Abstract:Intracellular recordings were made from rods in the superfused retina of the marine toad (Bufo marinus). It was found that injection of a brief depolarizing current pulse (0.04-1 nA) evoked a distinctive, long-lasting response, here called "the prolonged depolarization." The response appears to be regenerative, has a stereotypical waveform, is typically about 6 mV in amplitude and 3 s in duration, and has a relatively long recovery period (10-60 s). As a rule, the response cannot be directly evoked by light bu… Show more
“…Burkhardt et al (1988) showed evidence for three components in the surround responses of turtle cones: 1) an initial graded depolarization, 2) spikes, and 3) long regenerative events that lasted for many seconds and were termed “prolonged depolarizations.” Subsequent work showed that prolonged depolarizations are triggered by the regenerative activation of L-type Ca 2+ channels and exhibit a long-lasting plateau phase maintained by the activation of Ca 2+ -activated Cl − channels (Thoreson and Burkhardt, 1991; Barnes and Deschenes 1992). Prolonged depolarizing responses with similar waveforms have been observed in cones and rods from a number of species (turtle cones: Burkhardt et al, 1988; Cervetto and Piccolino, 1982; salamander cones: Lasansky, 1981; toad rods: Burkhardt et al, 1991; mouse rods: Babai and Thoreson, 2009). …”
Section: Negative Feedback From Horizontal Cells To Conessupporting
Lateral interactions in the outer retina, particularly negative feedback from horizontal cells to cones and direct feed-forward input from horizontal cells to bipolar cells, play a number of important roles in early visual processing, such as generating center-surround receptive fields that enhance spatial discrimination. These circuits may also contribute to post-receptoral light adaptation and the generation of color opponency. In this review, we examine the contributions of horizontal cell feedback and feed-forward pathways to early visual processing. We begin by reviewing the properties of bipolar cell receptive fields, especially with respect to modulation of the bipolar receptive field surround by the ambient light level and to the contribution of horizontal cells to the surround. We then review evidence for and against three proposed mechanisms for negative feedback from horizontal cells to cones: 1) GABA release by horizontal cells, 2) ephaptic modulation of the cone pedicle membrane potential generated by currents flowing through hemigap junctions in horizontal cell dendrites, and 3) modulation of cone calcium currents (ICa) by changes in synaptic cleft proton levels. We also consider evidence for the presence of direct horizontal cell feed-forward input to bipolar cells and discuss a possible role for GABA at this synapse. We summarize proposed functions of horizontal cell feedback and feed-forward pathways. Finally, we examine the mechanisms and functions of two other forms of lateral interaction in the outer retina: negative feedback from horizontal cells to rods and positive feedback from horizontal cells to cones.
“…Burkhardt et al (1988) showed evidence for three components in the surround responses of turtle cones: 1) an initial graded depolarization, 2) spikes, and 3) long regenerative events that lasted for many seconds and were termed “prolonged depolarizations.” Subsequent work showed that prolonged depolarizations are triggered by the regenerative activation of L-type Ca 2+ channels and exhibit a long-lasting plateau phase maintained by the activation of Ca 2+ -activated Cl − channels (Thoreson and Burkhardt, 1991; Barnes and Deschenes 1992). Prolonged depolarizing responses with similar waveforms have been observed in cones and rods from a number of species (turtle cones: Burkhardt et al, 1988; Cervetto and Piccolino, 1982; salamander cones: Lasansky, 1981; toad rods: Burkhardt et al, 1991; mouse rods: Babai and Thoreson, 2009). …”
Section: Negative Feedback From Horizontal Cells To Conessupporting
Lateral interactions in the outer retina, particularly negative feedback from horizontal cells to cones and direct feed-forward input from horizontal cells to bipolar cells, play a number of important roles in early visual processing, such as generating center-surround receptive fields that enhance spatial discrimination. These circuits may also contribute to post-receptoral light adaptation and the generation of color opponency. In this review, we examine the contributions of horizontal cell feedback and feed-forward pathways to early visual processing. We begin by reviewing the properties of bipolar cell receptive fields, especially with respect to modulation of the bipolar receptive field surround by the ambient light level and to the contribution of horizontal cells to the surround. We then review evidence for and against three proposed mechanisms for negative feedback from horizontal cells to cones: 1) GABA release by horizontal cells, 2) ephaptic modulation of the cone pedicle membrane potential generated by currents flowing through hemigap junctions in horizontal cell dendrites, and 3) modulation of cone calcium currents (ICa) by changes in synaptic cleft proton levels. We also consider evidence for the presence of direct horizontal cell feed-forward input to bipolar cells and discuss a possible role for GABA at this synapse. We summarize proposed functions of horizontal cell feedback and feed-forward pathways. Finally, we examine the mechanisms and functions of two other forms of lateral interaction in the outer retina: negative feedback from horizontal cells to rods and positive feedback from horizontal cells to cones.
