scholarly journals Effects of L-glutamate on the anomalous rectifier potassium current in horizontal cells of Carassius auratus retina.

1985 ◽  
Vol 358 (1) ◽  
pp. 169-182 ◽  
Author(s):  
A Kaneko ◽  
M Tachibana
1986 ◽  
Vol 55 (3) ◽  
pp. 499-513 ◽  
Author(s):  
E. M. Lasater

Horizontal cells from the retinas of white perch were isolated and maintained in cell culture for 3 days to 3 wk. Four morphologically distinct types of horizontal cells could be identified in culture and were labeled types H1, H2, H3, and H4. Whole-cell patch-clamp techniques were used to study the ionic currents present in the four cell types. In all cells, depolarizing commands above threshold elicited a fast-inward current followed by an outward current. The fast-inward current was abolished by tetrodotoxin (TTX) or 0 Na+ Ringer's, indicating the current was carried by Na+. In H1, H2, and H3 cells, the outward current, carried by K+, consisted of two components: a transient current (IA), blockable with 4-aminopyridine (4-AP), tetraethylammonium (TEA), or intracellular cesium and a sustained current that could be blocked with TEA. The H4 cell had only the sustained current. An inward rectifying K+ current (anomalous rectifier) was observed in the four cell types. The current was sensitive to the extracellular K+ concentration. Its activation showed two components: an instantaneous component and a slower component. The slow component becomes faster with greater hyperpolarizations. The four cell types possessed a small, sustained Ca2+ current that, under normal conditions, was masked by the inward Na+ current and outward K+ currents.


Author(s):  
Michael W. Country ◽  
Michael G. Jonz

Neurons of the retina require oxygen to survive. In hypoxia, neuronal ATP production is impaired, ATP-dependent ion pumping is reduced, transmembrane ion gradients are dysregulated, and [Ca2+]i increases enough to trigger excitotoxic cell death. Central neurons of the common goldfish (Carassius auratus) are hypoxia-tolerant, but little is known about how goldfish retinas withstand hypoxia. To study the cellular mechanisms of hypoxia tolerance, we isolated retinal interneurons (horizontal cells; HCs), and measured intracellular Ca2+ concentration ([Ca2+]i) with Fura-2. Goldfish HCs maintained [Ca2+]i throughout 1 h of hypoxia, whereas [Ca2+]i increased irreversibly in HCs of the hypoxia-sensitive rainbow trout (Oncorhynchus mykiss) with just 20 min of hypoxia. Our results suggest mitochondrial ATP-dependent K+ channels (mKATP) are necessary to stabilize [Ca2+]i throughout hypoxia. In goldfish HCs, [Ca2+]i increased when mKATP was blocked with glibenclamide or 5-HD, whereas an mKATP agonist (diazoxide) prevented [Ca2+]i from increasing in hypoxia in trout HCs. We showed that hypoxia protects goldfish HCs via mKATP channels. Glycolytic inhibition with 2-deoxyglucose increased [Ca2+]i, which was rescued by hypoxia in an mKATP-dependent manner. We found no evidence of plasmalemmal KATP channels in patch-clamp experiments. Instead, we confirmed the involvement of KATP in mitochondria with TMRE imaging, as hypoxia rapidly (<5 min) depolarized mitochondria in an mKATP-sensitive manner. We conclude that mKATP channels initiate a neuroprotective pathway in goldfish HCs to maintain [Ca2+]i and avoid excitotoxicity in hypoxia. This model provides novel insight into the cellular mechanisms of hypoxia tolerance in the retina.


1990 ◽  
Vol 64 (6) ◽  
pp. 1758-1766 ◽  
Author(s):  
J. M. Sullivan ◽  
E. M. Lasater

1. Horizontal cells (HCs) are second-order neurons in the retina that receive direct photoreceptor input. They rest at around -20 mV in the dark, because of the continuous release of neurotransmitter from photoreceptors. HCs respond to light with graded hyperpolarizations, which can reach -70 to -80 mV in the presence of very bright stimuli. 2. HCs from the retinas of white bass were isolated and maintained in culture. Potassium currents in three morphological types of HCs--H1, H2, and H4--were studied in culture with whole-cell, patch-clamp techniques, when sodium and calcium currents were blocked. 3. A transient outward potassium current (IA), with many characteristics of the A-current, was found in all H2s and H4s but only occasionally in H1s. The threshold for activation of this current was around -40 mV, a value more depolarized than usual for the A-current. The peak IA was typically smaller than 300 pA when the membrane was stepped from a holding potential of -70 mV to a command potential of -10 mV, the upper limit of the in vivo range of HC membrane potentials. Steady-state inactivation is expected to reduce the magnitude of IA in vivo. 4. A sustained outward potassium current (IK) was found in all types of HCs. This sustained potassium current did not activate until the membrane was stepped to potentials above -10 mV, a value much more depolarized than those reported for the delayed rectifier current in other neurons. As a result, IK is absent over the in vivo operating range of these cells. 5. No calcium-dependent potassium current was found in any cells.(ABSTRACT TRUNCATED AT 250 WORDS)


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