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L C Fritz

Publications and source records attributed to L C Fritz.

46 records · Page 3Linked to original sources
PubMed1983

Immunochemical properties and cytochemical localization of the voltage-sensitive sodium channel from the electroplax of the eel (Electrophorus electricus).

Immunochemical methods have been used to investigate questions concerning the relatedness of sodium channels from different sources and their distribution in the eel electroplax. The reagents employed were two monoclonal antibodies, 5D10 (Moore, H. -P. H., L. C. Fritz, M. A. Raftery, and J. P. Brockes (1982) Proc. Natl. Acad. Sci. U.S.A. 79: 1673-1677) and 5F3, and a rabbit antiserum; all three were directed against determinants present on the 250,000-dalton component of the eel sodium channel. In quantitative adsorption assays, the three reagents were effectively adsorbed by eel electroplax membranes but not by brain membranes from rat, frog, or chick. The rabbit antiserum bound to immobilized membranes of rat brain at a level only approximately 0.1% of that seen with electroplax membranes. The reactivity of the three reagents with the eel electroplax was further investigated by indirect immunofluorescence on frozen sections. Whereas 5D10 showed no detectable reactivity, the rabbit antiserum and, especially, 5F3 stained the electrically excitable caudal face of the electrocytes but not the inexcitable rostral face. The reactivity of 5F3 was examined in greater detail and showed occasional abrupt discontinuities where the membrane was not stained. The presence of positive 5F3 immunoreactivity appeared to be correlated with extracellular filamentous material.

Animals↗
PubMed1982

The ionic dependence of black widow spider venom action at the stretch receptor neuron and neuromuscular junction of crustaceans.

The effects of black widow spider venom (BWSV) on the crayfish stretch receptor and the lobster neuromuscular junction were examined. In crayfish stretch receptor neurons, BWSV caused a slight hyperpolarization followed by a large depolarization. The venom-induced depolarization of the stretch receptor was caused by an increase in membrane conductance to Na+ and Ca2+. Black widow spider venom also caused an increase in the frequency of miniature inhibitory postsynaptic potentials recorded in the stretch receptor. The ability of BWSV to increase the frequency of miniature excitatory postsynaptic potentials (MEPSPs) at the lobster neuromuscular junction was dependent on the divalent cation composition of the bathing medium. Ringer solutions containing Ca2+ supported the greatest venom-induced increase in MEPSP frequency, Mg2+ and Mn2+ supported a moderate increase in MEPSP frequency, while Co2+ and Zn2+ blocked this venom effect entirely. Black widow spider venom did not block axonal conduction in lobster walking leg axons or in the axon of the crayfish stretch receptor. The results suggest that in crustaceans, BWSV interacts specifically with membrane of the soma-dendritic region of the stretch receptor and with nerve terminal membrane, causing an increase in Na+ and Ca2+ conductance.

Animals↗
PubMed1982

Isolation and characterization of a monoclonal antibody against the saxitoxin-binding component from the electric organ of the eel Electrophorus electricus.

A monoclonal hybridoma cell line secreting antibody against the saxitoxin-binding component from the eel Electrophorus electricus has been isolated. The specificity of this monoclonal antibody was established by (i) its ability to immunoprecipitate bound [3H]saxitoxin from a detergent extract of electroplax membranes in a dose-dependent manner, (ii) the inability of unrelated monoclonal antibodies to immunoprecipitate the toxin-binding activity in a similar assay, and (iii) the ability of excess unlabeled tetrodotoxin to displace [3H]saxitoxin from the immunoprecipitated component. The antibody is of the subclass IgG1 and binds specifically to a polypeptide component of Mr approximately 250,000 on NaDodSO4/polyacrylamide gels. The antigenic determinant is associated with the same polypeptide component throughout the purification procedure, indicating that this component is not a result of artifactual aggregation or degradation during isolation. We conclude that the 250,000-dalton polypeptide is part of the saxitoxin binding/sodium channel protein in the native electroplax membrane.

Animals↗
PubMed1981

The effect of diamide on transmitter release and on synaptic vesicle population at vertebrate synapses.

