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S D Erulkar

Publications and source records attributed to S D Erulkar.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1981

Modulation of the neural control of the clasp reflex in male Xenopus laevis by androgens: a multidisciplinary study.

The neural control of the clasp reflex in male Xenopus laevis has been studied by using anatomical, electrophysiological, and biochemical techniques. Neurons in spinal segment 2 of castrated males accumulate label after injection of [3H]-dihydrotestosterone; these neurons are distributed within the rostral portions of the motoneuronal pools of the sternoradialis and flexor carpi radialis muscles. In vitro recordings from the nerve to the sternoradialis muscle in the isolated spinal cord preparation from castrated male Xenopus showed increased activation to paired dorsal root stimulation after addition of dihydrotestosterone to the bath. This increase could be prevented by prior administration of cycloheximide. The reducing enzyme testosterone 5 alpha-reductase is present and is selectively distributed in male Xenopus spinal cord. It is speculated that the androgens may alter patterns of neuronal activity leading to the "clasp" muscles and thereby influence myosin types within these muscles.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1980

Interactions among lumbar motoneurons on opposite sides of the frog spinal cord: morphological and electrophysiological studies.

Light and electron microscopy have been used to study the projections of dendrites from motoneurons in lumbar segments of the spinal cord of the frog following administration of horseradish peroxidase to cut ventral roots. Processes originating from motoneurons crossed to the opposite side of the spinal cord via the anterior commissure and made contact with dendrites and motoneuronal somata. Typically, in segments 6 to 8 the crossing dendrites showed irregular enlargements in diameter. Electrophysiological recordings were obtained both extracellularly from ventral roots and intracellularly from motoneuronal somata. In Ringer's solution containing 1 mM calcium, stimulation of a lumbar ventral root, elicited population responses with early and late components in the ventral root of the opposite side of the same segment. Only the early, short latency component remained in calcium-deficient Ringer's solution. In calcium-containing Ringer's solution, intracellular recording from an antidromically activated motoneuron showed an action potential with a short latency; this response was followed by excitatory postsynaptic potentials (epsps) from which action potentials could be generated. Contralateral ventral root stimulation also elicited in the same motoneuron a short latency action potential that was rarely followed by epsps. The short latency responses, that were elicited by stimulation of ventral roots of either side persisted in calcium-deficient Ringer's solution, but the epsps were abolished. Contralaterally elicited short latency responses were eliminated by section of the anterior commissure. We believe that electrically mediated crossed interactions among lumbar motoneurons may serve as a means of coordinating muscle groups of opposite sides that are used in movements that require bilateral synchronization, such as jumping and swimming.

Animals↗
PubMed1979

The bulbo-spinal indoleaminergic pathway in the frog.

The role of the bulbo-spinal indoleaminergic pathway of the frog was investigated. Using the isolated spinal cord preparation, responses of motoneurons of segments 9 and 10 to lateral column stimulation were recorded from ventral roots (LC-VRP) and by intracellularly placed microelectrodes. Control responses were compared to those obtained after addition of substances known to alter indoleaminergic synthesis or receptor activation. Responses from spinal cords of animals that were pretreated with indoleamine-depleting agents were compared to mean control responses. Procedures that inhibited indoleamine synthesis or blocked indoleamine receptors reduced motoneuronal activity. This was manifested as an increase in mean latency and a decrease in amplitude of the monosynaptic LC-VRP, an increased duration of suppression following an LC conditioning stimulus, and a decrease in spontaneous activity. In contrast to intracellularly recorded responses from control cords, those recorded under these conditions typically showed single spikes with longer latencies. Additions of indoleamine precursors to normal cords or to cords depleted of monoamines by reserpine shortened mean latencies, increased amplitudes of LC-elicited responses and caused an increase in spontaneous activity. These observations were recorded both extracellularly and intracellularly. Our results suggest that the bulbo-spinal indoleaminergic pathway modulates the output of motoneurons of the frog spinal cord.

5-Hydroxytryptophan↗
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

Quelling of spontaneous transmitter release by nerve impulses in low extracellular calcium solutions.

1. The effect of nerve stimulation on spontaneous transmitter release was studied at the frog neuromuscular synapse which was bathed in a solution containing very low extracellular calcium concentration. Conventional methods for intracellular and extracellular recording were used and the pattern of quantal liberation following the nerve stimulus was determined. 2. Stimulation of the motor nerve (at rates between 0.09 and 2Hz) caused a reduction in the frequency of the miniature e.p.p.s in comparison to the prestimulation values. 3. The mean distribution of the time of occurrence of the miniature e.p.p.s during the interstimulus period showed periodic oscillations. 4. The quelling effect of nerve stimulation on transmitter release is explained by the hypothesis that a low [Ca]o a reversed electrochemical gradient for calcium occurs and nerve stimulation causes an increased calcium conductance leading to calcium efflux which in turn temporarily reduces [Ca]i and transmitter release.

