Nelson Ralph, Bender Anna M, Connaughton Victoria P
Basic Neurosciences Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Rockville, Maryland 20892-9406, USA.
Vis Neurosci. 2008 Mar-Apr;25(2):155-65. doi: 10.1017/S0952523808080310.
GABA-mediated interactions between horizontal cells (HCs) and bipolar cells (BCs) transform signals within the image-processing circuitry of distal retina. To further understand this process, we have studied the GABA-driven membrane responses from isolated retinal neurons. Papain-dissociated retinal cells from adult zebrafish were exposed to GABAergic ligands while transmembrane potentials were monitored with a fluorescent voltage-sensitive dye (oxonol, DiBaC4(5)). In HCs hyperpolarizing, ionotropic GABA responses were almost never seen, nor were responses to baclofen or glycine. A GABA-induced depolarization followed by after hyperpolarization (dep/AHP) occurred in 38% of HCs. The median fluorescence increase (dep component) was 0.17 log units, about 22 mV. HC dep/AHP was not blocked by bicuculline or picrotoxin. Muscimol rarely evoked dep/AHP responses. In BCs picrotoxin sensitive, hyperpolarizing, ionotropic GABA and muscimol responses occurred in most cells. A picrotoxin insensitive dep/AHP response was seen in about 5% of BCs. The median fluorescence increase (dep component) was 0.18 log units, about 23 mV. Some BCs expressed both muscimol-induced hyperpolarizations and GABA-induced dep/AHP responses. For all cells, the pooled Hill fit to median dep amplitudes, in response to treatments with a GABA concentration series, gave an apparent k of 0.61 muM and an n of 1.1. The dep/AHP responses of all cells required both extracellular Na+ and Cl(-), as dep/AHP was blocked reversibly by Li+ substituted for Na+ and irreversibly by isethionate substituted for Cl(-). All cells with dep/AHP responses in zebrafish have the membrane physiology of neurons expressing GABA transporters. These cells likely accumulate GABA, a characteristic of GABAergic neurons. We suggest Na+ drives GABA into these cells, depolarizing the plasma membrane and triggering Na+, K+-dependent ATPase. The ATPase activity generates AHP. In addition to a GABA clearance function, these large-amplitude transporter responses may provide an outer plexiform layer GABA sensor mechanism.
γ-氨基丁酸(GABA)介导的水平细胞(HCs)与双极细胞(BCs)之间的相互作用在视网膜远端的图像处理电路中转换信号。为了进一步了解这一过程,我们研究了分离的视网膜神经元中GABA驱动的膜反应。将成年斑马鱼经木瓜蛋白酶解离的视网膜细胞暴露于GABA能配体,同时用荧光电压敏感染料(氧化腈,DiBaC4(5))监测跨膜电位。在水平细胞中,几乎从未观察到超极化的离子型GABA反应,对巴氯芬或甘氨酸的反应也未观察到。38%的水平细胞出现了GABA诱导的去极化继后超极化(dep/AHP)。荧光增加的中位数(去极化成分)为0.17对数单位,约22 mV。水平细胞的dep/AHP不受荷包牡丹碱或印防己毒素的阻断。蝇蕈醇很少诱发dep/AHP反应。在双极细胞中,大多数细胞出现了对印防己毒素敏感的、超极化的离子型GABA和蝇蕈醇反应。约5%的双极细胞出现了对印防己毒素不敏感的dep/AHP反应。荧光增加的中位数(去极化成分)为0.18对数单位,约23 mV。一些双极细胞既表现出蝇蕈醇诱导的超极化,也表现出GABA诱导的dep/AHP反应。对于所有细胞,对一系列GABA浓度处理的中位数去极化幅度进行汇总的希尔拟合,得出表观解离常数k为0.61 μM,n为1.1。所有细胞的dep/AHP反应都需要细胞外的Na+和Cl-,因为dep/AHP可被Li+替代Na+可逆性阻断,被羟乙基磺酸替代Cl-不可逆性阻断。斑马鱼中所有具有dep/AHP反应的细胞都具有表达GABA转运体的神经元的膜生理学特性。这些细胞可能积累GABA,这是GABA能神经元的一个特征。我们认为Na+将GABA驱动到这些细胞中,使质膜去极化并触发Na+,K+-依赖性ATP酶。ATP酶活性产生超极化后电位。除了GABA清除功能外,这些大幅度的转运体反应可能提供一种外网状层GABA传感机制。