶盖表面。另一方面,氟西汀治疗的动物显示可塑性有很大增强,未交叉的视网膜轴突发芽明显进入去神经支配区域。数据表明,氟西汀在新生和幼年中枢神经系统中诱导广泛的轴突重排,并在发育后期视网膜损伤后增强神经可塑性。

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