bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ionic basis for electrical properties of tonic fibres in rat extraocular muscles
Authors: Bondi Ardith Y. , Chiarandini D. J. 
Published: December 2014

1. The ionic conductances underlying some of the electrophysiological properties of multiply innervated or tonic fibres of rat extraocular muscles were examined in vitro with double‐barrelled micro‐electrodes.2. Exposure of the muscle to a Cl‐free saline did not change the effective resistance (Reff) of tonic fibres which was 5·14 ± 0·45 MΩ (n = 7) in control saline and 4·78 ± 0·45 MΩ (n = 12) in Cl‐free saline (P > 0·1). In contrast, in singly innervated or twitch fibres Cl removal increased Reff from 1·77 ± 0·21 MΩ (n = 19) to 2·69 ± 0·12 MΩ (n = 22) (P < 0·001).3. Tonic fibres with membrane potentials restored to ‐ 80 mV by injecting current responded to intracellular depolarizing pulses with a brief, slow response (slow peak potential) which added to the rising phase of the electrotonic potential. The slow peak potential began at a membrane potential of ‐ 40 to ‐ 35 mV and was graded. Increasing depolarizations evoked faster and larger responses which did not over‐shoot the zero level of membrane potential.4. The slow peak potential was not blocked by 10 μ
M‐D‐600 hydrochloride but was markedly reduced by the absence of Na and by 10 μ
M‐tetrodotoxin. The response was broadened about five times by 25 m
M‐tetraethylammonium.5. Raising bath temperature from 21‐25 °C to 37 °C reversibly depressed and shortened the slow peak potential but did not transform it into an action potential.6. It is concluded that the characteristic high Reff of tonic fibres results from a lack of a membrane conductance to Cl and that the slow peak potential involves the transient activation of Na and K channels which are pharmacologically similar to the respective channels of twitch fibres.
Evidence for a dual pelvic nerve influence on large bowel motility in the cat
Authors: Fasth S. , Hultén L. , Nordgren S. 
Published: December 2014

1. The effects of efferent electric pelvic nerve stimulation on colorectal motility and blood flow with emphasis on the motor responses in consecutive colonic and rectal segments were studied in anaesthetized cats. It was considered of particular interest to explore whether selective pharmacological blockade and graded nerve stimulations might reveal the presence of functionally differentiated efferent fibres controlling colonic motility.2. Pelvic nerve stimulation induced immediate and sustained colorectal contractions and a simultaneous increase of the over‐all colonic blood flow. The excitatory responses declined immediately on cessation of a shortlasting stimulation (< 2 min); after a longlasting one, however, the rectal contraction was maintained for several min.3. The colonic contraction on pelvic nerve stimulation remained unchanged after atropine but was delayed in onset. Moreover, in the transverse and distal colon it was preceded by a relaxation which was most pronounced in the distal part. The vasodilator response was unchanged.4. After atropine the rectal segment showed a purely relaxatory response. Despite continuous pelvic nerve stimulation the relaxation vanished, however, and rectal volume returned to resting level with 3‐5 min. On cessation of such a prolonged stimulation there was a marked rectal ‘after‐contraction’.5. The excitation thresholds for the efferent nerve fibres eliciting these different responses could not be separated. The motility and the vasodilator responses were not influenced by adrenergic or by serotoninergic blockade.6. The results indicate that direct preganglionic stimulation of the cat pelvic nerves activates intramural cholinergic excitatory neurones as well as non‐cholinergic excitatory neurones and furthermore, non‐adrenergic non‐cholinergic inhibitory neurones, which together result in most complex colonic and rectal motor responses. From a functional point of view these centrally controlled responses may well be independently controlled by separate preganglionic neurones though they do not differ concerning excitation thresholds.7. The effects are consistent with a dual function of the distal colon and rectum. Such a dual parasympathetic influence on the large bowel simulates the vagal control of the stomach, where specific vagal relaxatory fibres convey a reflex widening of the corpus‐fundus reservoir during food intake.
Specific features of smooth muscle cells recorded from the placental region of the myometrium of pregnant rats
Authors: Kanda S. , Kuriyama H. 
Published: December 2014

