Conduction velocities in amphibian skeletal muscle fibres exposed to hyperosmotic extracellular solutions.
Early quantitative analyses of conduction velocities in unmyelinated nerve studied in a constantly iso-osmotic volume conductor were extended to an analysis of the effects of varying extracellular osmolarities on conduction velocities of surface membrane action potentials in Rana esculenta skeletal muscle fibres. Previous papers had reported that skeletal muscle fibres exposed to a wide range of extracellular sucrose concentrations resemble perfect osmometers with increased extracellular osmolarity proportionally decreasing fibre volume and therefore diminishing fibre radius, a. However, classical electrolyte theory (Robinson and Stokes 1959, Electrolyte solutions 2nd edn. Butterworth & Co. pp 41-42) would then predict that the consequent increases in intracellular ionic strength would correspondingly decrease sarcoplasmic resistivity, R(i). An extension of the original cable analysis then demonstrated that the latter would precisely offset its expected effect of alterations in a on the fibre axial resistance, r(i), and leave action potential conduction velocity constant. In contrast, other reports (Hodgkin and Nakajima J Physiol 221:105-120, 1972) had suggested that R(i) increased with extracellular osmolarity, owing to alterations in cytosolic viscosity. This led to a prediction of a decreased conduction velocity. These opposing hypotheses were then tested in muscle fibres subject to just-suprathreshold stimulation at a Vaseline seal at one end and measuring action potentials and their first order derivatives, dV/dt, using 5-20 MOmega, 3 M KCl glass microelectrodes at defined distances away from the stimulus sites. Exposures to hyperosmotic, sucrose-containing, Ringer solutions then reversibly reduced both conduction velocity and maximum values of dV/dt. This was compatible with an increase in R(i) in the event that conduction depended upon a discharge of membrane capacitance by propagating local circuit currents through initially passive electrical elements. Conduction velocity then showed graded decreases with increasing extracellular osmolarity from 250-750 mOsm. Action potential waveforms through these osmolarity changes remained similar, including both early surface and the late after-depolarisation events reflecting transverse tubular activation. Quantitative comparisons of reduced-chi(2) values derived from a comparison of these results and the differing predictions from the two hypotheses strongly favoured the hypothesis in which R(i) increased rather than decreased with hyperosmolarity.
Chen
Zhongbo
Z
Physiological Laboratory, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK.
Hothi
Sandeep S
SS
Xu
Wei
W
Huang
Christopher L-H
CL
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism*; D003600:Cytosol / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D045604:Extracellular Fluid / Q000737:chemistry / Q000378:metabolism; D006982:Hypertonic Solutions / Q000494:pharmacology; D007552:Isotonic Solutions / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism*; D009994:Osmolar Concentration; D011893:Rana esculenta; D000077331:Ringer's Solution; D014783:Viscosity / Q000187:drug effects
D006982:Hypertonic Solutions; D007552:Isotonic Solutions; D000077331:Ringer's Solution