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Y Grossman

Publications and source records attributed to Y Grossman.

At least 55 records · Page 3Linked to original sources
PubMed1990

Pressure-induced tremor-associated activity in ventral roots in isolated spinal cord of newborn rats.

Hyperbaric pressure induces hyperexcitability, tremor, and convulsions in intact animals by mechanisms that are not understood. High pressure induces spontaneous electrical discharges in the spinal ventral roots which we call "tremor-associated activity" (TAA). This study examined the nature of TAA, its likely origins, and its possible contribution in the cervical roots to respiratory difficulties. Activity was recorded extracellularly from the cut cervical ventral roots C1 and C5 in an in vitro brainstem-spinal cord preparation from newborn rats. Under hyperbaric conditions spontaneous TAA was observed either between the typical respiratory bursts in C1 and C5 or immediately after the burst itself. Stimulating the trigeminal nerve at 1 Hz induced a direct excitatory medullospinal reflex which, at high pressure, was followed by a conspicuous TAA. The TAA evoked by the dorsoventral root reflex in isolated spinal cord under hyperbaric conditions was similar to that evoked by the medullospinal reflex. These findings suggest that basic TAA originates at the level of the spinal cord and may be triggered by various synaptic inputs. They further suggest that pressure-induced abnormal activity of the motoneuron pool innervating various respiratory muscles may contribute to respiratory problems encountered under hyperbaric conditions.

Animals↗
PubMed1989

Hyperbaric pressure depresses potentiation of polysynaptic medullospinal reflexes in newborn rats.

Hyperbaric pressure induces hyperexcitability and convulsions in intact animals by mechanisms that are not understood. In the present experiments we examined the effects of pressure on medullospinal reflexes and synaptic interactions in the vitro brainstem-spinal cord of newborn rats. Reflex activity was recorded extracellularly from the cut ventral root of the 1st cervical nerve; the Vth and Xth cranial nerves were stimulated. Exposure to pressure of 10.1 MPa increased the amplitude and duration of individual reflex responses. Hyperbaric pressure inhibited post-tetanic potentiation, reduced recovery time and decreased the marked heterosynaptic potentiation caused by Vth nerve stimulation on the Xth nerve reflex. Xth nerve stimulation caused weak heterosynaptic potentiation of the Vth nerve reflex and was not affected by pressure. In contrast to crustacean neuromuscular junction, hyperbaric pressure in the mammalian central nervous system enhanced single polysynaptic responses but depressed frequency-dependent potentiation of medullospinal reflexes.

Animals↗
PubMed1988

Pressure reversal of anaesthesia: a synaptic mechanism.

Hyperbaric pressure induces seizures and increases anaesthetic requirements ("pressure reversal of anaesthesia"), but both pressure and anaesthetic agents depress excitatory synaptic transmission. The present study has attempted to resolve this paradox. The interaction between helium pressure to 10.1 MPa and anaesthetic agents (pentobarbitone, halothane, methoxyflurane) was investigated at a crustacean glutaminergic excitatory neuromuscular junction which can be modulated by GABA inhibition. Both pressure and the anaesthetics depressed the singly evoked excitatory junctional potential (EJP). During repetitive stimulation, both pressure and pentobarbitone antagonized their own depressant effects by enhancing tetanic potentiation. The additive enhancement at 10.1 MPa was sufficient to increase the pentobarbitone-depressed response above the corresponding normobaric level. No significant antagonism between pressure and any of the anaesthetics was observed on the properties of EJP amplitude and time course, facilitation, potentiation or inhibition. Additivity rather than antagonism is the basis for pressure reversal of anaesthetic depression at this model synapse. The functional antagonism is therefore indirect, and probably involves multiple sites of action for both pressure and anaesthetics.

Action Potentials↗
PubMed1988

Synaptic integrative properties at hyperbaric pressure.

1. Because hyperbaric pressure profoundly depresses excitatory synaptic transmission, it has proved difficult to account for its excitatory effects in the CNS. We tested the hypothesis that hyperbaric pressure might increase excitation by enhancing facilitation and potentiation during repetitive synaptic activation, and/or by selectively depressing inhibitory synaptic transmission. Intracellular microelectrode recordings were obtained from crustacean muscle fibers innervated by single identifiable excitor and inhibitor motor neurons; the preparations were exposed to pressures of 0.1-10.1 MPa. 2. Hyperbaric pressure reduced the amplitude of the singly evoked excitatory junctional potential (EJP), enhanced paired-pulse facilitation, and increased the potentiation elicited by trains of stimuli. The potentiated EJP at 10.1 MPa approached the comparable response evoked at normobaric pressure. 3. Hyperbaric pressure also depressed inhibitory synaptic transmission, measured as depression of the EJP by the inhibitor motor neuron. However, pressure depressed excitatory and inhibitory synaptic transmission to the same extent. Thus there appears to be no selective effect of pressure on the GABA-activated chloride channel. The amplitude of the inhibited EJP at 10.1 MPa remained below that at normobaric pressure, even during repetitive stimulation. 4. The results do not support the hypothesis that pressure increases central excitation by selectively depressing inhibitory transmission per se; enhancement of potentiation, however, probably plays an important role. In this preparation, in which inhibitory transmission also displays facilitation, pressure did not increase overall excitation or alter the balance between excitation and inhibition. 5. These results predict that a pressure-excitable network should encompass excitatory synaptic connections which exhibit pronounced facilitation and inhibitory synapses with little or no facilitation.