The muscle membrane and contractile properties of placental and non‐placental regions of pregnant and postpartum myometria of the rat were investigated.1. The membrane potential of the myometrium varied during the progress of gestation, but the membrane potential in the placental region was consistently higher than that in the non‐placental region up to the last stage of gestation. The maximum difference in the membrane potential recorded from both regions was observed at 17‐21 days gestation.2. The conduction velocity of the excitation measured from muscle cells of the non‐placental region was consistently larger than that of the placental region at any stage of the gestation (7‐22 days). At 7 days gestation, the conduction velocity in the placental region could not be measured due to widely scattered values of the latencies for the spike generation. During the progress of gestation, the conduction velocity increased, and the value was consistently larger (about 10 times) in the nonplacental region than that in the placental region at any stage of gestation up to the last stage.3. The length constant of the tissue measured from the non‐placental region was larger (2·3 mm) than that in the placental region (1·1 mm) at 14 days gestation. The propagation of the excitation seems to be blocked from the cells of the non‐placental region to the placental region, but not vice versa.4. The shape of the spike in the non‐placental region changed markedly during the progress of gestation. The spike could be recorded from the cells of the placental region but not consistently. However, the electrical activity of muscle cells recorded at the full term was much the same in both regions.5. Various concentrations of [K]o or [Na]o modified the membrane potential. The differences in the membrane response to the above ionic environments appeared more significantly at the different stages of gestation, rather than topical differences.6. Sensitivity of the muscle cell membrane to oxytocin in the placental region was higher than that in the non‐placental region at any stage of gestation, while that to prostaglandin F2α was much the same in the cells recorded from both regions.7. At 8 days gestation, the circular muscle layer is lost from the area of implantation and only the longitudinal muscle layer remains. The width of the placenta and the thickness of the muscle layer increased during the progress of gestation.8. From the above results, the role of smooth muscle cells in the placental region is discussed in relation to hormonal controls in the myometrium, i.e. the activity of the muscle cell membrane in the placental region was markedly suppressed up to the last stage of gestation, however, there was no apparent direct relation between the inhibitory responses and the actions of progesterone.
Relations between the inactivation of sodium channels and the immobilization of gating charge in frog myelinated nerve
Authors: Nonner W. 
Published: December 2014

1. Single, voltage‐clamped nerve fibres of Rana esculenta were stimulated with ‘P/2’ pulse patterns for measuring Na and gating currents at 13 °C.2. Gating currents during test pulses to ‐ 122 or + 10 mV were measured after 45 msec conditioning steps to voltages between ‐ 122 and ‐ 18 mV. As the conditioning voltage was made more positive than ‐ 80 mV, the movable gating charge diminished along a sigmoid curve, approaching a value of nearly one third of the maximum charge. On the other hand, Na inactivation began at a more negative potential and proceeded to undetectable levels.3. After a depolarizing prepulse, both time constant and size of the charge movment depended less steeply on the test voltage than normally. The prepulse reduced gating currents associated with steps from ‐ 122 to test voltages ≥ ‐ 40 mV, but enhanced gating currents obtained with test voltages < ‐ 40 mV.4. Increasing the duration of a depolarizing pulse (‐ 54 to + 42 mV) reduced the fast ‘off’ gating current at the end of the pulse and enhanced a slow component. Their total charge corresponded approximately to that carried during the pulse. During depolarization, Na current inactivated in a fast and a slow phase. The fast phase was also reflected in the loss of fast charge movement (immobilization) as seen after the pulse was interrupted at various durations.5. The available Na current and the fast movement of gating charge diminished in parallel during prepulses more positive than ‐ 54 mV, and recovered in parallel upon repolarization to levels between ‐ 102 and ‐ 46 mV. During prepulses between ‐ 62 and ‐ 78 mV, however, Na inactivation occurred up to 4 times faster than charge immobilization. Also, at ‐ 78 mV, Na current was inactivated 3 times faster than it recovered.6. These findings indicate that Na inactivation and charge immobilization are linked, but proceed with high‐order kinetics. The simplest scheme that accounts for their relation is [Formula: see text] Depending on voltage, either state h2 (E > ‐ 45 mV) or h3 (E < ‐ 45 mV) becomes kinetically undetectable.7. A model of the Na channel is developed in which inactivation gains most of its voltage dependence by a coupling to the fast charge movement (activation). The model is shown to be quantitatively consistent with the results. In particular, the change of kinetics observed near ‐ 45 mV can be explained as an effect of the redistribution of charges on the inactivation process.
Co‐ordination of head and eyes in the gaze changing behaviour of cats
Authors: Blakemore Colin , Donaghy Michael 
Published: December 2014

