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.

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 CHANGES IN MEMBRANE CHARACTERISTICS OF HEART MUSCLE DURING INHIBITION

1956 ◽  
Vol 40 (1) ◽  
pp. 135-145 ◽  
Author(s):  
W. Trautwein ◽  
S. W. Kuffler ◽  
C. Edwards
Keyword(s):  
Membrane Potential ◽  
Time Course ◽  
Heart Beat ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Pulse Technique ◽  
Spatial Spread ◽  
Length Constant ◽  
Membrane Changes ◽  
Acetylcholine Concentration

Membrane characteristics were studied in isolated muscle strands from auricles of frogs using the "square pulse" technique. Changes in the time course and spatial spread of subthreshold electrotonic potentials were measured. If acetylcholine is applied in concentrations which cause slowing or stoppage of the heart beat, the following changes are produced: (a) the length constant (λ) of the membrane is reduced, (b) the time constant is shortened. The effects are reversible and increase with acetylcholine concentration. The membrane changes caused by acetylcholine dimmish with time. It is concluded that during acetylcholine inhibition, as well as during vagal inhibition, the conductance of the muscle membrane is increased. Appreciable changes in the resting membrane potential need not accompany inhibition.

Trauma-induced changes of skeletal muscle membrane: decreased K+ and increased Na+ permeability

1997 ◽  
Vol 83 (4) ◽  
pp. 1096-1103 ◽  
Author(s):  
S. J. Hong ◽  
C. C. Chang
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Outward Current ◽  
Membrane Resistance ◽  
Muscle Membrane ◽  
End Plate ◽  
Plateau Potential ◽  
Permeability Changes ◽  
Underlying Mechanisms ◽  
Induced Changes

Hong, S. J., and C. C. Chang.Trauma-induced changes of skeletal muscle membrane: decreased K+ and increased Na+ permeability. J. Appl. Physiol. 83(4): 1096–1103, 1997.—Trauma of skeletal muscle causes membrane depolarization and reduces membrane resistance. The underlying mechanisms were studied in isolated mouse phrenic nerve diaphragms subject to sharp transections of muscle. Depolarization was most marked at the vicinity (∼1 mm) of trauma, where the membrane potential dropped rapidly from about −80 mV to zero and repolarized to about −25 mV. At the end-plate region (located ∼3 mm away from the cut end), the membrane gradually attained a plateau potential around −45 mV. The magnitude of depolarization was not reduced by inhibition of Na+, Ca2+, or Cl− channel, whereas the progress of depolarization was delayed in low-Na+ medium. Activation of the K+ channel with lemakalim induced some hyperpolarization at damaged site but produced a glybenclamide-sensitive outward current and hyperpolarization of end-plate region to the levels before trauma, as if there was no diminution of transmembrane K+gradient in this area. Appropriate elevation of extracellular K+ to stimulate K+ conductance also hyperpolarized the end-plate region. The results suggest that depolarization at regions remote from trauma is related to decreased K+ and increased Na+ permeability. The cytoplasma compartmentalization and permeability changes may protect muscle fiber from trauma.

The resting membrane potential of white muscle from brown trout (Salmo trutta) exposed to copper in soft, acidic water

2000 ◽  
Vol 203 (14) ◽  
pp. 2229-2236 ◽  
Author(s):  
M.W. Beaumont ◽  
E.W. Taylor ◽  
P.J. Butler
Keyword(s):  
Membrane Potential ◽  
Brown Trout ◽  
Salmo Trutta ◽  
White Muscle ◽  
Low Ph ◽  
Ammonium Ion ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
Brown Trout Salmo Trutta

Previously, the distribution of ammonia between the intracellular and extracellular compartments has been used to predict a significant depolarisation of the resting membrane potential (E(M)) of white muscle from brown trout (Salmo trutta) exposed to a sub-lethal combination of copper and low pH. However, this prediction is based upon two assumptions (i) a relatively high membrane permeability for the ammonium ion with respect to that for ammonia gas and (ii) that this is unaltered by exposure to copper and low pH. Since there is conflicting evidence in the literature of the validity of these assumptions, in the present study E(M) was directly measured in white muscle fibres of trout exposed to copper and low pH (E(M)=−52.2+/−4.9 mV) and compared with that of unexposed, control animals (E(M)=−86.5+/−2.9 mV) (means +/− s.e.m., N=6). In confirming the predicted depolarisation, these data support the hypothesis of electrophysiological impairment as a factor in the reduction in the swimming performance of trout exposed to these pollutants. In addition, the results of this study support the role of a significant permeability of the muscle membrane to NH(4)(+) in determining the distribution of ammonia in fish.

