bluuebunny/crossref_metadata_2025_split huggingface dataset:
Changes in renal haemodynamics and kidney weight during pregnancy in the unanaesthetized rat
Authors: Davison J. M. , Lindheimer M. D. 
Published: December 2014

1. Glomerular filtration rate ([3H]inulin clearance) and renal plasma flow (PAH clearance) were measured in unanaesthetized Sprague‐Dawley rats early in pregnancy (8‐10 days) and near term (18‐20 days); the results were compared with studies in virgin litter‐mates. Evidence of kidney growth was sought by analysing renal dry weights as well as [14C]choline incorporation into membrane phospholipids of renal cortical slices.2. Inulin clearances were similar early in pregnancy (pregnant 2·36 ± 0·12 (
S.E. of mean) vs. non‐pregnant 2·33 ± 0·10 ml./min) but near term values were significantly increased (pregnant 2·80 ± 0·05 vs. non‐pregnant 2·39 ± 0·05 ml./min, P < 0·001). PAH clearances were similar in pregnant and litter‐mate control animals at each stage of the study.3. Total renal weight increased significantly both early and late in pregnancy, but renal dry weights as well as [14C]choline incorporation were similar in pregnant and non‐pregnant animals both at 8‐10 days gestation and near term.4. Data confirm our previous findings on renal haemodynamics in anaesthetized rats. Observations that renal dry weight and [14C]choline incorporation into phospholipids are similar in litter‐mate pregnant and control animals suggests that renal enlargement in this species is due to increments in water content and not to accelerated growth.
Calcium efflux from Myxicola giant axons: effects of extracellular calcium and intracellular EGTA
Authors: Abercrombie Ronald F. , Sjodin Raymond A. 
Published: December 2014

1. 45Ca efflux was examined in Myxicola giant axons injected with 45CaCl2 or various concentrations of 45Ca/EGTA buffers. In axons injected with 45CaCl2, the Cao‐dependent Ca efflux in 1 m
M‐Cao was about half that in 10 m
M‐Cao.2. Axons injected with 45Ca/EGTA buffers consistently showed two types of results: in one type (B type), K½ for Cao activation was less than 1 m
M‐Cao. In the other type of result (A type), there was an additional Ca activation of Ca efflux. This additional efflux exhibited a linear dependence on Cao when the Cao values ranged between 1 m
M‐Cao and 10 m
M‐Cao.3. The B‐type result remained unchanged when the injected Ca/EGTA concentrations were varied. The A type result, however, changed as a function of Ca/EGTAi in the following way: (a) at a constant ratio of Ca/EGTAi = 8/10, the megnitude of the linear component of the Cao‐activated Ca efflux was reduced by increasing the intracellular concentration of (Ca/EGTA) buffer; and (b) at a ratio Ca/EGTA = 1/10, the linear component of the Cao‐activated Ca efflux appeared to acquire a slower time response to changes in Cao.4. Nao acts synergistically with Cao to produce the linear component of the Ca‐activated Ca efflux seen in the A type result.5. With axons containing 45Ca/EGTA buffers (total EGTAi = 1 m
M), changing the Ca/EGTA ratio by repetitive injections of CaCl2 did not increase 45Ca efflux by as great an amount as would be predicted if Cai2+ were controlled by the EGTA buffer alone.6. Cai2+ (measured by arsenazo III absorbance) is influenced by Cao irrespective of the presence of 1 m
M‐EGTA buffer inside the axon. There was a variability in the sensitivity of Cai to Cao that resembled the variability found in 45Ca efflux measurements.7. 45Ca influx is not affected by the concentration of Ca/EGTA buffer injected into the cell and appears to be only slightly, if at all, affected by increasing ionized Cai2+ from 0·016 to 0·56 μ
M in the injection medium.8. These results are consistent with the interpretation that the Ca efflux system of the Myxicola giant axon, or something controlling it, can exist in more than one state. One of these states, which exhibited a large Cao‐dependent Ca efflux, may represent axons in which Cai is poorly controlled by the natural endogenous Ca buffers.
Enhancement of synaptic function in cat motoneurones during peripheral sensory regeneration
Authors: Gallego R. , Kuno M. , Núñez R. , Snider W. D. 
Published: December 2014

