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γ-氨基丁酸(GABA)诱导出生后家兔视网膜神经元胞内钙离子浓度([Ca2+]i)升高。

GABA-induced increases in [Ca2+]i in retinal neurons of postnatal rabbits.

作者信息

Huang B O, Redburn D A

机构信息

Department of Ophthalmology and Visual Science, University of Texas-Houston Medical School 77030, USA.

出版信息

Vis Neurosci. 1996 May-Jun;13(3):441-7. doi: 10.1017/s0952523800008117.

DOI:10.1017/s0952523800008117
PMID:8782371
Abstract

Previous studies have indicated that gamma-aminobutyric acid (GABA) plays an important trophic role in the synapse formation between horizontal cells and photoreceptors in postnatal rabbit retina. However, the mechanism of the GABA effect has not been identified. Using fluo-3 Ca2+ imaging and confocal laser scanning microscopy we examined the effect of GABA on [Ca2+]i during postnatal retinal development. GABA (100 microM) evoked a fast and transient increase of [Ca2+]i in selected populations of freshly dissociated retinal cells from postnatal rabbits. This increase was apparent on postnatal day 1 and reached a maximum on day 5. Little increase in [Ca2+]i was observed in retinal cells isolated from adult rabbits. GABA receptor antagonists, picrotoxin and bicuculline, significantly reduced the response. The GABAB agonist, baclofen, did not evoke any [Ca2+]i changes. The GABA-induced increase in [Ca2+]i was observed in all retinal layers in neonatal retinal whole-mount explants. In the outer retina, the increase was seen in cone photoreceptors which were specifically labeled with peanut agglutinin (PNA). The GABA-induced increase in [Ca2+]i may provide an important mechanism for regulating cone synaptogenesis in the outer plexiform layer of the postnatal retina.

摘要

先前的研究表明,γ-氨基丁酸(GABA)在新生兔视网膜水平细胞与光感受器之间的突触形成中发挥重要的营养作用。然而,GABA作用的机制尚未明确。我们使用fluo-3 Ca²⁺成像和共聚焦激光扫描显微镜检查了GABA在视网膜发育过程中对[Ca²⁺]i的影响。GABA(100微摩尔)可使新生兔新鲜分离的视网膜细胞特定群体中的[Ca²⁺]i快速短暂升高。这种升高在出生后第1天很明显,并在第5天达到最大值。在成年兔分离的视网膜细胞中未观察到[Ca²⁺]i有明显升高。GABA受体拮抗剂匹鲁卡品和荷包牡丹碱可显著降低该反应。GABAB激动剂巴氯芬未引起任何[Ca²⁺]i变化。在新生视网膜全层外植体的所有视网膜层中均观察到GABA诱导的[Ca²⁺]i升高。在外视网膜中,在用花生凝集素(PNA)特异性标记的视锥光感受器中可见这种升高。GABA诱导的[Ca²⁺]i升高可能为调节新生视网膜外网状层中的视锥突触形成提供重要机制。

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