Bumps, the elementary excitatory events of the Limulus ventral nerve photo receptor following a weak flash of light were recorded under voltage clamp conditions. The statistical distribution of various bump parameters and their changes caused by weak conditioning pre-illumination are described, and the influence of lowered external Ca2+-concentration together with normal or raised Mg2+-concentration (15 °C).1) Weak conditioning pre-illumination causes desensitization: the bump current amplitude, bump duration , bump area (current-integral), and the bump latency are diminished, the more, the stronger the conditioning flash, i.e. the light adaptation. Very weak conditioning pre-illumination causes facilitation, expressed by an increase in number and size of the observed bumps. The average bump latency, however, is already shortened under these conditions.2) Lowering the external Ca2+-concentration from 10 mmol/l to 250 (µmol/1 has its primary effect on the dark -adapted photoreceptor (without substantially reducing the ability for light adaptation ). It causes the following average changes: the amplitudes, durations, current-integrals, and the latencies of current bumps are greatly enlarged and the number of bumps is raised.3) Raised magnesium concentration from 50 to 100 mmol/l can partially compensate for the lack of calcium ; however, it enhances the effect of calcium deficiency on the latency, i.e. it further enlarges the average latencies. The results can be explained on the basis of our model of bump generation by two assumptions.1) Lowering the external calcium concentration causes a decrease in the cytosolic Ca2+-level without substantially reducing the intracellular calcium stores from which the light-adapting calcium release is fed. The lowered cytosolic Ca2+-concentration induces an “extra” dark adaptation resulting in greater bumps and more bumps exceeding the threshold of recognition. The bump latency, however, which behaves differently from all other bump parameters, is determined by a separate calcium -dependent reaction where magnesium competes with calcium antagonistically. 2) Facilitation is due to cooperativity of transmitter binding in order to open the ion channels
The intracellular arsenazo signal indicating the transient light-evoked change in cytosolic Ca2+ (or Sr2+) concentration was measured in Limulus ventral photoreceptor simultaneously with the receptor potential at 15 °C. The decline of the arsenazo signal has two phases (D1 and D2) when the photoreceptor is bathed in physiological saline. 1. When calcium is replaced by strontium in the superfusate both receptor potential and arsenazo signal are markedly increased in amplitude and the membrane potential is hyper polarized. The decline of the arsenazo signal is prolonged and becomes monophasic; the fast phase D1 of the decline disappears. 2. In strontium saline under voltage clamp conditions the slope of the monophasic decline of the arsenazo signal is the steeper the more negative the membrane voltage. 3. After replacing sodium by lithium in the superfusate the rise of the receptor potential and of the arsenazo signal are not much altered. The decline of the arsenazo signal, however, is slowed down more than 3-fold; this is due to the complete suppression of the fast phase D1 and the retardation of the slow phase D2 of the calcium re-decline. Interpretation: 1. The Na-C a exchanger can accept strontium as a calcium substitute. Strontium has a weaker desensitizing action than calcium. Strontium is not-or only very little -taken up by the endoplasmic cisternae. 2. In sodium-free lithium saline the Na-C a exchanger, the Na-K ATPase and the calcium uptake system of the endoplasmic cisternae do not function. Therefore the intracellular calcium level rises.
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