Selective inhibition by hydrocortisone of 3H-normetanephrine formation during 3H-transmitter release elicited by nerve stimulation in the isolated nerve-muscle preparation of the cat nictitating membrane

1975 ◽  
Vol 287 (3) ◽  
pp. 261-275 ◽  
Author(s):  
M. A. Luchelli-Fortis ◽  
S. Z. Langer
Keyword(s):  
Nerve Stimulation ◽  
Transmitter Release ◽  
Selective Inhibition ◽  
Muscle Preparation ◽  
Nictitating Membrane ◽  
Cat Nictitating Membrane ◽  
Nerve Muscle

scholarly journals GLUTAMATE UPTAKE BY A STIMULATED INSECT NERVE MUSCLE PREPARATION

1970 ◽  
Vol 46 (2) ◽  
pp. 300-307 ◽  
Author(s):  
Isabelle R. Faeder ◽  
Miriam M. Salpeter
Keyword(s):  
Electron Microscope ◽  
Nerve Stimulation ◽  
Neuromuscular Junctions ◽  
Tissue Concentration ◽  
Glutamate Uptake ◽  
Muscle Preparation ◽  
Glutamate Concentration ◽  
Chemical Studies ◽  
Nerve Muscle ◽  
Cellular Compartments

Recent reports suggest that glutamate may be the excitatory neuromuscular transmitter in insects. In this study, glutamate uptake by isolated cockroach nerve muscle preparations was investigated by means of chemical and electron microscope radioautographic techniques. We found that the preparation had a high affinity for glutamate and that nerve stimulation enhanced glutamate uptake. Chemical studies showed that the average tissue concentration of glutamate bound during a 1 hr incubation period in 10-5 M glutamate-3H after nerve stimulation was 2.8 x 10-5 M. Less than 1% of the radioactivity was present in the perchloric acid-precipitated protein fraction. Using electron microscope radioautography, we observed that sheath cells showed the highest glutamate concentration of all cellular compartments. Uptake was greater at neuromuscular junctions than in other regions of the tissue. The data suggest a possible mechanism for transmitter inactivation and protection of synapses from high blood glutamate.

Effect of armin on synaptic transmission in the frog nerve-muscle preparation

1981 ◽  
Vol 91 (6) ◽  
pp. 774-777 ◽  
Author(s):  
I. I. Krivoi ◽  
V. I. Kuleshov ◽  
D. P. Matyushkin ◽  
V. I. Sanotskii ◽  
I. A. Shabunova
Keyword(s):  
Synaptic Transmission ◽  
Muscle Preparation ◽  
Nerve Muscle

scholarly journals Changes in miniature endplate potential frequency during repetitive nerve stimulation in the presence of Ca2+, Ba2+, and Sr2+ at the frog neuromuscular junction.

1981 ◽  
Vol 77 (5) ◽  
pp. 503-529 ◽  
Author(s):  
J E Zengel ◽  
K L Magleby
Keyword(s):  
Nerve Stimulation ◽  
Transmitter Release ◽  
Neuromuscular Junctions ◽  
Fourth Power ◽  
Bathing Solution ◽  
Frog Neuromuscular Junction ◽  
Repetitive Nerve Stimulation ◽  
Time Constants ◽  
Endplate Potential ◽  
Induced Changes

Miniature endplate potentials (MEPPs) were recorded from frog sartorious neuromuscular junctions under conditions of reduced quantal contents to study the effect of repetitive nerve stimulation on asynchronous (tonic) quantal transmitter release. MEPP frequency increased during repetitive stimulation and then decayed back to the control level after the conditioning trains. The decay of the increased MEPP frequency after 100-to 200-impulse conditioning trains can be described by four components that decayed exponentially with time constants of about 50 ms, 500 ms, 7 s, and 80 s. These time constants are similar to those for the decay of stimulation-induced changes in synchronous (phasic) transmitter release, as measured by endplate potential (EPP) amplitudes, corresponding, respectively, to the first and second components of facilitation, augmentation, and potentiation. The addition of small amounts of Ca2+ or Ba2+ to the Ca2+-containing bathing solution, or the replacement of Ca2+ with Sr2+, led to a greater increase in the stimulation-induced increases in MEPP frequency. The Sr-induced increase in MEPP frequency was associated with an increase in the second component of facilitation of MEPP frequency; the Ba-induced increase with an increase in augmentation. These effects of Sr2+ and Ba2+ on stimulation-induced changes in MEPP frequency are similar to the effects of these ions on stimulation-induced changes in EPP amplitude. These ionic similarities and the similar kinetics of decay suggest that stimulation induced changes in MEPP frequency and EPP amplitude have some similar underlying mechanisms. Calculations are presented which show that a fourth power residual calcium model for stimulation-induced changes in transmitter release cannot readily account for the observation that stimulation-induced changes in MEPP frequency and EPP amplitude have similar time-courses.

