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Biomedical subjects

H Meiri

Publications and source records attributed to H Meiri.

At least 55 records · Page 3Linked to original sources
PubMed1985

The fusogenic substance dimethyl sulfoxide enhances exocytosis in motor nerve endings.

Fusion of synaptic vesicles with the surface membrane of the nerve terminal is a key step in synaptic transmission, which normally requires the entry of calcium ions into the cell. We report that this fusion and the subsequent liberation of transmitter can also be induced by the fusogenic substances DMSO (dimethyl sulfoxide) and PEG (poly(ethylene glycol)). Calcium ions and DMSO exhibit a synergistic effect in the fusion of synaptic vesicles with the axolemma, resembling their action on fusion phenomena in liposomes.

Action Potentials↗
PubMed1985

A monoclonal immunotoxin acting on the Na+ channel, with properties similar to those of a scorpion toxin.

We describe the properties of a monoclonal antibody against the Na+ channel. The antibody, 72.38, competitively inhibited (Ki = 1.5 X 10(-9) M) the binding of an 125I-labeled toxin from the Brazilian scorpion Tityus serrulatus (125I-TiTX gamma) to Na+ channels of rat brain membranes. No significant inhibition of binding of a number of other Na+ channel toxins was observed. The inhibition of 125I-TiTX gamma binding also was observed with the solubilized Na+ channel from rat brain membranes (Ki = 2 X 10(-9) M). Antibody 72.38 antagonized 125I-TiTX gamma binding to Na+ channels from different animal species (fish, avian, and mammalian) and from different tissues (electroplax, brain, heart, and muscle). Moreover, 72.38 has been used for immunofluorescence labeling of Na+ channels in rat sciatic nodes of Ranvier and cultured dorsal root ganglion cells. Electrophysiological experiments on rat muscle cells fully confirmed the similarity between TiTX gamma and 72.38 seen in binding experiments. Both produce slow oscillations of the membrane potential accompanied by bursts of action potentials which are due to a selective action on the Na+ channel. TiTX gamma and 72.38 are without effect on the ion selectivity of the Na+ channel, but they both drastically change the voltage-dependence of activation and inactivation of the Na+ channel.

Animals↗
PubMed1985

Modification of Vmax of canine cardiac Purkinje fibers and of the effects of lidocaine by SC-72-14.

We used standard microelectrode techniques to determine the effects of SC-72-14, a monoclonal antibody to the fast sodium channel, on the transmembrane potentials and Vmax of canine cardiac Purkinje fibers, and to study the interactions of the monoclonal antibody with lidocaine. SC-72-14 was prepared with receptor-rich membrane fragments of homogenized eel electroplax as the antigen. It reduced Vmax in a concentration-dependent fashion, and depressed membrane responsiveness, as well. These effects were attributable specifically to SC-72-14, and not to other substances in the vehicle. At slow rates of stimulation, the actions of SC-72-14 and lidocaine on Vmax equaled the sum of their effects, administered alone. These results are consistent with the interpretation that SC-72-14 and the local anesthetic did not compete for the same binding site. In contrast, at fast stimulation rates, the use-dependent blocking effects of lidocaine were suppressed by SC-72-14. The basis for the interference with the use-dependent action of lidocaine is not readily apparent, but may be the result of SC-72-14-induced changes in channel state, receptor affinity for drug, or the availability of ionized drug molecules. These possibilities all await further testing.

Animals↗
PubMed1984

Monoclonal antibodies associated with sodium channel block nerve impulse and stain nodes of Ranvier.

Monoclonal antibodies were generated against native eel electroplax sodium channels in their natural membrane. These antibodies block nerve conduction in rat central (optic) and peripheral (sciatic) nerve. The antibody binding to eel electroplax membrane fragments and to rat brain synaptosomes can be modulated by neurotoxins. Thus it implies that active sites of the sodium channels are immunogenic in their natural membrane. Unlike the antibodies described in the past, our antibodies recognize antigenic determinants which are associated with the physiological activity of the channel and have been conserved through evolution.

Animals↗
PubMed1984

Local application of calcium-modulating agents to a crushed goldfish optic nerve modifies visual recovery.

The effects of various Ca2+-modulating agents on regeneration in the optic nerve of goldfish were determined by assaying recovery of visual function. One to three daily applications of the agents were made at the site of an optic nerve crush beginning within 3 days after the lesion. Application of calcium ionophore A-23187 significantly shortened the time required for reappearance of the startle reaction to a bright light. Some shortening of recovery time was also observed with application of high-Ca2+ Ringer's solution. A significant effect was obtained with 1% and 6% dimethylsulfoxide (DMSO). When A-23187 was combined with DMSO, a further enhancement was seen if the original DMSO effect had been weak, whereas a strong DMSO effect was reduced in the presence of A-23187. The effect of DMSO alone or DMSO in combination with A-23187 was blocked by the calcium-chelating agent EGTA. These results indicated that increased entry of Ca2+ into the regenerating axons or supporting cells may be responsible for the enhanced rate of recovery. There was no histologic evidence that the faster recovery was due to accelerated axon outgrowth, but the packing density of the regenerating axons was increased. We postulate that the recovery-enhancing agents may act by promoting axonal interactions leading to the reestablishment of the correct retinal projection, or by facilitating the function of the regenerating synaptic terminals.

