Effect of denervation on a steady electric current generated at the end‐plate region of rat skeletal muscle.

Betz, William J.; Caldwell, John H.; Harris, G L

doi:10.1113/jphysiol.1986.sp016037

Cited by 15 publications

(9 citation statements)

References 37 publications

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“…5 shows the effect in a 10-ddenervated muscle fiber of replacing normal Krebs with a Cl--free solution . As described previously - (Betz et al, 1986), the effect on V, (A) in a denervated fiber is quite different from that observed for normal fibers . We never observed in denervated fibers the transient depolarization that, in normal muscle, precedes the steady state hyperpolarization .…”

Section: Effects Of Removing External CL -mentioning

confidence: 51%

Evidence for active chloride accumulation in normal and denervated rat lumbrical muscle.

Harris¹,

Betz²

1987

The Journal of General Physiology

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Intraceilular CI-activity (aict) was measured with Cl--sensitive microelectrodes in normal and denervated rat lumbrical muscle. In normal muscle bathed in normal Krebs solution, a~l lay close to that predicted by the Nernst equation• The addition of 9-anthracene carboxylic acid, which blocks CI-conductance, caused alcl to increase far above that predicted by a passive distribution. Furosemide (10 vM) reversibly blocked this accumulation• After muscle denervation, a~l progressively increased for 1-2 wk. The rise occurred in two stages. The initial stage (1-3 d after denervation) reflected passive CIaccumulation owing to membrane depolarization. At later times, a~l continued to increase, with no further change in membrane potential, which suggests an active uptake mechanism. This rise approximately coincided with the natural reduction in membrane conductance to CI-that occurs several days after denervation. Na + replacement, K + replacement, and furosemide each reversibly blocked the active CI-accumulation in denervated muscle. Quantitative estimates suggested that there was little difference between Ci-flux rates in normal and denervated muscles. The results can be explained by assuming that, in normal muscle, an active accumulation mechanism operates, but that CI-lies close to equilibrium owing to the high membrane conductance to CI-. The rise• i m acl after denervation can be accounted for by the membrane depolarization, the reduction in membrane Cl-conductance, and the nearly unaltered action of an inwardly directed CI-"pump."

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Section: Effects Of Removing External CL -mentioning

confidence: 51%

Evidence for active chloride accumulation in normal and denervated rat lumbrical muscle.

Harris¹,

Betz²

1987

The Journal of General Physiology

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“…There was an initial hyperpolarization of about 30 mV before Em suddenly dropped to stabilize at around -35 mV (cf. Betz et al 1986). This behaviour is similar to that of the cardiac Purkinje fibre under normal conditions, where K.+ removal causes an immediate drop in Em to around -35 mV (e.g.…”

Section: Effect Of Removal Of External K+mentioning

confidence: 99%

“…There was an initial hyperpolarization of about 30 mV before Em suddenly dropped to stabilize at around -35 mV (cf. Betz et al 1986 Ellis, 1977;Gadsby & Cranefield, 1977) and is possibly caused by reduction of the K+ conductance (inward rectification). Readdition of K+ resulted in a large and rapid hyperpolarization in which Em became more negative than before the removal of K+.…”

Section: Effect Of Removal Of External K+mentioning

confidence: 99%

“…In experiments relying mainly on brief, independent impalements with voltage and Cl--sensitive electrodes, Harris & Betz (1987) showed that the high a', of denervated muscle was reversibly reduced to that predicted from a passive distribution by the removal of external Na+ or K+ or by application of frusemide. Thus Na+, K+, Cl-co-transport seems likely to be responsible (see also Betz et al 1984;Betz, Caldwell & Harris, 1986). …”

Section: Introductionmentioning

confidence: 99%

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Intracellular chloride and the mechanism for its accumulation in rat lumbrical muscle.