Action Potentials↗
PubMed1978

The role of calcium ions in tetanic and post-tetanic increase of miniature end-plate potential frequency.

1. The role of Ca ions in transmitter release changes, during and after high frequency stimulation of the motor nerve (10--100 Hz), was examined at the frog neuromuscular junction. 2. The stimulation-induced changes in miniature end-plate potential frequency (f) resembled the changes in end-plate potential amplitude recently described by Magleby and Zengel (1975, 1976). 3. The effects of tetanic stimulation on f under inward electrochemical gradient for Ca ions were compared with those under reversed gradient and four differences were found: (a) The increase in f during the tetanus under reversed Ca gradient conditions is much smaller than with an inward Ca gradient. (b) The increase in f under reversed Ca gradient is preceded by a small decrease in f, whereas with an inward Ca gradient an immediate increase in f is observed. (c) After the termination of the tetanus with a reversed Ca gradient, there is a further increase in f, compared to a decrease with an inward Ca gradient. (d) The augmentation phase of post-tetanic potentiation was practically abolished. 4. The experimental results are explained by assuming that high frequency nerve stimulation causes an increase in transmitter release by at least two distinct processes: influx of Ca ions through the presynaptic membrane and release of Ca ions from intracellular stores. It is suggested that Na ions couple nerve activity to intracellular release of Ca.

Action Potentials↗
PubMed1977

Extracellular potassium and trasmitter release at the giant synapse of squid.

1. The effects of changes in extracellular K concentration, [K]0, on synaptic transmission were studied at the squid giant synapse with intracellular recording from the presynaptic terminal and post-synaptic axon. 2. The amplitudes of both the presynaptic spike and the e.p.s.p. varied inversely with [K]0. On the average, a 10 mV change in spike height was accompanied by a 3-1 mV change in e.p.s.p. amplitude. 3. The amplitude of the presynaptic spike after-hyperpolarization (AH) varied inversely with [K]0. On the average, increasing [K]0 resulted in a 20% change in e.p.s.p. amplitude per mV change in presynaptic spike AH. 4. Repetitive antidromic stimulation of the post-synaptic giant axon resulted in an exponential decline in the post-synaptic spike AH, a depolarization of the presynaptic membrane potential and a reduction in the AHs of presynaptic spikes. This suggests that the K which accumulates in the extracellular spaces around the post-synaptic axon also affects the presynaptic terminal. 5. Repetitive antidromic stimulation of the post-synaptic axon resulted in a reduction in the amplitude of e.p.s.p.s. elicted by stimulation of the presynaptic axon. The reduction in e.p.s.p. amplitude relative to the change in presynaptic spike AH was quantitatively close to the change produced by increasing [K]0, suggesting that the reduction in e.p.s.p. amplitude is due to the accumulation of extracellular K at the presynaptic terminal. 6. Repetitive stimulation of the presynaptic axon reduced the amplitudes of the e.p.s.p. and the presynaptic spike AH. On the average, a 1 mV change in presynaptic spike AH was accompanied by a 204% change in e.p.s.p. amplitude, suggesting that K accumulation may only contribute to a small extent, under these conditions, to the depression of transmitter release.

Action Potentials↗
PubMed1976

Modulation of synaptic transmitter release by repetitive postsynaptic action potentials.

The effect of repetitive action potentials in the postsynaptic axon on the release of synaptic transmitter from the presynaptic terminal was investigated at the squid giant synapse. Repetitive antidromic stimulation of the postsynaptic axon resulted in a reduction in the excitatory postsynaptic potential (EPSP). The reduction in transmitter release was accompanied by a decrease in the presynaptic spike after-hyperpolarization (AH). Increasing the concentration of extracellular potassium ions also reduced the EPSP and decreased the amplitude of the presynaptic spike AH. The reduction in transmitter release resulting from repetitive postsynaptic impulses is attributed to the accumulation of extracellular potassium ions. It is proposed that the accumulation of extracellular potassium ions resulting from repetitive postsynaptic activity may modulate synaptic transmission and function as an integrative mechanism in the nervous system.

Action Potentials↗