Zhou Chengwen, Dacheux Ramon F
Department of Ophthalmology, University of Alabama at Birmingham, Birmingham 35294-0009, USA.
Vis Neurosci. 2004 Mar-Apr;21(2):181-8. doi: 10.1017/s0952523804042099.
Physiological properties of ligand-activated currents were characterized for morphologically identified AII amacrine cells in the rabbit retina by using whole-cell recordings in a superfused retina slice preparation. The AII amacrine cells were identified based on their distinct narrow-field, bistratified morphology. In the present study, the whole-cell recordings from AII amacrine cells synaptically isolated from presynaptic influences demonstrated the presence of glutamate AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid) receptors, but no kainate receptors. The presence of only AMPA receptors on rabbit AII amacrine cells is in contrast to an earlier study on rabbit AII amacrine cells by Bloomfield and Xin (2000), but consistent with previous studies on rat AII amacrine cells. In addition, NMDA (N-methyl-D-aspartate) -activated currents blocked by the NMDA antagonist D-AP7 (D-2-amino-7-phosphonoheptanoic acid) were found on the AII amacrine cells. These most likely extrasynaptic NMDA-activated currents were attenuated by the presence of Co2+ interacting with Mg2+ and Ca2+ as they competed for divalent cation-binding sites within the NMDA channel. AII amacrine cells also possessed GABA (gamma-aminobutyric acid) -activated currents that were unaffected by the GABAc receptor antagonist TPMPA (1,2,5,6-tetrahydropyridine-4-yl methylphosphinic), but were completely blocked by the GABA(A) antagonist bicuculline. This indicates that the major inhibitory inputs were mediated by only GABA(A) receptors located directly on the AII amacrine cells. Furthermore, although the AII amacrine cells were glycinergic amacrine cells, they also possessed glycine-activated currents that may be mediated by autoreceptors.
通过在视网膜切片灌流制备中使用全细胞膜片钳记录,对兔视网膜中形态学上已鉴定的AII无长突细胞的配体激活电流的生理特性进行了表征。AII无长突细胞是根据其独特的窄视野、双分层形态来鉴定的。在本研究中,从AII无长突细胞进行的全细胞膜片钳记录在突触上分离了突触前影响,结果表明存在谷氨酸AMPA(α-氨基-3-羟基-5-甲基-4-异恶唑丙酸)受体,但没有海人藻酸受体。兔AII无长突细胞上仅存在AMPA受体,这与Bloomfield和Xin(2000年)早期对兔AII无长突细胞的研究相反,但与先前对大鼠AII无长突细胞的研究一致。此外,在AII无长突细胞上发现了被NMDA拮抗剂D-AP7(D-2-氨基-7-磷酸庚酸)阻断的NMDA(N-甲基-D-天冬氨酸)激活电流。这些最有可能是突触外的NMDA激活电流,由于Co²⁺与Mg²⁺和Ca²⁺相互作用并竞争NMDA通道内的二价阳离子结合位点,而被减弱。AII无长突细胞还具有GABA(γ-氨基丁酸)激活电流,该电流不受GABAc受体拮抗剂TPMPA(1,2,5,6-四氢吡啶-4-基甲基次膦酸)的影响,但被GABA(A)拮抗剂荷包牡丹碱完全阻断。这表明主要的抑制性输入仅由直接位于AII无长突细胞上的GABA(A)受体介导。此外,尽管AII无长突细胞是甘氨酸能无长突细胞,但它们也具有可能由自身受体介导的甘氨酸激活电流。