Effects of quantal content, membrane potential, and cholinoceptor density on the time course of end-plate currents in the rat under during acetylcholinesterase inhibition

1992 ◽  
Vol 24 (3) ◽  
pp. 167-174
Author(s):  
R. A. Giniatullin ◽  
A. B. Shvetsov
Keyword(s):  
Membrane Potential ◽  
Time Course ◽  
Acetylcholinesterase Inhibition ◽  
Quantal Content ◽  
End Plate

Effects of Sodium Fluoride on Nerve-Muscle Transmission

1956 ◽  
Vol 186 (2) ◽  
pp. 278-282 ◽  
Author(s):  
K. Koketsu ◽  
R. W. Gerard
Keyword(s):  
Membrane Potential ◽  
Threshold Voltage ◽  
Time Course ◽  
Muscle Membrane ◽  
Fluoride Ion ◽  
Normal Muscle ◽  
End Plate ◽  
Increased Sensitivity ◽  
Nerve Muscle ◽  
Muscle Responses

Anticurare action of NaF at the neuromuscular junction is demonstrated and analyzed for various stages of impulse transmission from nerve to muscle. The e.p.p. of preparations blocked by d-tubocurarine is augmented by 0.5–10 mm NaF. The e.p.p. amplitude is increased about 2.5 times by 0.5–1 mm, nearly three times by 3 mm or higher concentrations, and some prolongation occurs. The e.p.p. of a preparation blocked by tetanization is also augmented promtly by NaF, and transmission is restored. In this case, the threshold voltage for propagated muscle responses is lowered. NaF has no effect on the normal muscle membrane potential, even in the end-plate region —nor has it any effect on the electrical threshold. The end-plate depolarization produced by acetylcholine is considerably increased by NaF; and the curve of NaF concentration against the increase of depolarization is identical with that of the increase of e.p.p. The time course of acetylcholine depolarization, when augmented by small concentrations of NaF produce some prolongation of the falling limb, but the curve is still quite different from one augmented by eserin. NaF has no effect on the frequency of spontaneous e.p.p.s, but it considerably augments the height of each individual miniature e.p.p. The augmentation of the e.p.p. produced by NaF is not explained by an anticholinesterase action; it is mainly due to an increased sensitivity of the end-plate to acetylcholine induced by the fluoride ion.

scholarly journals Early morphological remodeling of neuromuscular junction in a murine model of diabetes

2000 ◽  
Vol 89 (6) ◽  
pp. 2235-2240 ◽  
Author(s):  
M. A. Fahim ◽  
M. Y. Hasan ◽  
W. B. Alshuaib
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Time Course ◽  
Neuromuscular Junctions ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
End Plate ◽  
Intramuscular Nerves ◽  
Skeletal Muscle Weakness ◽  
C57bl Mice

Although skeletal muscle weakness is documented in diabetes, the time course for its development is not established. The present study examined the dorsiflexor muscle from animals that had been diabetic for 2 wk. Adult male c57BL mice were injected once with streptozotocin (STZ) to induce diabetes (60 mg/kg ip). Two weeks later, resting membrane potential and miniature end-plate potentials were recorded, and electron microscopy was utilized for ultrastructural evaluations. After STZ-induced diabetes, both resting membrane potential and miniature end-plate potentials were reduced. Nerve terminals showed less synaptic vesicles and had degenerated mitochondria. Furthermore, in the intramuscular nerves, disorganization of microtubules and neurofilaments was evidenced. Myelin-like figures were present in intramuscular nerves, neuromuscular junctions, and muscle fibers. At the muscle level, mitochondria were swollen, with disorganization of their cristae, disruption of T tubules, and myofibers with more deposition of glycogen granules. The present results revealed early STZ-induced nerve and muscle alterations. Observed ultrastructural modifications resemble those of motoneuron disorders and aging processes. These changes are possibly related to alterations in Ca2+ mobilization across muscle membrane. Other mechanisms such as free radical-mediated actions may also be implicated in STZ-induced effects on skeletal muscle.

scholarly journals Desensitization onset and recovery at the potassium-depolarized frog neuromuscular junction are voltage sensitive.