Catecholaminergic automatic activity in the rat pulmonary vein: electrophysiological differences between cardiac muscle in the left atrium and pulmonary vein

2009 ◽  
Vol 297 (1) ◽  
pp. H102-H108 ◽  
Author(s):  
Nicolas Doisne ◽  
Véronique Maupoil ◽  
Pierre Cosnay ◽  
Ian Findlay
Keyword(s):  
Membrane Potential ◽  
Electrical Activity ◽  
Cardiac Muscle ◽  
Left Atrium ◽  
Pulmonary Vein ◽  
Pulmonary Veins ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Ectopic Activity ◽  
Automatic Activity

Ectopic activity in cardiac muscle within pulmonary veins (PVs) is associated with the onset and the maintenance of atrial fibrillation in humans. The mechanism underlying this ectopic activity is unknown. Here we investigate automatic activity generated by catecholaminergic stimulation in the rat PV. Intracellular microelectrodes were used to record electrical activity in isolated strips of rat PV and left atrium (LA). The resting cardiac muscle membrane potential was lower in PV [−70 ± 1 (SE) mV, n = 8] than in LA (−85 ± 1 mV, n = 8). No spontaneous activity was recorded in PV or LA under basal conditions. Norepinephrine (10−5 M) induced first a hyperpolarization (−8 ± 1 mV in PV, −3 ± 1 mV in LA, n = 8 for both) then a slowly developing depolarization (+21 ± 2 mV after 15 min in PV, +1 ± 2 mV in LA) of the resting membrane potential. Automatic activity occurred only in PV; it was triggered at approximately −50 mV, and it occurred as repetitive bursts of slow action potentials. The diastolic membrane potential increased during a burst and slowly depolarized between bursts. Automatic activity in the PV was blocked by either atenolol or prazosine, and it could be generated with a mixture of cirazoline and isoprenaline. In both tissues, cirazoline (10−6 M) induced a depolarization (+37 ± 2 mV in PV, n = 5; +5 ± 1 mV in LA, n = 5), and isoprenaline (10−7 M) evoked a hyperpolarization (−11 ± 3 mV in PV, n = 7; −3 ± 1 mV in LA, n = 6). The differences in membrane potential and reaction to adrenergic stimulation lead to automatic electrical activity occurring specifically in cardiac muscle in the PV.

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)

Effect of nicotine and acetylcholine on crustacean muscle membrane potential

1986 ◽  
Vol 61 (2) ◽  
pp. 807-809
Author(s):  
R. F. Taylor ◽  
D. T. Frazier
Keyword(s):  
Membrane Potential ◽  
Muscle Tension ◽  
Muscle Cells ◽  
Abdominal Muscle ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Crustacean Muscle ◽  
Standard Glass ◽  
Before And After ◽  
Receptor Organ

We have investigated the effect of nicotine and acetylcholine on the resting membrane potential of the crayfish extensor muscle in order to determine whether crustacean muscle can be activated by cholinergic compounds. Intracellular recordings from individual deep extensor abdominal muscle cells were made using standard glass microelectrode techniques. The resting membrane potential was measured before and after treatment with glutamate, nicotine, and acetylcholine. Glutamate, which is a known activator of crayfish muscle, was used to determine whether the muscle cell preparation was viable and capable of responding to any of the test substances. Our results confirm that application of glutamate is associated with a depolarization of the muscle membrane. However, muscle cells showed no depolarization after treatment with nicotine (50 microM) or acetylcholine (66 microM). These results argue against the notion that increases in muscle tension may be responsible for the increased receptor organ discharge observed in the presence of nicotine. Rather, it supports the hypothesis that nicotine is acting directly on the mechanoreceptor membrane to change its sensitivity.

Limits to the Development of Fast Neuromuscular Transmission in Zebrafish

2001 ◽  
Vol 86 (6) ◽  
pp. 2951-2956 ◽  
Author(s):  
Pierre Drapeau ◽  
Robert R. Buss ◽  
Declan W. Ali ◽  
Pascal Legendre ◽  
Richard L. Rotundo
Keyword(s):  
Time Course ◽  
Neuromuscular Junctions ◽  
Synaptic Cleft ◽  
Muscle Membrane ◽  
High Concentration ◽  
Limited Region ◽  
Neuromuscular Synapses ◽  
Transmission Electron ◽  
Order Of Magnitude ◽  
High Concentrations

Zebrafish embryos have small and slow miniature end-plate currents (mEPCs), whereas only a few days later larval mEPCs are an order of magnitude larger and faster, being among the fastest of all neuromuscular synapses. To identify the bases for these changes we compared, in embryos and larvae, the properties and distributions of acetylcholine (ACh) receptors (AChRs) and acetylcholinesterase (AChE) as well as the ultrastructure of the developing neuromuscular junctions (NMJs). To mimic synaptic release, patches of muscle membrane were exposed briefly (for 1 ms) to a saturating concentration (10 mM) of ACh. The AChR deactivation kinetics were twice as slow in embryos compared with larvae. In both embryos and larvae, AChRs demonstrated open channel block by millimolar ACh, and this was detected during mEPCs, indicating that a high concentration of ACh is released at immature and mature NMJs. AChR and AChE distributions were compared using the selective fluorescently conjugated labels α-bungarotoxin and fasciculin 2, respectively. In larvae, punctate AChR clusters were detected whereas junctional AChE staining was less intense than that found at adult NMJs. Transmission electron microscopy revealed immature nerve endings in embryos that were closely juxtaposed to the surrounding muscle cells, whereas mature larval NMJs had a wider synaptic cleft with a conspicuous basal lamina over a limited region of synaptic contact. Our results indicate that ACh is released at high concentrations at immature NMJs, but its clearance is prolonged and the AChRs are dispersed, resulting in a slow mEPC time course until a mature cleft appears with densely packed faster AChRs and abundant AChE.

Sign in / Sign up

Export Citation Format

Share Document