Animals↗
PubMed1987

Increased axonal excitability during exposure to hyperbaric oxygen.

The effect of high oxygen pressure on neural function was studied in the isolated nervous system of the cockroach. Intracellular and extracellular action potentials were recorded from single giant axons during exposure to 7 ATA (atmosphere absolute) (1 ATA = 0.1 MPa) of oxygen. Axonal excitability was measured as changes in stimulus strength-duration relationship. Initially, a transient increase in the rheobase current was observed followed by a significant decline to 75% of air control values. This decrease was accompanied by a parallel increase in the membrane time constant. The results demonstrate that hyperbaric oxygen increases axonal excitability. Such changes are consistent with the epileptogenic properties of high oxygen pressure.

Animals↗
PubMed1986

Pressure and temperature modulation of conduction in a bifurcating axon.

A bifurcating crustacean motor neuron, which serves an integrative function by selectively controlling output to its daughter branches, was examined for its behavioral response to changes in pressure and in temperature when each was varied while the other was held constant, and when both were varied together. The neuron was exposed to helium pressure between 1 and 200 ATA and temperatures between 9 and 22 degrees C. The response of the neuron to pressure changes was biphasic and time dependent. Immediately following a pressure change, action potential amplitude and conduction velocity increased, and the ability of the branch point to pass high frequency trains improved; after 15-20 min at pressures above 35 ATA these measures were depressed below control values. The curve relating functional measures to temperature displayed a time-dependent hysteresis, fast warming leading to values for amplitude, velocity, and branchpoint capacity which corresponded to those made at a point 3-5 degrees C higher during slow cooling. The delayed depressant effects of compression and cooling were synergistic. Low temperature significantly enhanced the effects of pressure on amplitude and conduction velocity; high pressure increased the Q10 of both measures. However, slow cooling antagonized the transient compression-induced excitability increase, and prolonged exposure to hyperbaric pressure diminished the temperature hysteresis. The complex time-dependent changes in this branching axon's ability to conduct are related to previously described changes in membrane potential properties. The responses of this axon to pressure changes are different from responses of other axons studied at hyperbaric pressure. Thus, even within relatively stereotyped axon membrane the effects of pressure are not generalizeable among cells. The possible relevance of these findings to the high pressure nervous syndrome (HPNS) is discussed.

Animals↗
PubMed1985

Spectral characterization of ciliary beating: variations of frequency with time.

Ciliary beating frequency in tissue culture from frog palate and isolated lung was optically examined using instrumentation that was adjusted to measure a fraction of the surface area of a single ciliary cell. Consecutive 1-s segments of the analogue signal were fast Fourier transformed (FFT) to obtain a power spectrum. At room temperature, these power spectra changed over time from 1 s to the next. Each spectrum contained several dominant frequencies of similar intensities. Cooling the preparation resulted in a single-peak spectrum that was constant over time. A mathematical model is proposed to simulate these findings. The results and the mathematical model support the hypothesis that ciliary beating frequency fluctuates over short periods of time.

Animals↗
PubMed1984

Conduction block in a branching axon innervating two muscles under physiological conditions.

The escape reflex of the lobster consists of a series of tail flips resulting from alternating activity of the abdominal flexor and extensor muscles. Electromyographic (EMG) activity was recorded from the medial (DEAM) and the lateral (DEAL1) deep abdominal extensor muscles during free swimming. During the escape response, the muscles were active either synchronously or separately, at frequencies of 100-120 Hz. This activity pattern could be generated either by central programming, or by a peripheral mechanism such as frequency-dependent differential conduction block into one of the two branches of the common excitor axon (C.Ex) innervating these muscles. In order to explore the latter possibility in a living animal, we left the DEAM and DEAL1 muscles innervated only by the C.Ex from the tested segment. This was accomplished by manually cutting all other axons in the nerve under visual control. During escape responses in six successfully dissected animals, we found 27 sudden failures of the DEAM responses and only three in DEAL1. The failures were usually preceded by an increase in the delay of the response. These findings strongly suggest that conduction block occurs in the M branch innervating the DEAM under physiological conditions.

Animals↗
PubMed1984

Pressure and temperature: time-dependent modulation of membrane properties in a bifurcating axon.

