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Articles by Evan Vickers in JoVE
JoVE Neuroscience
Patch-clamp Mått kapacitans och Ca 2 + Imaging vid enstaka nervterminaler i näthinnan Slices
The Vollum Institute, Oregon Health and Science University
Här beskriver vi ett protokoll för beredning av agar inbäddade-retinal skivor som är lämpliga för elektrofysiologi och Ca2 + avbildning. Denna metod gör att man kan studera band-typ synapser i näthinnan mikrokretsar med direkt patch-clamp inspelningar av enstaka presynaptiska nervändslut.
Other articles by Evan Vickers on PubMed
Hemichannel-mediated and PH-based Feedback from Horizontal Cells to Cones in the Vertebrate Retina
Recent studies designed to identify the mechanism by which retinal horizontal cells communicate with cones have implicated two processes. According to one account, horizontal cell hyperpolarization induces an increase in pH within the synaptic cleft that activates the calcium current (Ca(2+)-current) in cones, enhancing transmitter release. An alternative account suggests that horizontal cell hyperpolarization increases the Ca(2+)-current to promote transmitter release through a hemichannel-mediated ephaptic mechanism.
Allosteric Modulation of Retinal GABA Receptors by Ascorbic Acid
Ionotropic GABA receptors (GABA(A) and GABA(C)) belong to the Cys-loop receptor family of ligand-gated ion channels. GABA(C) receptors are highly expressed in the retina, mainly localized at the axon terminals of bipolar cells. Ascorbic acid, an endogenous redox agent, modulates the function of diverse proteins, and basal levels of ascorbic acid in the retina are very high. However, the effect of ascorbic acid on retinal GABA receptors has not been studied. Here we show that the function of GABA(C) and GABA(A) receptors is regulated by ascorbic acid. Patch-clamp recordings from bipolar cell terminals in goldfish retinal slices revealed that GABA(C) receptor-mediated currents activated by tonic background levels of extracellular GABA, and GABA(C) currents elicited by local GABA puffs, are both significantly enhanced by ascorbic acid. In addition, a significant rundown of GABA puff-evoked currents was observed in the absence of ascorbic acid. GABA-evoked Cl(-) currents mediated by homomeric ρ(1) GABA(C) receptors expressed in Xenopus laevis oocytes were also potentiated by ascorbic acid in a concentration-dependent, stereo-specific, reversible, and voltage-independent manner. Studies involving the chemical modification of sulfhydryl groups showed that the two Cys-loop cysteines and histidine 141, all located in the ρ(1) subunit extracellular domain, each play a key role in the modulation of GABA(C) receptors by ascorbic acid. Additionally, we show that retinal GABA(A) IPSCs and heterologously expressed GABA(A) receptor currents are similarly augmented by ascorbic acid. Our results suggest that ascorbic acid may act as an endogenous agent capable of potentiating GABAergic neurotransmission in the CNS.
Light-evoked Lateral GABAergic Inhibition at Single Bipolar Cell Synaptic Terminals is Driven by Distinct Retinal Microcircuits
Inhibitory amacrine cells (ACs) filter visual signals crossing the retina by modulating the excitatory, glutamatergic output of bipolar cells (BCs) on multiple temporal and spatial scales. Reciprocal feedback from ACs provides focal inhibition that is temporally locked to the activity of presynaptic BC activity, whereas lateral feedback originates from ACs excited by distant BCs. These distinct feedback mechanisms permit temporal and spatial computation at BC terminals. Here, we used a unique preparation to study light-evoked IPSCs recorded from axotomized terminals of ON-type mixed rod/cone BCs (Mb) in goldfish retinal slices. In this preparation, light-evoked IPSCs could only reach axotomized BC terminals via the lateral feedback pathway, allowing us to study lateral feedback in the absence of overlapping reciprocal feedback components. We found that light evokes ON and OFF lateral IPSCs (L-IPSCs) in Mb terminals having different temporal patterns and conveyed via distinct retinal pathways. The relative contribution of rods versus cones to ON and OFF L-IPSCs was light intensity dependent. ACs presynaptic to Mb BC terminals received inputs via AMPA/KA- and NMDA-type receptors in both the ON and OFF pathways, and used TTX-sensitive sodium channels to boost signal transfer along their processes. ON and OFF L-IPSCs, like reciprocal feedback IPSCs, were mediated by both GABA(A) and GABA(C) receptors. However, our results suggest that lateral and reciprocal feedback do not cross-depress each other, and are therefore mediated by distinct populations of ACs. These findings demonstrate that retinal inhibitory circuits are highly specialized to modulate BC output at different light intensities.
