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Biomedical subjects

Z Vogel

Publications and source records attributed to Z Vogel.

At least 109 records · Page 6Linked to original sources
PubMed1980

Do human platelets have opiate receptors?

In their study of prostaglandin E1 (PGE1)-sensitive adenylate cyclase (AC) in rat brain homogenates, Collier and Roy claimed that the activity of this enzyme is inhibited by opiates. They also proposed that opiates exert their analgesic and allied effects by inhibiting AC of neurones that are normally stimulated by E prostaglandins. Studies using neuroblastoma x glioma hybrid cells supported this hypothesis. However, subsequent studies with mammalian brain and rat brain tissue slices yielded conflicting results. PGE1 also inhibits platelet aggregation, probably through activation of platelet AC. Gryglewski et al. showed that morphine inhibits the anti-aggregating effect of PGE1 on ADP- and adrenaline-induced platelet aggregation, and suggested that the inhibition by morphine is mediated through platelet AC activity. We report here our attempts to reproduce the results of Gryglewski et al. and our examination of the effect of morphine on PGE1-sensitive AC activity in platelet lysates and on PGE1-induced accumulation of cyclic AMP in intact platelets. The possible existence of opiate receptors in platelets was also assessed by direct binding studies with 3H-etorphine. In contrast to Gryglewski et al., we could not detect any effect of opiates on the aggregation of human platelets, nor did we find any other evidence supporting the presence of opiate receptors in these cells. Thus we conclude that the presence of opiate receptors in human platelets is unlikely.

Adenylyl Cyclases↗
PubMed1980

Localization of alpha-bungarotoxin binding sites in synapses of the developing chick retina.

Alpha-bungarotoxin binding sites in chick retina from 12 days in ovo to hatching, were visualized at the ultrastructural level by use of a 1:1 conjugate of horseradish peroxidase with alpha-bungarotoxin. At all stages binding sites in the inner plexiform layer were localized in synapses, predominantly on or near the postsynaptic membrane. Localization of binding sites was found in bipolar and amacrine-cell synapses which appeared morphologically immature as well as in more well developed synapses. The results suggest that alpha-bungarotoxin-binding synapses, tentatively considered to be nicotinic cholinergic, are formed throughout the course of synaptogenesis, and that the aggregation of nicotinic receptors occurs early in the formation of these synapses.

Age Factors↗
PubMed1980

Inactivation of enkephalin by brain enzymes.

Two distinct enzymatic activities capable of hydrolyzing enkephalin are present in the brain. The major activity was shown to be a neutral aminopeptidase which hydrolyzes Leu-enkephalin (Leu-Enk) with a Km of 2 X 10(-5) M. This activity was inhibited by heavy metal ions (i.e. Zn++, Cd++), by sulfhydryl blocking reagents, and by the antibiotics bacitracin and puromycin. In contrast, these two antibiotics had no effect on the hydrolysis of Leu-Enk by either rat serum or commercial leucine aminopeptidase. The integrity of both the glycosidic and peptide bonds in the puromycin molecule was required for its inhibitory activity. On the other hand, modifications of the sugar moiety had relatively little effect, allowing the design of puromycin analogs which were inactive with regard to protein synthesis inhibition but still capable of inhibiting brain aminopeptidase. Puromycin was also shown to inhibit enkephalin degradation by homogenates of guinea pig ileum and to prolong the depressant effect of enkephalin on the electrically induced contractions of the ileum. The second enzymatic activity in brain homogenate was found to sediment with the synaptic plasma membrane fraction and cleave Leu-enkephalin into Tyr-Gly-Gly and Phe-Leu with a Km of 2.2 X 10(-5) M and pH optimum between 6.5 and 7.0. This endopeptidase was inhibited by metal chelating agents and by thiols but was insensitive to puromycin and to p-chloromercuribenzoate. In contrast to the aminopeptidase some cleavage of (D-Ala2)Met-Enk x amide by the endopeptidase was observed.

Aminopeptidases↗
PubMed1979

Alpha-bungarotoxin-horseradish peroxidase conjugate: preparation, properties and utilization for the histochemical detection of acetylcholine receptors.

A method is presented for the efficient conjugation of horseradish peroxidase to alpha-bungarotoxin. The 1:1 molar conjugate obtained is purified to completion by gel filtration on Sephadex G-100, followed by ion exchange chromatography on CM-Sephadex. The conjugate retains half of the activity of unmodified horseradish peroxidase and binds effectively to the nicotinic acetylcholine receptor of muscle. The conjugate is proven to be useful reagent for the histochemical staining of the receptor on muscle fibers for light and electron microscopy.

Acetylcholine↗
PubMed1978

A factor from neurons increases the number of acetylcholine receptor aggregates on cultured muscle cells.

There is an increase in the number of acetylcholine (AcCho) receptor aggregates on striated embryonic mouse myotubules when they are cocultured with clonal neuroblastoma-glioma hybrid cells. Medium conditioned by hybrid cells contains a factor which increases the number of AcCho receptor aggregates on myotubes cultured from mouse, rat or chick muscle. AcCho receptor-aggregating activity was present in medium conditioned by the neuroblastoma parent clone but was not detected in medium conditioned by cells of the parent glioma clone, fibroblasts, or HeLa cells. The factor increased the aggregation of AcCho receptors within 24 hr without a significant increase in the total number of AcCho receptors, and its action did not depend on myotube protein synthesis. The factor appears to rearrange the distribution of myotube AcCho receptors either by aggregating mobile AcCho receptors or by stabilizing labile receptor aggregates.

Cells, Cultured↗
PubMed1976

Localization of acetylcholine receptors during synaptogenesis in retina.

Nicotinic acetylcholine receptors are synthesized in chick embryo retina before synapses appear. Most of the receptors are found associated with neurites in the inner synaptic layer of the retina; later in development the receptors appear in the outer synaptic layer. Cells dissociated from retina and cultured in vitro form aggregates and also sort out into regions comprised either of neurites or cell bodies. Most of the nicotinic acetylcholine receptors of aggregates are found associated with neurite regions. The receptor distribution of cultured retina cells thus resembles that of intact retina.

Age Factors↗
PubMed1976

Synapse and acetylcholine receptor synthesis by neurons dissociated from retina.

Neurons dissociated from chick embryo retina and cultured from more than 1 x 10(8) synapses per mg of protein. At least three types of synapses are synthesized which resemble those of the intact retina. In addition, two populations of neurons were found, those with nicotinic acetylcholine receptors and those without the receptors.

Acetylcholine↗
PubMed1976

Immunoperoxidase localization of alpha bungarotoxin: a new approach to myasthenia gravis.

The IPBT method has made it possible to precisely visualize the AChR. Normal distribution of AChR is at the peaks of the postjunctional folds of the muscle sarcolemmal membrane with a small amount present on the axonal tip as well. Denervated muscle fibers have extrajunctional AChR. In MG, there are also denervated-appearing fibers but these do not have extrajuctional AChR with the IPBT stain. To explain this, we have been able to demonstrate a serum factor capable of blocking the binding of alpha-BuTx to the AChR and have shown for the first time that this factor is capable of acting at the neuromuscular junction itself. This blocking factor may play a major role in causing the weakness of MG.

Acetylcholine↗