Animals↗
PubMed1983

Adrenocorticotropic hormone causes long-lasting potentiation of transmitter release from frog motor nerve terminals.

Exposure of frog neuromuscular preparations to adrenocorticotropic hormone for several minutes increased both nerve-evoked and spontaneous transmitter release for several hours. No changes in postsynaptic sensitivity to transmitter were detected. The long-lasting potentiation shows little sensitivity to changes in extracellular calcium concentration and seems to be entirely presynaptic in origin.

Action Potentials↗
PubMed1983

Comparison of ultrastructural changes in proximal and distal segments of transected giant fibers of the cockroach Periplaneta americana.

When the giant axons of the cockroach Periplaneta americana are transected the proximal segment (the part connected to the soma) regenerates by tip sprouting and the distal segment degenerates. The initial ultrastructural response (24-48 h post-transection) occurring in the cut ends of the proximal and distal segments are similar. This response includes the disappearance of neurotubules; appearance of amorphous material in the axoplasm and a gradual accumulation of large numbers of small mitochondria, vesicles of various sizes and smooth endoplasmic reticulum. The axolemma in the region of organelle accumulation invaginates and glial processes are present in the invagination. The similarity of the changes that occur in the cut ends of the proximal and distal segments indicates that the primary reaction to axotomy is of a local nature and does not depend on the soma. Two to four days after transection, the cut end of the distal axonal segment reveals signs of degeneration. These include the appearance of swollen mitochondria, lysosomes, myelinated bodies and shrinking of the axon. In addition there is a massive proliferation of glial processes around the degenerating axons. Sprouting from the tip of the proximal segment starts 5--7 days post axotomy. Sprouts were identified as profiles containing few neurotubules, many vesicles and abundant smooth endoplasmic reticulum. 'Growth cone-like' structures were identified. The ultrastructural reorganization of the cut end of the proximal segment is discussed in relation to changes in membrane properties of the regenerating tip, as previously described by us.

Animals↗
PubMed1982

Regulatory role of intracellular sodium ions in neurotransmitter secretion.

Calcium ions are the main inducer of quantal transmitter release of the frog neuromuscular junction; but even in their virtual absence from the extracellular medium, nerve stimulation causes a prolonged augmentation of transmitter release. These facts led to the hypothesis that an accumulation of intracellular sodium can serve as a slow secondary regulator of neurosecretion. Three lines of evidence presented in this article substantiate this hypothesis: firstly, veratridine, which is known to increase sodium fluxes through the voltage-dependent sodium channels, increases transmitter release after nerve stimulation. Secondly, monensin, which was shown to induce sodium transport through nerve membranes, increases evoked transmitter release, tetanic potentiation and posttetanic potentiation. Thirdly, sodium-filled phosphatidylcholine liposomes increase transmitter release. These effects of sodium are probably not due to a direct effect on the transmitter release mechanism, but are caused by sodium-induced calcium translocation from intracellular stores.

Animals↗
PubMed1981

Membrane conductance and action potential of a regenerating axonal tip.

The electrical membrane properties of axotomized and regenerating giant axons from the nerve cord of the cockroach Periplaneta americana were studied. Immediately after axotomy there was a decrease in resting potential, input resistance, and action potential amplitude near the cut end. This decrease was followed by the disappearance of the sodium-dependent action potential; an increase in the resting membrane conductance to K+, Na+, and Ca2+; and the appearance of a calcium-dependent action potential.

Action Potentials↗
PubMed1981

The action of the sodium ionophore, monensin, or transmitter release at the frog neuromuscular junction.

The action of the sodium ionophore, monensin, on spontaneous and evoked transmitter release at the frog neuromuscular junction was studied. Ringer's solutions with low calcium concentrations (0.4 mM or 0 Ca 1 mM EGTA) were used to bathe the preparation. Following addition of monensin in the bathing solution: (1) substantial increases in miniature end-plate potential frequency occurred; (2) tetanic nerve stimulation caused increases in potentiation of approximately 10 times over control values; (3) there was a dual action on the amplitude of the end-plate potential. We conclude that sodium ions take part in the regulation of transmitter release at the neuromuscular junction.

Animals↗
PubMed1980

Regulation of acetylcholine liberation from presynaptic nerve terminals.

