When photosynthesis of the blue‐green alga Anacystis nidulans was measured as 14CO2‐fixation, the inhibitory effect of DCMU at low concentrations was greatest when mainly Photosystem 1 (PS 1) (excitation at 446 or 687 nm) was operative. At concentrations above 10‐6M the inhibition on 14CO2‐fixation was greatest when mainly Photosystem 2 (PS 2) was operative (excitation at 619). During excitation of PS 1, the excretion of glycolate was stimulated at low concentrations of DCMU (5 × 10‐8M and lower), while higher concentrations inhibited excretion. All concentrations of DCMU inhibited glycolate excretion when mainly PS 2 was excited. The curves showing the relative effect of DCMU on the two photosystems, measured as PS 1/PS 2, had opposite shapes for 14CO2‐fixation and glycolate excretion. An increase in 14CO2‐fixation coincided with a decrease in glycolate excretion and vice versa. It appears that the increased rate of photosynthesis when mainly PS 1 was operative relative to that when mainly PS 2 was excited, increases the consumption of glycolate in an oxidation process associated with the excitation of PS 1, resulting in less excretion of glycolate to the medium. The influence of DCMU inhibition on labelled amino acid pools connected to the glycolate pathway (glycine‐serine) is quite similar to that for 14CO2‐fixation. At concentrations below 10‐6M DCMU, inhibition of 14CO2‐ incorporation into the amino acids was greatest when PS 1 was excited, while at the higher concentrations tested, inhibition was greater when PS 2 was excited. We conclude that the metabolism of glycine and serine is closely connected to the rate of photosynthesis.

In Sinapis alba, the Emerson enhancement effect, measured as CO2 uptake, was significantly lower in an O2‐free atmosphere than in normal air. Photorespiration, when measured as 14CO2 release after a period of 14C‐photosynthetic labeling in white or monochromatic light, was reduced during photosynthetic enhancement. The 14C‐glycolate pool and the 14C‐labeled amino acids associated with the glycolale pathway (glutamate, glycine and serine) decreased during photosynthetic enhancement when Pholosyslem I was ‘overexcited’. This demonstrates that photosynthesis and photorespiration are oxygen dependent and that photorespiration is wavelength dependent in Sinapis alba. The effect of oxygen on pholosynthetic enhancement and photorespiraion, as well as the effect of wavelength on these processes suggest that light is involved not only in the production of glycolate, but also in its further metabolism. It seems that Photosystem I is a key factor in the regulation of glycolate metabolism. Furthermore, the product from the consumption of glycolate in a reaction associated with Pholosystem 1 does not seem to be metabolized via the glycolate pathway.

Rat synaptosomal plasma membranes were extracted with a detergent (CHAPS, a zwitterionic derivative of cholic acid), μ and δ opioid receptor binding and adenylate cyclase activities were tested in the intact membranes and in the supernatants from detergent treated membranes. The 6000 x g/8 min. supernatant contained μ receptor binding equal to 33% of the μ receptor binding measured in the untreated membranes. When the detergent treated membranes were sedimented at (50,000 x g/10 min.), 23% of the μ receptor binding was recovered in the supernatant. After a 100,000 x g/30 min. centrifugation the supernatant contained 10% of the μ receptor binding when compared to untreated membranes. Of the 5 receptor binding found in intact membranes, 10% or less was recovered in the 3 supernatants described above. Furthermore, the μ and δ receptor binding were distributed differently among particles in the supernatants. This indicates differences in the chemical properties of the μ and δ opioid receptors. Adenylate cyclase assays showed that the G/F site of this enzyme complex was inactivated in the supernatants from detergent treated membranes parallel to the δ receptor binding decrease. However, the catalytic part of adenylate cyclase was present in the supernatants and seemed resistant to the detergent.

In vitro p and 6 opioid receptor binding is known to be influenced by ions. High affinity 3H-SKF10047 and 3H-ethylketocyclazocine binding sites are found in brain membranes and postulated to be similar to p opioid receptor binding. To investigate this postulate, we have studied how the high affinity binding of 3H-SKF10047, 3H-ethylketocyclazocine, a tritiated p agonist, p antagonist and 6 agonist is altered when the radioreceptor binding assay incubation buffer is changed. The binding of 3H-ethylketocyclazocine and the p antagonist (3H-naloxone) is highest in isotonic HEPES buffer, while the binding of the p (3Hdihydromorphine) and 6 ('H-D-ala-D-leu-enkephalin) agonist is highest in hypotonic Tris-HC1 buffer. 3H-SKF10047 binding is similar in the two buffers. The inhibition of 3H-ethylketocyclazocine, 3H-SKF10047 and tritiated p and 6 opioid ligands by seven unlabeled ligands is then compared in the two buffers. Morphine chloride is a more potent inhibitor of 3H-ethylketocyclazocine binding and tritiated p ligand in hypotonic Tris-HC1 buffer than in isotonic HEPES buffer. The potency of naloxone, nalorphine, SKF10047, D-ala-Dleu-enkephalin, cyclazocine and phencyclidine in inhibiting 3H-ethylketocyclazocine binding is independent of the buffer system. None of the seven unlabelled substances change potency with buffer change when inhibiting the 1.2 nM 'H-SKF10047 binding. In sum our results show that 1 nM 3H-ethylketocyclazocine binding is influenced by buffer change in a manner very similar to p ligand binding, while the 1.2 nM 3H-SKF10047 binding is only slightly influenced by buffer change and therefore different from p ligand binding.

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