1. Saccadic changes of gaze have been studied in conscious cats implanted with electro‐oculographic electrodes to register eye position and held in a device for measuring head position.2. When the head is free to move, almost all saccades larger than 4 deg in amplitude are accompanied by head rotation. This head movement starts at a variable delay after the beginning of the eye movement. Most frequently, the latency is 30 msec.3. After finishing its saccade, the eye rotates retrogressively in the orbit so as to maintain a constant direction of gaze during the remaining portion of the head movement. This compensatory eye movement has an average gain of 0·96 in the absence of visual feed‐back.4. The duration and peak velocity characteristics of head‐fixed saccades were measured. A typical horizontal saccade of 20 deg in amplitude attains a peak velocity of 250 deg/sec and lasts 110 msec. The duration—amplitude relationship increases by 2·1 msec/deg.5. Saccades aimed obliquely within the orbit possess the same duration/peak—velocity/amplitude relationships as purely horizontal saccades. Consequently, the horizontal component of an oblique saccade lasts longer, and has a lower peak velocity, than a purely horizontal saccade of the same amplitude as this component. This finding is discussed in relation to brain‐stem control of oblique saccades.6. A saccade is initially programmed to achieve the desired gaze change without aid from the head. Consequently, the saccade is slowed down so as to prevent gaze overshoot when the head moves too. Since this saccadic attenuation occurs even during passive head movement, it must be due to feed‐back from peripheral sensors of head rotation, and probably represents the initial stage of the compensatory eye movement.7. Since the axes of horizontal head and eye rotation are horizontally separated, it may be predicted that the gain of compensatory eye movements must rise as the viewing distance decreases if they are to maintain fixation during head movements. This prediction was confirmed.
Studies on the mechanisms of renin release from rat kidney slices: calcium, sodium and metabolic inhibition
Authors: Lyons H. Jay 
Published: December 2014

1. The coincident release of renin and lactic dehydrogenase (LDH) from rat renal cortical tissue slices was studied during calcium depletion, metabolic inhibition, and with the addition of ouabain (1 m
M) to the incubation medium.2. The results indicate that although LDH accumulated in the medium during incubation, the pattern was dissimilar to that of renin. Ouabain significantly inhibited renin release in calcium containing medium, but had no effect on LDH release. Renin release was potentiated in calcium ‘free’ media, while calcium depletion reduced the release of LDH.3. The addition of potassium cyanide (2 m
M) significantly inhibited the release of renin from these tissue slices. Cyanide was ineffective, however, when administered in calcium ‘free’ medium.4. At reduced incubation temperatures (5 °C) the release of both renin and LDH were significantly reduced.5. Medium sodium depletion caused a significant inhibition of renin release. The simultaneous removal of calcium from the medium did not restore renin release to control levels.6. These results are not consistent with the hypothesis that spontaneous renin release during calcium depletion and metabolic inhibition is a result of cell enlargement and increased membrane permeability. On the other hand, the in vitro release of renin during these experiments appeared to be inversely related to the intracellular concentration of calcium.
The variance of sodium current fluctuations at the node of Ranvier
Authors: Sigworth F. J. 
Published: December 2014

