Electrogenic responses elicited by transmembrane depolarizing current in aerated body wall muscles ofDrosophila melanogaster larvae

Summary Electrical excitability of the longitudinal ventrolateral body wall muscle of the third instar larva ofDrosophila melanogaster was demonstrated. This is in contrast to previous papers which have reported that this muscle is electrically inexcitable. It was found that an air supply to the muscle through the tracheoles is essential for maintaining its excitability. In an aerated preparation, the muscle maintained a resting potential of around –80 mV for more than 1.5 h, while a nonaerated muscle depolarized to about –30 mV within 30 min. Muscles with resting potentials larger than –70 mV showed graded regenerative potentials with a double-peaked configuration in response to transmembrane depolarizing current. A tetrodotoxin- (TTX-)sensitive, voltage-dependent inward sodium current, and a tetraethylammonium-(TEA-)sensitive, voltage-dependent outward potassium current were found to be responsible for the first peak of the electrogenic response of this muscle. The rising phase of the second peak was caused by a cobalt/manganese-sensitive, voltage-dependent inward calcium current that had a threshold level near –40 mV. Elimination by TEA or barium of the delayed rectification following the first peak caused the second peak to be triggered at a lower threshold. The second peak was profoundly elongated by barium, and this effect was antagonized by external calcium. Thus, the falling phase of the second peak was most likely driven by a calcium-dependent, outward potassium current.     

Monoclonal Antibodies Specific for NADH-Ferricyanide Reductase Domain of Spinach Leaf Nitrate Reductase

Two monoclonal antibodies, 17(3)9 and 36(79)4, were preparedagainst nitrate reductase from Spinacia oleracea L. leaves.An enzyme-linked immunosorbent assay showed that 17(3)9, butnot 36(79)4, reacted more strongly to heat-denatured than nativeantigen. These antibodies inhibited NADH-nitrate reductase aswell as its various partial activities including reduced methylvilogen-nitrate reductase, reduced flavin mononucleotide-nitratereductase and NADH-cytochrome c reductase activities, but notNADH-ferricyanide reductase activity. Immunoblotting after electrophoreticseparation of nitrate reductase fragments obtained by Staphyrococcusaureus V8 protease digestion of native enzyme revealed thatthe two monoclonal antibodies bind to different epitopes locatedon the 28 kDa of the NADH-ferricyanide reductase domain. (Received October 2, 1987; Accepted June 9, 1988)     

Antidepressants and seizure-interactions at the GABA-receptor chloride-ionophore complex

Convulsive seizures are a potential side effect of antidepressant drug treatment and can be produced by all classes of antidepressants. It is also known that some convulsant and anticonvulsant drug actions are mediated by the GABA-receptor chloride-ionophore complex. Drugs acting at this complex appear to induce convulsions by inhibiting chloride conductance through the associated chloride channel. Using the method of GABA-stimulated 36Cl-uptake by rat cerebral cortical vesicles, we show that some antidepressant drugs (imipramine, amitryptyline, and mianserine) can inhibit the GABA-receptor chloride uptake, and that the degree of chloride channel inhibition by these drugs correlates with the frequency of convulsive seizures induced by them.     

Somatomedin-C in the kidney of streptozotocin diabetic rats

To evaluate the possible role of somatomedin-C, insulin-like growth factor I, in renal hypertrophy in early diabetes, kidney tissue SmC concentrations were measured in streptozotocin-induced (80 mg/kg ip) diabetic rats. Body weight, liver weight, plasma SmC concentration, and SmC concentration in the liver of diabetic rats were significantly lower than those of controls. Seven days after induction of diabetes, the kidney weight (898 +/- 95 mg) in diabetic rats was significantly greater than that in controls (755 +/- 69 mg), while SmC concentration in the kidney of diabetic rats (1.7 +/- 0.3 U/g kidney) was significantly lower than that of control rats (5.4 +/- 0.6 U/g kidney). These results suggest that renal SmC may not have an important role in renal hypertrophy in early stages of diabetes and that renal production of SmC may be impaired by insulin deficiency in rats.