“…Regenerative potentials have been recorded in rods during the recovery phase of the light response when the retina was treated with TEA to block potassium channels (Fain & Quandt, 1980; Fain et al 1980). A prolonged depolarization was also observed in rods after injection of brief depolarizing current pulses in cells with high internal chloride (Thoreson & Burkhardt, 1991; Burkhardt et al 1991). In 20% of cones in turtle retina, feedback from horizontal cells evokes a spike (Piccolino & Gerschenfeld, 1980).…”
In the dark-adapted salamander retina, spikes could be elicited from rods under normal physiological conditions. Spike activity was observed in rods during the recovery phase of the response to saturating light. These action potentials were calcium spikes, blocked by cadmium and L-type calcium channel blockers. In response to light stimuli that saturate the rod peak response, calcium action potentials occurred with a delay that depended on light intensity, with stronger light increasing spike latency. Therefore, these spikes encode rod visual information at light intensities beyond rod saturation. Postsynaptic currents of similar time course were observed in second and third order neurones. Since rods exposed to brighter light stimuli produced more delayed spike activity, these signals might contribute to negative afterimages.
“…In two rods, we observed large, prolonged depolarizing responses with waveforms similar to prolonged depolarizing responses found in rods and cones of other species (Burkhardt et al . 1988, 1991; Thoreson & Burkhardt, 1991; Barnes & Deschenes, 1992). These earlier studies showed that prolonged depolarizing responses begin when an initial small depolarization (e.g., due to activation of Ca 2+ -activated Cl − channels by CICR) stimulates the regenerative activation of voltage-gated Ca 2+ channels.…”
We tested whether calcium-induced calcium release (CICR) contributes to synaptic release from rods in mammalian retina. Electron micrographs and immunofluorescent double labeling for the sarco/ endoplasmic reticulum Ca 2+ -ATPase (SERCA2) and synaptic ribbon protein, ribeye, showed a close association between ER and synaptic ribbons in mouse rod terminals. Stimulating CICR with 10 μM ryanodine evoked Ca 2+ increases in rod terminals from mouse retinal slices visualized using confocal microscopy with the Ca 2+ -sensitive dye, Fluo-4. Ryanodine also stimulated membrane depolarization of individual mouse rods. Inhibiting CICR with a high concentration of ryanodine (100 μM) reduced the ERG b-wave but not a-wave consistent with inhibition of synaptic transmission from rods. Ryanodine (100 μM) also inhibited light-evoked voltage responses of individual rod bipolar cells (RBCs) and presumptive horizontal cells recorded with perforated patch recording techniques. A presynaptic site of action for ryanodine's effects is further indicated by the finding that ryanodine (100 μM) did not alter currents evoked in voltage-clamped RBCs by puffing the mGluR6 antagonist, (RS)-α-cyclopropyl-4-phosphonophenylglycine (CPPG), onto bipolar cell dendrites in the presence of the mGluR6 agonist L-(+)-2-amino-4-phosphonobutyric acid (L-AP4). Ryanodine (100 μM) also inhibited glutamatergic outward currents in RBCs evoked by electrical stimulation of rods using electrodes placed in the outer segment layer. Together, these results indicate that, like amphibian retina, CICR contributes to synaptic release from mammalian (mouse) rods. By boosting synaptic release in darkness, CICR may improve the detection of small luminance changes by postsynaptic neurons.
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