1. Single myelinated nerve fibres 12‐17 μm in diameter from Rana temporaria and Rana pipiens were voltage clamped at 2‐5 °C. Potassium currents were blocked by internal Cs+ and external tetraethylammonium ion. Series resistance compensation was employed.2. Sets of 80‐512 identical, 20 ms depolarizations were applied, with the pulses repeated at intervals of 300‐600 ms. The resulting membrane current records, filtered at 5 kHz, showed record‐to‐record variations of the current on the order of 1%. From each set of records the time course of the mean current and the time course of the variance were calculated.3. The variance was assumed to arise primarily from two independent sources of current fluctuations: the stochastic gating of sodium channels and the thermal noise background in the voltage clamp. Measurement of the passive properties of the nerve preparation allowed the thermal noise variance to be estimated, and these estimates accounted for the variance observed in the presence of tetrodotoxin and at the reversal potential.4. After the variance σ2 was corrected for the contribution from the background, its relationship to the mean current I could be fitted by the function σ2 = iI—I2/N expected for N independent channels having one non‐zero conductance level. The single channel currents i corresponded to a single‐channel chord conductance γ = 6·4 ± 0·9 pS (S.D.; n = 14). No significant difference in γ was observed between the two species of frogs. The size of the total population of channels ranged from 20,000 to 46,000.5. The voltage dependence of i corresponded closely to the form of the instantaneous current—voltage relationship of the sodium conductance, except at the smallest depolarizations. The small values of i at small depolarizations may have resulted from the filtering of high‐frequency components of the fluctuations.6. It is concluded that sodium channels have only two primary levels of conductance, corresponding to ‘open’ and ‘closed’ states of the channel.7. The fraction pmax of channels open at the time of the peak conductance was found to be 0·59 ± 0·08 (S.D.; n = 5) and 0·9 ± 0·1 (S.D.; n = 3) for depolarizations to ‐5 and +125 mV, respectively. (50 ms hyperpolarizations to ‐105 mV preceded the depolarizations in each case.) These values are similar to those predicted by Hodgkin‐Huxley kinetics.8. Fluctuations in the firing threshold of neurones are expected from the stochastic gating of sodium channels. A prediction of the size of these fluctuations based on the measured properties of the channels gives a value of about 1% for the relative spread, which agrees with experimental values in the literature.
Luminal acidification by the perfused rat cauda epididymidis
Authors: Au C. L. , Wong P. Y. D. 
Published: December 2014

1. Acid secretion by the rat cauda epididymidis was studied by microperfusion of the epididymal duct and by measuring the pH of the perfusate at a constant pCO2 using a micro pH sensitive electrode. The rate of acidification was expressed as the rate of fall of intraluminal bicarbonate per cm duct per min.2. When the cauda epididymal duct was perfused with normal bicarbonate solution, the luminal bicarbonate concentration fell at a rate of 0.59 ± 0.39 n‐equiv cm−1 min−1 (mean ±
s.e., n = 22).3. The rate of luminal acidification was independent of the perfusion rate but was dependent on the concentration of bicarbonate in the perfusion fluid. The rate of fall of luminal bicarbonate increased with increasing bicarbonate concentration and showed saturation at an intraluminal bicarbonate concentration of 25 m‐mole/l.4. Acidification was abolished in the absence of intraluminal sodium ions. This may suggest a linked sodium reabsorption and hydrogen ion secretion.5. Acidification of the luminal fluid was studied under different acid‐base conditions. In animals undergoing metabolic acidosis, the rate of acidification was enhanced, and conversely in animals undergoing metabolic alkalosis, the rate was depressed.6. Intravenous infusion of acetazolamide into rats at a dose rate of 20 mg/kg.hr markedly inhibited the acidification process. This effect was still observed in animals undergoing metabolic acidosis. Acetazolamide (10−5
m) applied luminally was found to have no effect but higher concentration (10−4
m) was found to inhibit acidification by 50%.7. The role of acidification of the epididymal fluid in sperm maturation was discussed.
A comparison of the horizontal and vertical vestibulo‐ocular reflexes of the rabbit
Authors: Barmack N. H. 
Published: December 2014