Acetylcholine is liberated from motor nerve terminals either as a molecular leakage or as quantal packages; the latter form of release is responsible for signaling across the neuromuscular synapse. Three main factors determine the number of quanta liberated by the nerve impulse: the degree of presynaptic depolarisation, the frequency of activation of the nerve terminal, and calcium ion concentration in the extracellular medium. These factors seem to act yb changing the free calcium ion concentration [Ca]in in the presynaptic nerve terminal. Thus, processes that change [Ca]in will determine efficiency of synaptic transmission. These processes include fluxes of calcium ions across the presynaptic membrane and reversible translocation by intracellular organelles such as mitochondria, vesicles and soluble molecules. The level of intracellular [Ca] can be changed by ion-containing liposomes. One of the main physiological determinants of the level of transmitter release is potentiation, where the increase in transmitter release is caused by transmembranal processes and intracellular translocation.

Acetylcholine↗
PubMed1980

Primary and secondary regulation of quantal transmitter release: calcium and sodium.

Calcium is the prime regulator of quantal acetylcholine liberation at the neuromuscular junction; its entry through the presynaptic membrane and the level of free [Ca]in most probably determine the number of transmitter quanta liberated by the nerve impulse. The level of free [Ca[in, in turn, is controlled by a number of subcellular elements: mitochondria, endoplasmic reticulum, vesicles, macromolecules and the surface membrane. The action potential induced calcium entry is not the only factor responsible for coupling nerve terminal depolarization with increased transmitter release; increased transmitter release occurs also in the virtual absence of calcium ions in the extracellular medium, when a reversed electrochemical gradient for calcium probably exists during action potential activity. Several lines of evidence suggest that the entry of sodium ions is responsible for this augmented transmitter release: the tetanic potentiation observed under reversed calcium gradient is blocked by tetrodotoxin; tetanic and post-tetanic potentiation are augmented and prolonged by ouabain; the amplitude of the extracellular nerve action potential is reduced with high-frequency stimulation, in parallel with increased spontaneous quantal release. In addition, sodium-filled egg-lecithin liposomes augment quantal liberation. The augmentory effect of sodium on transmitter release is probably due to an intracellular calcium translocation, since no preferred timing after the action potential is observed. Thus, the level of [Na]in in the presynaptic nerve terminal can control indirectly the efficiency of synaptic transmission.

Acetylcholine↗
PubMed1978

Intracellular and extracellular calcium ions in transmitter release at the neuromuscular synapse.

The theme of this presentation has been to show that the control of transmitter release at the neuromuscular synapse is achieved by extracellular and intracellular calcium. For the fast information transfer represented by the end-plate potential, the electrochemical gradient for calcium across the presynaptic membrane and the associated calcium conductance seem to play the primary role. For slower processes such as tetanic and posttetanic potentiation, the combined effect of both sources for calcium determine the amount of transmitter liberated.

Acetylcholine↗
PubMed1978

Changes in transmitter release induced by ion-containing liposomes.

The changes in quantal transmitter release induced by egg phosphatidylcholine liposomes with different internal ionic composition were examined at the frog neuromuscular junction by using conventional electrophysiological techniques. It was found that liposomes containing calcium or sodium ions increase both evoked and spontaneous transmitter release, while liposomes containing potassium do not. The results suggest that phosphatidylcholine liposomes are able to transfer their aqueous medium into the presynaptic nerve terminal.

Acetylcholine↗
PubMed1978

Clumping and oscillations in evoked transmitter release at the frog neuromuscular junction.

1. Time series analysis of evoked transmitter release was performed at the frog neuromuscular synapse. 2. Clumping of end-plate potentials with similar amplitude was found in the time domain. 3. At low quantal contents periodic oscillations were observed with a period of 14 sec. 4. Clumping and oscillations are phenomena of presynaptic origin. 5. The results are explained on the hypothesis that periodic fluctuations occur in Ca concentration inside the presynaptic nerve terminal.

Animals↗
PubMed1978

Adrenergic influences on rabbit oviduct: effect of muscle size and ovarian hormones.

This study attempts to distinguish between a direct action of ovarian steroids on adrenergic neurons in the oviduct and an indirect effect mediated by changes in muscle size. Mature rabbits were treated as follows: group 1, ovariectomized and a polyethylene catheter (1 mm OD) inserted into isthmus of one oviduct (CT) with contralateral oviduct as control (C); group 2, normal, estrous animals with one intubated isthmus (ET) and contralateral control (E). Fourteen days postoperatively, oviducts were removed and muscle-wall thickness, norepinephrine (NE) content, and response to nerve stimulation were measured. Although castration atrophy was prevented in CT, NE content of CT was significantly less than C, 0.032 +/- 0.07 versus 1.09 +/- 0.10 nmol. NE content of ET was also significantly less than E (1.32 +/- 0.03 versus 1.81 +/- 2.0) despite a greater wall thickness of ET. It was concluded that: a) withdrawal of ovarian hormones reduces NE contents by a direct action on nerves; b) moderate stretch, per se, increases muscle size and reduces NE content; c) nerve stimulation induces muscle contraction despite large reduction in transmitter content.

Adrenergic Fibers↗