A crustacean bifurcating motor neuron that selectively controls output to its daughter branches was exposed to helium pressure of 1-200 atmospheres (atm) and temperatures of 9-22 degrees C. The membrane responses of this integrative axon were monitored by intra- and extracellular recording, macropatch clamp, and Vaseline gap voltage clamp. The response of the neuron to pressure changes was biphasic and time dependent. Initially there was an increase in action potential amplitude and rate of rise, in magnitude of the inward sodium current, in conduction velocity, and in the ability of the branch point to conduct at high frequency. After 10-20 min at a given pressure above 35 atm, these functional measures declined to levels below control. Action potential duration increased throughout. In addition, membrane resting potential was depolarized by 10-15 mV, and input resistance increased. Pressure-related depolarization was not seen in an axon pretreated with ouabain, a result consistent with pressure inhibition of the electrogenic sodium pump in this axon. Cooling induced changes opposite to the initial effects and similar to the delayed effects of pressure in all measures, including action potential amplitude, rise time, duration, membrane potential, membrane resistance, inward current amplitude, conduction velocity, and ability to conduct at high frequency. This axon differs from other axons that have been studied at hyperbaric pressure in the bimodal nature of its response and in the magnitude of pressure-related depression of membrane properties related to excitability.

Animals↗
PubMed1983

Cyclic AMP reduction of frequency following ability in peripheral axons.

Radioimmunoassays for cAMP demonstrated that a beta-adrenergic agonist, isoproterenol, increased cAMP levels in isolated frog sciatic nerve. Dibutyryl cAMP (db-cAMP) and isoproterenol reduced the amplitude of the compound action potential and decreased the ability of the Xenopus sciatic nerve to follow high frequency stimulation. Similar effects of db-cAMP and a phosphodiesterase inhibitor were seen on intracellularly recorded action potentials of single lobster peripheral axons. These results suggest that cAMP can modulate the electrophysiological response properties of both myelinated and unmyelinated axons.

1-Methyl-3-isobutylxanthine↗
PubMed1981

Extracellular potassium activity during frequency-dependent conduction block of giant axons in the metathoracic ganglion of the cockroach.

In the metathoracic ganglion (T3) of the cockroach, extracellular potassium activity (aK) was measured with ion-sensitive microelectrodes and intracellular recordings were simultaneously made from giant axons (GAs) during high frequency stimulation of the connectives. Blockade of spike conduction through T3 was associated with intraganglionic aK rises of 0.2-0.5 mM, which were only 10% of the periaxonal aK rises suggested from GA depolarizations. When aK in the bath was increased 10-fold, GA conduction block during 1 Hz stimulation did not occur until much higher levels of aK and GA depolarization were achieved. The results suggest that glial sheaths surrounding GAs significantly impede K+ movement, and may thus prevent non-specific axonal interactions, and that stimulus-induced conduction block is not primarily due to K+-induced depolarization and consequent Na+-inactivation.

Action Potentials↗
PubMed1979

A common origin of voltage noise and generator potentials in statocyst hair cells.

Voltage noise, generator potentials, and hair movements in the Hermissenda statocyst were analyzed. Motile hairs on the cyst's luminal surface moved as rods through +/- 10 degrees Hz when free and at 7 Hz when loaded with the weight of the statoconia (at 120 degrees C). For hair cells oriented opposite to a centrifugal force vector, rotation caused depolarization and increase of voltage noise variance. The depolarizing generator potential and the increase in voltage noise variance were similarly reduced by perfusion with zero external sodium or chloral hydrate. Cooling, perfusion with zero external sodium or chloral hydrate reduced the movement frequencies of the hairs but increased their range of motion. The same treatments reduced voltage noise variance and increased input resistance of the hair cell membrane. The results indicate that voltage noise and hair cell generator potential have a common origin: exertion of force on statocyst hairs by the weight of statoconia. The collision of statoconia with the motile hairs, not the hairs' bending, produces most of the voltage noise.

Action Potentials↗
PubMed1979

Differential conduction block in branches of a bifurcating axon.

1. Propagation of action potentials at high frequency was studied in a branching axon of the lobster by means of simultaneous intracellular recording both before and after the branch point. 2. Although the branching axon studied has a geometrical ratio close to one (perfect impedance matching) conduction across the branch point failed at stimulation frequencies above 30 Hz. 3. The block of conduction after high frequency stimulation occurred at the branch point per se. The parent axon and daughter branches continued to conduct action potentials. 4. Conduction block after high frequency stimulation appeared first in the thicker daughter branch and only later in the thin branch. 5. With high frequency stimulation there was a 10-15% reduction in amplitude of the action potential in the parent axon, a corresponding decrease in the rate of rise of the action potential, a 25-30% decrease in conduction velocity, marked increase in threshold and prolongation of the refractory period. In addition the membrane was depolarized by 1-3 mV. 6. Measurements of the membrane current using the patch clamp technique showed a large decrease in the phase of inward current associated with the action potential, before the branching point. 7. The small membrane depolarization seen after high frequency stimulation is not the sole cause of the conduction block. Imposed prolonged membrane depolarization (8 mV for 120 sec) was insufficient to produce conduction block. 8. In vivo chronic extracellular recordings from the main nerve bundle (which contains the parent axon) and the large daughter branch revealed that: (a) the duration and frequency of trains of action potentials along the axons exceeded those used in the isolated nerve experiments and (b) conduction failure in the large daughter branch could be induced in the whole animal by electrical stimulation of the main branch as in the isolated preparation. 9. Possible mechanisms underlying block of conduction after high frequency stimulation in a branching axon are discussed.

Action Potentials↗