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Deprivation of external calcium causes sudden potentiation of the twitch response of single muscle fibers. The potentiation was 64 4-8 %. Potentiation is simultaneous with membrane depolarization occurring after Ca +÷ removal. This depolarization amounted to 9 4-2 my. Ca ++ removal also alters the action potential. 3 rain after calcium withdrawal, action potential amplitude fell by 36 4-3 my; maximum rates of rise and fall of the spike decreased by 55 4-5 and 63 4-5 % respectively. Changes in shape of the A. P. differ from those seen with other potentiators of the twitch response, such as Zn ++. After short exposure to calcium-free media, potassium-induced contractures show potentiation of peak tension. The S-shaped curve relating potassium contracture tension to log [K]o shifts to the left after such treatment. Calcium deprivation also increased the rate of relaxation of the contractures. This effect depends on the duration of calcium deprivation, and is probably related to the effect of calcium lack on the membrane. The change in relaxation occurred immediately after calcium deprivation, and was reversed by sudden readmission of calcium. Relaxation of twitch and tetanus responses also were affected by Ca lack, but not as rapidly as potassium contractures. The results suggest that external calcium is not directly involved in the process responsible for tension development, supporting the view that this process is mediated by translocation of intracellular calcium. The relaxation process, however, appears to be rapidly affected by deprivation of external calcium.Normally the contractile response of muscle fibers is triggered by the lowering of the fiber m e m b r a n e potential to a threshold value at which the excitationcontraction coupling (ECC) process begins to be effective (1--4). T h e hypothesis which postulated t h a t calcium ions entering the fibers from the extracellular space upon depolarization of the m e m b r a n e activated the contractile material (5, 6) appears to be inadequate on the basis of theoretically calculated diffusion delays (4,7,8). However, the presence in the interior of the fiber of the system of transverse tubules which open out directly into the external space could reduce such delays (9, 10).

The effects on the Schwann cell electrical potential of external ionic concentrations and of K-strophanthoside were investigated. Increasing (K)o depolarized the cell. The potential is related to the logarithm of (K)o in a quasi-linear fashion. The linear portion of the curve has a slope of 45 mv/tenfold change in (K)o. Diminutions of (Na)o and (C1)o produced only small variations in the potential. Calcium and magnesium can be replaced by 44 mM calcium without altering the potential. Increase of (Ca)o to 88 mM produced about 10 mv hyperpolarization. The cell was hyperpolarized by 11 mv and 4 mv within 1 min after applying K-strophanthoside at concentrations of 10 .8 and 10 -5 M, respectively. No variations of cellular potassium, sodium, or chloride were observed 3 rain after applying the glycoside. The hyperpolarization caused by 10 .3 M K-strophanthoside was not observed when (K)o was diminished to 1 or 0.1 m~ or was increased to 30 mM. At a (K)o of 30 mu, 10 .2 M strophanthoside was required to produce the hyperpolarizing effect. In high calcium, the cell was further hyperpolarized by the glycoside. The initial hyperpolarization caused by the glycoside was followed by a gradual depolarization and a decrease of the cellular potassium concentration. The results indicate that the Schwann cell potential of about --40 mv is due to ionic diffusion, mainly of potassium, and to a cardiac glycoside-sensitive ion transport process.Previous work (1, 2) carried out in single nerve fibers of the squid, Sepioteuthis sepioidea, revealed t h a t across the plasma m e m b r a n e of the S c h w a n n cell (Del Rio H o r t e g a ' s peripheral glial cell), there is an electrical potential difference of a p p r o x i m a t e l y -4 0 my, the interior negative with respect to the outside solution. It was found also that the m a g n i t u d e of the S c h w a n n cell electrical potential, even the largest recorded, is always smaller t h a n the resting potential of the neighboring axon. This electrical potential remains a p p a r e n t l y unchanged, within 1 my, during the c o n d u c t i o n of a single nerve impulse. 47The Journal of General Physiologyon May 11, 2018 jgp.rupress.org Downloaded from http://doi.org/10.1085/jgp.51.1.47 Published Online: 1 January, 1968 | Supp Info:The present investigation was undertaken to determine the nature of this electrical potential difference across the Schwann cell plasma membrane. The experiments deal with: (I) the effects on the Schwann cell and axon electrical potentials of different external potassium, sodium, chloride, and calcium concentrations, and (II) the effects on the electrical potential and the electrolyte concentrations of the Schwann cell of a cardiac glycoside, K-strophanthoside, added to normal seawater and to seawater with different potassium and calcium concentrations. The effect of the glycoside on the axon resting and action potentials was determined also in the same nerve fibers.The results of the present work indicate that the Schwann cell electrical poten...

In fifty-seven resting nerve fibers of the squid Sepioteuthis sepioidea impaled from outside to inside, three potential difference (PD) levels were recorded. In twelve nerve fibers the position of the tip of the micropipette, when it was recording one of the I'D levels, was labeled with carmine, and the minute spot of dye was localized histologically. The first t,D level of --10 to --26 my, was located in the endoneurium cells; the second level, formed by a single PD of --33 to --46 mv, was located in the Schwann cell; and the third level, formed by a single eD of --50 to --65 my, was located in the axon. In sixteen nerve fibers the independence among these PD levels was demonstrated as follows. One micropipette was inserted inside the axon for recording its I'D; a second one was inserted inside one endoneurinm cell or inside one Schwann cell for recording the PD; and a third micropipette was inserted inside the axon to supply current to depolarize the axon. When the axon was depolarized no significant change was observed in the PD of either the endoneurium cell or the Schwann cell. In all nerve fibers action potentials were registered from the axon only. This identifies the axolemma (axon plasma membrane) as the excitable membrane. I N T R O D U C T I O NPhysiologists h a v e traditionally assumed t h a t the electrical p o t e n t i a l differences w h i c h c h a r a c t e r i z e the nerve fiber d u r i n g rest a n d d u r i n g the p r o p a g ation of an impulse occur across a surface m e m b r a n e of the nerve fiber. T h e identification of the structure c o r r e s p o n d i n g to the excitable m e m b r a n e of a n e r v e fiber has been a challenging p r o b l e m in neurobiology. S c h m i t t (1, 2), has suggested t h a t the excitable m e m b r a n e m a y be a c o m p o s i t e of the a x o l e m m a ( p l a s m a m e m b r a n e of the a x o n p r o p e r ) a n d the S c h w a n n i o47

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