1978 ◽  
Vol 71 (3) ◽  
pp. 285-299 ◽  
Author(s):  
B Scubon-Mulieri ◽  
R L Parsons
Keyword(s):  
Membrane Potential ◽  
Neuromuscular Junction ◽  
Time Constant ◽  
Time Course ◽  
Voltage Dependence ◽  
Onset Time ◽  
Control Voltage ◽  
Frog Neuromuscular Junction ◽  
End Plate ◽  
Voltage Dependent

The influence of voltage on the time-course of desensitization onset and recovery has been studied at the frog neuromuscular junction. The activation-desensitization sequence was determined from carbachol-induced end-plate currents in potassium-depolarized fibers voltage-clamped either to -40 mV or +40 mV. The time-course of both desensitization onset and recovery developed exponentially, with onset occurring more rapidly than recovery. Desensitization onset was voltage dependent, the onset time constant being 8.3 +/- 1.3 s (11 fibers) at -40 mV and 19.3 +/- 3.4 s (15 fibers) at +40 mV. Recovery from desensitization was also influenced by voltage. The extent of recovery after 2 min was 80.4 +/- 6.3% in those fibers voltage-clamped to -40 mV and 57.4 +/- 3.6% in those fibers voltage-clamped to +40 mV. The voltage dependence of desenistization onset and recovery did not result from a difference in ability to control voltage at these two levels of membrane potential. These results demonstrate that in the potassium-depolarized preparation the processes controlling both desensitization onset and recovery of sensitivity from the desensitivity from the desensitized state are influenced by membrane voltage.

Inositol-1,4,5-trisphosphate injection mimics fertilization potentials in sea urchin eggs

1986 ◽  
Vol 250 (2) ◽  
pp. C340-C344 ◽  
Author(s):  
B. E. Slack ◽  
J. E. Bell ◽  
D. J. Benos
Keyword(s):  
Membrane Potential ◽  
Partial Response ◽  
Sea Urchin ◽  
Time Course ◽  
Strongylocentrotus Purpuratus ◽  
Sea Urchin Eggs ◽  
Low Calcium ◽  
Inositol 1,4,5 Trisphosphate

The effects of inositol-1,4,5-trisphosphate (IP3) and of diacylglycerol (DAG) and its analogues on the membrane potential of eggs from the sea urchin Strongylocentrotus purpuratus were examined. Injection of IP3 into eggs resulted in a change in membrane potential that was similar in magnitude and time course to the fertilization potential elicited by sperm attachment. In low-calcium seawater, IP3 injection elicited a partial response. DAG and its analogues phorbol myristyl acetate and 1-oleoyl-2-acetylglycerol did not affect membrane potential either when applied by perfusion or when injected. The results indicate that IP3, but not DAG or its analogues, may be involved in the generation of the fertilization potential triggered by the interaction of sperm with sea urchin eggs.

Electrical properties and innervation of fibers in the orbital layer of rat extraocular muscles

1989 ◽  
Vol 61 (1) ◽  
pp. 116-125 ◽  
Author(s):  
J. Jacoby ◽  
D. J. Chiarandini ◽  
E. Stefani
Keyword(s):  
Electrical Properties ◽  
Nerve Stimulation ◽  
Action Potentials ◽  
Time Course ◽  
Lucifer Yellow ◽  
Extraocular Muscles ◽  
Resting Potential ◽  
Inferior Rectus ◽  
End Plate ◽  
Orbital Layer

1. The inferior rectus muscle of rat, one of the extraocular muscles, contains two populations of multiply innervated fibers (MIFs): orbital MIFs, located in the orbital layer of the muscle and global MIFs, found in the global layer. The electrical properties and the responses to nerve stimulation of orbital MIFs were studied with single intracellular electrodes and compared with those of twitch fibers of the orbital layer, MIFs of the global layer, and tonic fibers of the frog. 2. About 90% of the orbital MIFs did not produce overshooting action potentials. In these fibers the characteristics and time course of the responses to nerve stimulation varied along the length of the fibers. Within 2 mm of the end-plate band of the muscle, the responses consisted of several small end-plate potentials (EPPs) and a nonovershooting spike. Distal to 2 mm, the responses in most fibers consisted of large and small EPPs with no spiking response. Some fibers produced very small spikes surmounted on large EPPs. 3. Overshooting action potentials were observed in approximately 10% of the orbital MIFs recorded between the end-plate band and 2 mm distal. The presence or absence of action potentials was not related to the magnitude of the resting potential of the fibers. 4. The threshold of nerve stimulated responses in orbital MIFs was the same as that in orbital twitch fibers. A large number of orbital MIFs had latencies equal to those for the orbital twitch fibers recorded at the same distance from the end-plate band, but the average latency was greater in the MIFs. The latency of orbital MIFs was about one-half of that for the MIFs of the global layer. The values for the effective resistance and membrane time constant of orbital MIFs fell between those for orbital twitch fibers on the one hand, and global MIFs and frog tonic fibers on the other. 5. In order to compare electrical properties with innervation patterns, fibers identified electrophysiologically as orbital MIFs were injected with the fluorescent dye Lucifer yellow and then traced in Epon-embedded, serial transverse sections. In addition to numerous superficial endings distributed along the fibers, a single "en plaque" ending was also found in the end-plate band that resembled the end plates of the adjacent orbital twitch fibers. 6. From these results we conclude that the electrical activity of orbital MIFs varies along the length of the fibers.(ABSTRACT TRUNCATED AT 400 WORDS)