Effect of Hypertonicity on Augmentation and Potentiation and on Corresponding Quantal Parameters of Transmitter Release

1999 ◽  
Vol 81 (3) ◽  
pp. 1428-1431 ◽  
Author(s):  
Hong Cheng ◽  
Michael D. Miyamoto
Keyword(s):  
Nerve Stimulation ◽  
Transmitter Release ◽  
Ringer Solution ◽  
Hypertonic Solution ◽  
Repetitive Nerve Stimulation ◽  
Quantal Transmitter Release ◽  
Before And After ◽  
Miniature Endplate Potentials ◽  
Endplate Potentials ◽  
Made In

Effect of hypertonicity on augmentation and potentiation and on corresponding quantal parameters of transmitter release. Augmentation and (posttetanic) potentiation are two of the four components comprising the enhanced release of transmitter following repetitive nerve stimulation. To examine the quantal basis of these components under isotonic and hypertonic conditions, we recorded miniature endplate potentials (MEPPs) from isolated frog ( Rana pipiens) cutaneous pectoris muscles, before and after repetitive nerve stimulation (40 s at 80 Hz). Continuous recordings were made in low Ca2+ high Mg2+ isotonic Ringer solution, in Ringer that was made hypertonic with 100 mM sucrose, and in wash solution. Estimates were obtained of m (no. of quanta released), n (no. of functional release sites), p (mean probability of release), and vars p (spatial variance in p), using a method that employed MEPP counts. Hypertonicity abolished augmentation without affecting potentiation. There were prolonged poststimulation increases in m, n,and p and a marked but transient increase in vars p in the hypertonic solution. All effects were completely reversed with wash. The time constants of decay for potentiation and for vars p were virtually identical. The results are consistent with the notion that augmentation is caused by Ca2+ influx through voltage-gated calcium channels and that potentiation is due to Na+-induced Ca2+ release from mitochondria. The results also demonstrate the utility of this approach for analyzing the dynamics of quantal transmitter release.

Nerve—Muscle Preparations of the Nictitating Membrane

Smooth Muscle ◽  
1975 ◽  
pp. 457-468 ◽  
Author(s):  
U. Trendelenburg ◽  
G. Haeusler
Keyword(s):  
Nictitating Membrane ◽  
Nerve Muscle

Effect of Bothrops insularis venom on the mouse and chick nerve-muscle preparation

Toxicon ◽  
1993 ◽  
Vol 31 (10) ◽  
pp. 1237-1247 ◽  
Author(s):  
J.C. Cogo ◽  
J. Prado-Franceschi ◽  
M.A. Cruz-Hofling ◽  
A.P. Corrado ◽  
L. Rodrigues-Simioni
Keyword(s):  
Muscle Preparation ◽  
Nerve Muscle

scholarly journals I. Croonian Lecture .—Observations on isolated nerve (with particular reference to carbon dioxide)

1897 ◽  
Vol 188 ◽  
pp. 1-101 ◽  
Keyword(s):  
Weak Link ◽  
Nerve Degeneration ◽  
Muscle Preparation ◽  
Marked Contrast ◽  
Functional Failure ◽  
Du Bois ◽  
Motor End Plates ◽  
Nerve Muscle ◽  
Long Endurance ◽  
Experimental Disturbance

As was pointed out ten years ago by Wedenski, from telephone observations of the negative variation, by Waller, from galvanometric observations of the same, and by Bowditch from the observation of long-persisting excitability in the nerves of temporarily curarised mammals, nerve is now admitted to be practically inexhaustible. The apparent exhaustion of nerve when a nerve-muscle preparation is submitted to prolonged excitation is, as was first demonstrated in Bernstein’s experiment, not an exhaustion of nerve, but an exhaustion of the organ of intermediation between nerve and muscle, which, as pointed out by Waller, is the weak link in the neuro-muscular chain, being the point at which functional failure is first manifested, in fatigue, in nerve degeneration, in intoxication by curare (Bernard), and at death. Taking as the sign of action artificially excited in a nerve, the negative variation of its current of rest (du Bois-Reymond) or current of injury (Hermann), the long endurance by nerve of excitation excessive in strength and in length, is well shown by prolonged photographic records of the galvanometric indications, which exhibit little or no decline, in marked contrast with similar records of the negative variation of muscle which declines pari passu with the declining contraction due to fatigue of the motor end plates. This steady regularity of response renders nerve pre-eminently suitable to the systematic study of its experimental disturbance.

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