Diamide, a sulfhydryl-oxidizing agent, has previously been shown to cause acetylcholine release in two preparations in the absence of added Ca2+. Similarities in action between diamide and alpha-latrotoxin, a component of black widow spider venom which causes transmitter release with no added Ca2+, and which seems to require a disulfide bond for its action, led us to study further the transmitter-releasing properties of diamide. In rat cerebral cortical slices we show that diamide, like alpha-latrotoxin, released all transmitters studied; GABA, acetylcholine, norepinephrine and dopamine. The response reached a peak after a delay (5-15 min), in contrast to the much faster release evoked by high K+ (within 3 min). Diamide-induced GABA release was found to occur equally well in the absence of added Ca2+, and was blocked when diamide was reduced prior to addition. Our ultrastructural studies of the frog neuromuscular junction showed that whereas alpha-latrotoxin caused the elimination of synaptic vesicles, diamide did not. Dithiothreitol, a disulfide-reducing agent, also caused GABA release, but this effect was Ca2+-dependent, blocked by high Mg2+, and occurred without delay. These observations comparing the 3 transmitter-releasing agents have further delineated the sulfhydryl/disulfide-group involvement in transmitter release and have demonstrated that dithiothreitol is operating at a different site from either alpha-latrotoxin or diamide.

Acetylcholine↗
PubMed1980

Lobster neuromuscular junctions treated with black widow spider venom: correlation between ultrastructure and physiology.

Black widow spider venom (BWSV) causes marked physiological and morphological alterations at the lobster neuromuscular junction. BWSV is also active at vertebrate neuromuscular junctions but the component which acts on the lobster preparation is different from the one which affects vertebrates. Following exposure to BWSV, lobster neuromuscular junctions showed elevated frequencies of spontaneous miniature synaptic potentials for 15-30 min. Nerve-evoked synaptic potentials became blocked during this period. Subsequently, spontaneous miniature potentials disappeared and less frequent 'giant' spontaneous potentials appeared. Ultrastructural examination of excitatory and inhibitory nerve terminals showed that both types were affected by venom treatment. In untreated terminals, synaptic vesicles were grouped near the dense specialized membranes of the synapses. Soon after venom treatment, the synaptic vesicles were dispersed throughout the terminals and many larger and elongated vesicular structures were apparent. At the time of appearance of 'giant' spontaneous potentials, few synaptic vesicles were seen in the terminals, but large irregular vacuoles were present. Many mitochondria within the nerve terminals were swollen or disrupted, while nearby muscle mitochondria remained normal in size and appearance. Very few presynaptic dense bodies ('active zones') were seen at synapses of affected terminals. The observations are consistent with the hypothesis that BWSV allows an abnormal amount of Ca2+ to enter the nerve terminals, causing the various physiological and morphological changes.

Animals↗
PubMed1979

Avermectin B1a irreversibly blocks postsynaptic potentials at the lobster neuromuscular junction by reducing muscle membrane resistance.

Avermectin B1a, a macrocyclic lactone with broad spectrum anthelmintic activity, affects neuromuscular transmission in the lobster stretcher muscle. Perfusion of the muscle with 1-10 microgram of the drug per ml eliminates inhibitory postsynaptic potentials within a few minutes. Intracellularly recorded excitatory postsynaptic potentials are gradually reduced in amplitude over 20-30 min, and their falling phases become faster; there is no effect, however, on extracellularly recorded excitatory potentials. Avermectin B1a reduced the input resistance of the muscle fibers with a time course similar to that of the reduction of excitatory potentials. Washing for up to 2 hr with drug-free solution fails to reverse the drug's effects. However, perfusion with 20 microgram of picrotoxin per ml results in recovery of the excitatory potentials and input resistance. Avermectin B1a also blocks the firing of the crayfish stretch receptor neuron, and this block is also reversed by picrotoxin. We hypothesize that the reduction in excitatory postsynaptic potentials after avermectin B1a treatment is caused solely by reduction in membrane resistance; additional experiments suggest that the reduction in membrane resistance is due to the opening of membrane Cl- channels, perhaps including those regulated by gamma-aminobutyric acid at the inhibitory synapse.

Animals↗