A study of the effect of X-rays on the electrical properties of mammalian nerve and muscle

1963 ◽  
Vol 157 (969) ◽  
pp. 536-561 ◽  
Keyword(s):  
Dose Rate ◽  
Action Potentials ◽  
Time Course ◽  
Low Dose ◽  
High Dose ◽  
X Rays ◽  
Low Dose Rate ◽  
End Plate ◽  
Small Doses ◽  
Motor End Plate

Resting potentials, action potentials, and miniature end-plate potentials have been re­corded from isolated phrenic-diaphragm preparations of the rat during and after irradiation with X-rays. Relatively small doses of a few thousand roentgens have no obvious effect on the preparation for many hours but larger doses, of the order of 70 to 150 kr irreversibly block neuromuscular transmission. The block is not accompanied by any change in the size of action potentials, resting potentials, membrane constants or miniature potentials recorded in the muscle with intracellular electrodes, or in the size of action potentials recorded in the nerve. Records made at the motor end-plate show that the cause of the block is a ‘pre-synaptic ’ failure of impulse propagation in the intramuscular part of the nerve. The time course of the failure depends largely on the rate at which X-rays are delivered to the pre­paration: at a high dose-rate (70kr/min) the block develops rapidly and is accompanied by an increase in the frequency of miniature potentials; at a low dose-rate (7 kr/min) larger doses are required, the latency is longer and the miniature potentials continue at a normal frequency. The sequence in which different parts of the muscle become blocked, the abrupt nature of the failure at an individual motor end-plate, and the increase in frequency of the miniature potentials together suggest that the action of X-rays is to block conduction in the nerve near its terminals, possibly by depolarizing points where the axons branch and the safety factor for the propagation of impulses is low. The results reported in this paper do not support the hypotheses that small doses of X-rays at a high or a low dose-rate lead to an initial 'enhancement' of function or that they produce immediate and reversible changes in the permeability of excitable membranes to ions.

Conductance changes underlying a late synaptic hyperpolarization in hippocampal CA3 neurons

1987 ◽  
Vol 58 (1) ◽  
pp. 160-179 ◽  
Author(s):  
J. J. Hablitz ◽  
R. H. Thalmann
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Time Course ◽  
Membrane Potentials ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Voltage Sensitivity ◽  
Base Line ◽  
Membrane Hyperpolarization ◽  
Ca3 Neurons

1. Single-electrode current- and voltage-clamp techniques were employed to study properties of the conductance underlying an orthodromically evoked late synaptic hyperpolarization or late inhibitory postsynaptic potential (IPSP) in CA3 pyramidal neurons in the rat hippocampal slice preparation. 2. Late IPSPs could occur without preceding excitatory postsynaptic potentials at the resting membrane potential and were graded according to the strength of the orthodromic stimulus. The membrane hyperpolarization associated with the late IPSP peaked within 140-200 ms after orthodromic stimulation of mossy fiber afferents. The late IPSP returned to base line with a half-decay time of approximately 200 ms. 3. As determined from constant-amplitude hyperpolarizing-current pulses, the membrane conductance increase during the late IPSP, and the time course of its decay, were similar whether measurements were made near the resting membrane potential or when the cell was hyperpolarized by approximately 35 mV. 4. When 1 mM cesium was added to the extracellular medium to reduce inward rectification, late IPSPs could be examined over a range of membrane potentials from -60 to -140 mV. For any given neuron, the late IPSP amplitude-membrane potential relationship was linear over the same range of membrane potentials for which the slope input resistance was constant. The late IPSP reversed symmetrically near -95 mV. 5. Intracellular injection of ethyleneglycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid or extracellular application of forskolin, procedures known to reduce or block certain calcium-dependent potassium conductances in CA3 neurons, had no significant effect on the late IPSP. 6. Single-electrode voltage-clamp techniques were used to analyze the time course and voltage sensitivity of the current underlying the late IPSP. This current [the late inhibitory postsynaptic current (IPSC)] began as early as 25 ms after orthodromic stimulation and reached a peak 120-150 ms following stimulation. 7. The late IPSC decayed with a single exponential time course (tau = 185 ms). 8. A clear reversal of the late IPSC at approximately -99 mV was observed in a physiological concentration of extracellular potassium (3.5 mM).(ABSTRACT TRUNCATED AT 400 WORDS)