1. The gain and phase of the horizontal (H.v.o.r.) and vertical (V.v.o.r.) vestibulo‐ocular reflexes were measured in rabbits. The V.v.o.r. was evoked by sinusoidal rolls about the longitudinal axis of the rabbit. This axis was maintained at different orientations with respect to the earth horizontal axis: V.v.o.r. 0°, prone; V.v.o.r. 90°, ‘nose‐up’; V.v.o.r. 180°, supine; V.v.o.r. 0°L, left side down.2. In contrast to the H.v.o.r., the V.v.o.r. 0° had a higher gain (eye velocity/head velocity) and a smaller phase lead (eye position + 180° with respect to head position) at low frequencies of sinusoidal vestibular stimulation (± 10 deg, 0·005‐0·05 Hz). At higher frequencies (0·05‐0·8 Hz), the H.v.o.r. and V.v.o.r. 0° were equivalent in both gain and phase.3. The low‐frequency gain of the V.v.o.r. was smallest in the ‘nose‐up’ orientation. The V.v.o.r. 90° was equivalent in both gain and phase to the H.v.o.r. over the entire range of frequencies tested (0·005‐0·8 Hz). Threshold angular accelerations for the H.v.o.r. and V.v.o.r. 90° were below 0·04 deg/sec2.4. The compensatory eye movements of the H.v.o.r. were frequently interrupted by anticompensatory re‐setting eye movements. These anticompensatory re‐setting eye movements were present in the V.v.o.r. 90°, but not in the V.v.o.r. 0°.5. An estimate gain and phase of the otolithic component of the V.v.o.r. 0° was derived by subtraction of the V.v.o.r. 90° (semicircular canal signal) from the V.v.o.r. 0° (semicircular canal signal+otolith signal). This procedure was based on the assumption that the signals from the otolith organs and vertical semicircular canals combine linearly.6. The V.v.o.r. 180° provided an interesting test of the assumption of linear combination of otolithic and semicircular canal signals by reversing the phase of the modulated otolithic signal. The data indicated that the V.v.o.r. 180° is non‐linear.
The magnesium dependence of sodium‐pump‐mediated sodium—potassium and sodium—sodium exchange in intact human red cells
Authors: Flatman Peter W. , Lew Virgilio L. 
Published: December 2014

1. The magnesium content of human red blood cells was controlled by varying the magnesium concentration in the medium in the presence of the ionophore A23187. The new magnesium levels attained were very stable, which allowed the magnesium dependence of the sodium pump to be investigated.2. The effects of magnesium were shown to occur at the inner surface of the red cell membrane for the range of magnesium concentrations tested (10−7 to 6 × 10−3
m).3. At intracellular ionized magnesium concentrations below 0.8 m
m the activation of ouabain‐sensitive sodium—potassium exchange by internal ionized magnesium could be resolved into two or three components: (a) a small component, about 5% of the maximum flux, which is apparently independent of the ionized magnesium concentration below 2 μ
m, (b) a saturating component with a K½ of between 30 and 45 μ
m, and possibly (c) a component which increases linearly with ionized magnesium concentration and which only becomes apparent at concentrations above 0.1 m
m.4. At intracellular ionized magnesium concentrations below 0.8 m
m, activation of ouabain‐sensitive sodium—sodium exchange by internal ionized magnesium could be resolved into two components: (a) a small component, about 6% of the maximal flux, which is apparently independent of the ionized magnesium concentration below 2 μ
m, and (b) a saturating component with a K½ of about 9 μ
m. At ionized magnesium concentrations between about 0.2 and 0.8 m
m the rate of sodium—sodium exchange remained constant at the maximal level.5. The intracellular concentration of ATP decreased and the ADP concentration increased as the magnesium content of the cells was reduced from the normal level. A small increase in ATP and a small decrease in ADP was seen when the magnesium content was increased above the normal level. The variation in the ATP: ADP ratio from 2.5 at very low magnesium levels to about 6 at normal magnesium levels can account, at least in part, for the different K½ values of sodium—potassium and sodium—sodium exchange.6. When the concentration of ionized magnesium was increased above about 0.8 m
m both sodium—potassium and sodium—sodium exchange were inhibited. Sodium—sodium exchange was more strongly inhibited than sodium—potassium exchange.7. The possible sites of action of magnesium in the sodium pump cycle are discussed.