We have tested the proposal that the light-sensitive conductance in Drosophila is composed of two independent components by comparing the wild-type conductance with that in mutants lacking one or the other of the putative light-sensitive channel subunits, TRP and TRPL. For a wide range of cations, ionic permeability ratios in wild type were always intermediate between those of trp and trpl mutants. Effective channel conductances derived by noise analysis in wild type were again intermediate (17 pS; c.f. 35 pS in trp and 4 pS in trpl) and also showed a complex voltage dependence, which was quantitatively explained by the summation of TRPL and TRP channels after taking their different reversal potentials into account. Although La3+ partially blocked the light response in wild-type photoreceptors, it increased the effective single channel conductance. The results indicate that the wild-type light-activated conductance is composed of two separate channels, with the properties of TRP- and TRPL-dependent channels as determined in the respective mutants.

Discrete events (quantum bumps) elicited by dim light were analysed in whole‐cell voltage clamp of photoreceptors from dissociated Drosophila ommatidia. Bumps were automatically detected and analysed for amplitude, rise and decay times, and latency. The bump interval and amplitude distributions, and the ‘frequency of seeing’ curve conformed to Poisson predictions for the absorption of single photons. At resting potential (‐70 mV), bumps averaged 10 pA in peak amplitude with a half‐width of ca 20 ms, representing simultaneous activation of ca 15 channels. The macroscopic response to flashes containing up to at least 750 photons were predicted by the linear summation of quantum bumps convolved with their latency dispersion. Bump duration was unaffected by lowering the extracellular Ca2+ concentration ([Ca2+]o) from 1.5 to 0.5 mM, but increased >10‐fold between 0.5 mM Ca2+ and 0 Ca2+. Bump amplitude was constant over the range 1.5‐100 μM, but decreased ca 5‐ to 10‐fold at lower Ca2+ concentrations. Bump latency increased by ca 50 % between 1.5 mM and 100 μM Ca2+o but returned to near control levels in Ca2+‐free solutions. At intermediate [Ca2+]o bumps were biphasic with a slow rising phase followed by rapid amplification and inactivation. This behaviour was mimicked in high [Ca2+]o by internal buffering with BAPTA, but not EGTA. This suggests that Ca2+ influx through the light‐sensitive channels must first raise cytosolic Ca2+ to a threshold level before initiating a cycle of positive and negative feedback mediated by molecular targets within the same microvillus. Quantum bumps in trp mutants lacking the major class of light‐sensitive channel were reduced in size (mean 3.5 pA) representing simultaneous activation of only one or two channels; however, a second rarer (10 %) class of large bump had an amplitude similar to wild‐type (WT) bumps. Bumps in trpl mutants lacking the second class of light‐sensitive channel were very similar to WT bumps, but with slightly slower decay times. In InaDP215 mutants, in which the association of the TRP channels with the INAD scaffolding molecule is disrupted, bumps showed a defect in quantum bump termination, but their amplitudes and latencies were near normal.

No abstract

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

Im Jahre 1918 synthetisierten E. FISCHER und M. BERGMANN~) auf zwei verschiedenen Wegen die l-Triacetylgalloyl-2.3.4.6-tetraacetyl-~-glucose (Heptaacetyl-Pglucogallin) und erhielten durch Ammonolyse das Glucogallin selbst. Ein Jahr spaters) gewannen sie die anomere I-Triacetylgalloyl-2.3.4.6-tetraacetyl-a-glucose (Heptaacetyl-a-glucogallin), entacetylierten auch diese Verbindung mit alkoholischem Ammoniak und erhielten eine nicht kristallisierte, ziemlich stark rechtsdrehende Substanz, 1) XXIX. Mitteilung: 0. TH. SCHMIDT und R. ECKERT, Liebigs Ann. Chem. 618,71 (1958). 2 ) H. REUSS, Dissertation Univ. Heidelberg 1957. 3) 0. TH. SCHMIDT und J. HEROK, Liebigs Ann. Chem. 587, 63 (1954). 4) E. FISCHER und M. BERGMANN, Ber. dtsch. chem. Ges. 51, 1760 (1918). 5 ) E. FISCHER und M. BERCMANN, Ber. dtsch. chem. Ges. 52, 829 (1919). 9 ) G. ZEMPL~N und E. PACSU, Ber. dtsch. chem. Ges. 62, 1613 (1929). 10) vgl. auch die ebenso durchgefiihrte Entacetylierung der Heptaacetyl-glucogalline, 11) Die Beteiligung einer solchen Form an der Mutarotation des a-Glucogallins hat schon auf S. 145, 146 unter 6) und 8). J. HEROK in seiner Dissertation, Univ. Heidelberg 1954, diskutiert.