Aickin

Betz

Harris

1989

The Journal of Physiology

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SUMMARY1. Double-barrelled Cl--sensitive microelectrodes have been used to measure the intracellular Cl-activity (a',) and membrane potential (Em) in rat lumbrical muscles. The mean Cl-equilibrium potential (Ecl), calculated from the measured aC1 in sixty fibres, was 29 + 25 mV (S.D. of an observation) less negative than Em. The value of a', was higher than would be expected for a passive distribution, by a mean 1P4 + 1 2 mm. The mean Em was -59-5 + 8-2 mV. 3. If lack of selectivity of the Cl--sensitive ion exchanger and the intracellular presence of interfering anions, assumed to be responsible for the apparent al1 recorded in Cl--depleted fibres, were also responsible for the apparently non-passive Cl-distribution recorded under normal conditions, the difference between the calculated EC1 and Em would increase at more negative potentials. This was not observed over a range of Em values between -46 and -84 mV. 4. Inhibition of the Cl-permeability by application of 9-anthracene carboxylic acid (9-AC) resulted in an immediate rise in ai1 and hyperpolarization. An ai1 up to 40 mm higher, or eleven times higher, than that predicted by a passive distribution was recorded. Application of 9-AC after depletion of intracellular Cl-in Cl--free solution had no effect on either the apparent ai1 or Em.5. It is concluded that Cl-ions are actively accumulated by the skeletal muscle fibre and that the Cl-distribution therefore normally exerts a depolarizing influence.6. In the presence of 9-AC and nominal absence of CO2 and HC03-, readdition of Cl-to Cl--depleted fibres resulted in a substantial rise in a', and a small, maintained 7. Neither application of CO2 and HCQ3-nor application of DIDS (4,4'-diisothiocyanostilbene-2,2'-disulphonic acid) had any effect on the accumulation of Cl-ions. This suggests that Cl--HC03-exchange is not involved.8. Removal of Na+ or K+ resulted in a limited rise in a'1 such that EC1 approximated to Em. Removal of both cations had no greater effect than the absence of only one. Readdition of the cations caused an immediate accumulation of Cl-ions and divergence of Ec1 from Em. This was largely inhibited by the presence of frusemide. These results suggest that a Na+, K+, Cl-co-transport mechanism is responsible for the inward transport of Cl-.

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“…For example, binding of Ba 2+ to IRK occurs within 20-200 ms of the ion's presentation [3,29,36], and membrane resistance increases within 30 s [25], but actual membrane depolarization requires several minutes [7,10,15,19,25,37]. While in principle, such discrepancies could result from the absence or inactivity of IRK under the special conditions of the different experiments, that notion has been ruled out by single-cell measurements via the cell-attached patch procedure, where single IRK channel activity was recorded, and their blockade was compared with changes of the background cellular current [16].…”

Section: Introductionmentioning

confidence: 99%

In skeletal muscle the relaxation of the resting membrane potential induced by K+ permeability changes depends on Cl? transport

Foppen

2004

Pfl�gers Archiv European Journal of Physiology

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In resting skeletal muscle the potassium permeability is determined by the permeability of the inwardly potassium rectifier. Continuous resting membrane potential measurements are done to follow the relaxation of the membrane potential upon changes in potassium permeability. Inhibition of the inwardly potassium rectifier, by extracellular application of 80 microM Ba(2+), causes the cell to depolarize with mean time constants as follows: in control 127+/-7 s ( n=23), in the presence of bumetanide, as an inhibitor of the Na(+)/K(+)/2Cl(-) cotransporter, 182+/-23 s ( n=7), in hypertonic media (340 mosmol/kg) 90.4+/-5 s ( n=7) and in reduced chloride medium 64+/-8 s ( n=5). The depolarizing relaxation of the membrane potential induced by reduction of extracellular potassium produces similar results. These time constants are at least three orders of magnitude slower than the time constants reported in the literature for the inhibition of the inwardly potassium rectifier. Chloride transport affects the relaxation of the membrane potential. A further characterization of chloride transport is done by following the relaxation of the membrane potential upon application of chloride transport modulators. It is argued that the electroneutral cotransporter, for which a flux was preliminarily estimated of 13.4 pmol cm(-2) s(-1), has a considerable role in the processes related to the resting membrane potential.

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Effect of denervation on a steady electric current generated at the end‐plate region of rat skeletal muscle.

Cited by 15 publications

References 37 publications

Evidence for active chloride accumulation in normal and denervated rat lumbrical muscle.

Evidence for active chloride accumulation in normal and denervated rat lumbrical muscle.

Intracellular chloride and the mechanism for its accumulation in rat lumbrical muscle.

In skeletal muscle the relaxation of the resting membrane potential induced by K+ permeability changes depends on Cl? transport

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