Partial Uncoupling of Neurotransmitter Release From [Ca2+]i by Membrane Hyperpolarization

1999 ◽  
Vol 81 (6) ◽  
pp. 3044-3053 ◽  
Author(s):  
R. Ravin ◽  
H. Parnas ◽  
M. E. Spira ◽  
I. Parnas
Keyword(s):  
Membrane Potential ◽  
Neurotransmitter Release ◽  
Quantal Content ◽  
Presynaptic Membrane ◽  
Release Process ◽  
Membrane Hyperpolarization ◽  
Quantal Release ◽  
Asynchronous Release ◽  
Frequency Of Stimulation ◽  
Different Levels

Partial uncoupling of neurotransmitter release from [Ca2+]i by membrane hyperpolarization. The dependence of evoked and asynchronous release on intracellular calcium ([Ca2+]i) and presynaptic membrane potential was examined in single-release boutons of the crayfish opener neuromuscular junction. When a single bouton was depolarized by a train of pulses, [Ca2+]iincreased to different levels according to the frequency of stimulation. Concomitant measurements of evoked release and asynchronous release, from the same bouton, showed that both increased in a sigmoidal manner as a function of [Ca2+]i. When each of the depolarizing pulses was immediately followed by a hyperpolarizing pulse, [Ca2+]i was elevated to a lesser degree than in the control experiments, and the rate of asynchronous release and the quantal content were reduced; most importantly, evoked quantal release terminated sooner. The diminution of neurotransmitter release by the hyperpolarizing postpulse (HPP) could not be entirely accounted for by the reduction in [Ca2+]i. The experimental results are consistent with the hypothesis that the HPP reduces the sensitivity of the release machinery to [Ca2+]i, thereby not only reducing the quantal content but also terminating the quantal release process sooner.

Gating currents in the node of Ranvier: voltage and time dependence

1975 ◽  
Vol 270 (908) ◽  
pp. 483-492 ◽  
Keyword(s):  
Membrane Potential ◽  
Time Constant ◽  
Time Course ◽  
Voltage Dependence ◽  
Sudden Change ◽  
Node Of Ranvier ◽  
Ionic Currents ◽  
Gating Currents ◽  
Myelinated Nerve ◽  
Sodium Conductance

Like the axolemma of the giant nerve fibre of the squid, the nodal membrane of frog myelinated nerve fibres after blocking transmembrane ionic currents exhibits asymmetrical displacement currents during and after hyperpolarizing and depolarizing voltage clamp pulses of equal size. The steady-state distribution of charges as a function of membrane potential is consistent with Boltzmann’s law (midpoint potential —33.7 mV; saturation value 17200 charges/(μm 2 ). The time course of the asymmetry current and the voltage dependence of its time constant are consistent with the notion that due to a sudden change in membrane potential the charges undergo a first order transition between two configurations. Size and voltage dependence of the time constant are similar to those of the activation of the sodium conductance assuming m 2 h kinetics, The results suggest the presence of ten times more sodium channels (5000/μm2) in the node of Ranvier than in the squid giant axon with similar sodium conductance per channel (2-3 pS),

Persistence of mitochondrial competence during myocardial autolysis

1987 ◽  
Vol 252 (5) ◽  
pp. H985-H989
Author(s):  
W. Rouslin
Keyword(s):  
Membrane Potential ◽  
Time Course ◽  
Reductase Activity ◽  
Electron Flow ◽  
Coenzyme Q ◽  
Full Potential ◽  
Irreversible Loss ◽  
Control Activity ◽  
Inner Membrane ◽  
Potential Development

The rate of irreversible loss of mitochondrial phosphorylating respiratory function with NAD-linked substrates during zero flow myocardial autolysis at 37 degrees C was gradual and relatively linear with time, progressing at about 1% of the control activity per minute. State 3 respiratory rates and initial rates of inner membrane potential development dropped off in close parallel with one another as well as with NADH-coenzyme Q (CoQ) reductase activity, suggesting that oxygen uptake as well as membrane potential development were rate limited by the increasing impairment of electron flow through complex I. Although the initial rate of membrane potential development dropped off gradually, the time course for the loss of the ability to ultimately develop and hold a full potential was slower still, there being only a moderate impairment of this ability at 80 min of autolysis. This sustained ability to develop and hold a membrane potential after more than 1 h of autolysis suggested that inner membrane leakiness contributed little or not at all to the functional impairment observed. The irreversible loss of mitochondrial inner membrane competence emerged in these studies as a relatively late development in the sequence of cellular alterations which characterize the myocardial ischemic process.

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