1. Monosynaptic excitatory post‐synaptic potentials (e.p.s.p.s) were recorded from medial (m.g.) and lateral gastrocnemius (l.g.) motoneurones in the cat 2‐30 weeks after crushing the m.g. nerve.2. The mean amplitudes of homonymous and heteronymous e.p.s.p.s evoked from the m.g. nerve were initially depressed (2‐3 weeks after injury) and subsequently reached levels greater than normal for a period (8‐12 weeks) before slowly declining to about 70% of the normal values (by week 30).3. Monosynaptic e.p.s.p.s evoked in m.g. motoneurones from the intact l.g. nerve showed neither initial depression nor subsequent alterations following crush of the m.g. nerve.4. By the eighth week after nerve crush, about 70% of Group I and Group II sensory fibres in the m.g. nerve responded to muscle stretch, about 15% had regenerated into the muscle but did not respond to muscle stretch, and the remainder failed to regenerate across the neuroma formed by the nerve crush.5. Homonymous, monosynaptic e.p.s.p.s produced by impulses in single sensory fibres responding to stretch of the m.g. muscle were recorded 8 weeks after crush of the m.g. nerve. Their amplitude distribution was indistinguishable from that obtained in normal, unoperated cats. Thus, there was no evidence that functionally reinnervated sensory fibres are responsible for the enhanced phase of composite e.p.s.p.s observed during peripheral regeneration.6. When the m.g. nerve had been sectioned and prevented from regenerating into the muscle for 8 weeks, the amplitudes of homonymous and heteronymous e.p.s.p.s evoked from the m.g. nerve were significantly smaller than those observed in control animals. Thus, there was no evidence that non‐regenerating sensory fibres are responsible for the enhanced phase of composite e.p.s.p.s after nerve crush.7. It is suggested that the sensory fibres responsible for abnormally large composite e.p.s.p.s following nerve crush are those that regenerate into the muscle but do not achieve functional reinnervation. This possibility is discussed in relation to the increase in central synaptic efficacy observed after prolonged disuse of the sensory pathway.
Does glial uptake affect GABA responses? An intracellular study on rat dorsal root ganglion neurones in vitro
Authors: Desarmenien M. , Feltz P. , Headley P. M. 
Published: December 2014

1. Using single barrel pipettes, intracellular records were obtained from surface neurones of isolated rat dorsal root ganglia (DRG) impaled under microscopic vision.2. Responses to γ‐aminobutyric acid (GABA) were elicited either by ionophoresis or by placing drops of concentrated GABA solutions directly into the flow of superfusing Ringer. Using this latter method it was estimated that the GABA concentration eliciting threshold (≃ 1 mV) responses was 3‐20 μ
M.3. Short (≤ 1 sec) ionophoretic or drop administrations of GABA elicited depolarizing responses associated with an increased membrane conductance. With longer applications the initial depolarization was not sustained but decayed to a lower plateau level (desensitization) associated with a minimal conductance change.4. Low chloride superfusions did not affect subsequent responses to GABA unless GABA was also administered during the low chloride superfusion, in which case responses declined markedly. This suggests that GABA caused appreciable chloride fluxes when it was administered regularly (e.g. for 1 sec every minute).5. Glial GABA uptake was inhibited by adding 1 m
M‐β‐alanine or 0·25 m
M‐chlorpromazine to the bicarbonate‐Ringer superfusate or by substituting lithium for sodium in a Tris‐Ringer superfusate. Uptake inhibition had no consistent effect on any of the parameters studied, namely membrane potential, input resistance, amplitude and time course of responses to GABA, and GABA desensitization.6. Muscimol and isoguvacine, which are probably not substrates for the glial GABA carrier, elicited responses with time course and desensitization characteristics indistinguishable from those of responses to GABA.7. GABA superfused at concentrations as low as 1 μ
M could reduce responses to ionophoretic GABA, i.e. cause a desensitization of GABA receptors.8. It is concluded firstly that in DRG, glial uptake does not affect the amplitude or time course of responses to GABA when the neurone under study is close to the source of GABA; and secondly that desensitization can occur independently of GABA uptake.9. The findings are discussed in relation to their possible relevance to GABA systems in the central nervous system.
Current—voltage relations in the rod photoreceptor network of the turtle retina
Authors: Copenhagen D. R. , Owen W. G. 
Published: December 2014

1. Electrical coupling between rod photoreceptors was studied in the eyecup preparation of the snapping turtle, Chelydra serpentina, using intracellular micro‐electrodes.2. The spatial profiles of rod responses to a long narrow slit of light were determined. The peak response amplitudes were found to decline exponentially as the slit was moved from the most sensitive position in the receptive field of each rod. The mean length constant was 55·7 μm.3. Rods were simultaneously impaled in pairs and electrical coupling was demonstrated between the rods in seventeen of these pairs. No coupling was observed between rods separated by more than 110 μm. The transfer resistance, defined as the ratio of potential in the second rod (coupled potential) to the current injected into the first rod, varied from 0·2 to 13·2 MΩ.4. The waveform of the coupled potential was time varying, exhibiting a peak and subsequent relaxation phase. The time course of the relaxation phase was voltage‐dependent. At the cessation of current, the coupled potential rebounded beyond the resting potential and then decayed to the dark potential.5. Plots of input current versus coupled potential showed strong outward‐going rectification, chord transfer resistances being as much as 3·5 times lower for depolarizing currents.6. Simultaneous impalements were made of pairs of neighbouring red‐sensitive cones, of horizontal cells and rods, and of red‐sensitive cones and rods. No evidence of coupling between cones and rods were found, nor could feed‐back from horizontal cells onto rods be demonstrated; however, coupling between red‐sensitive cones was found. This coupling exhibited neither the marked time‐varying nor voltage‐dependent properties that characterize the rod‐rod coupling.7. Individual rods were impaled with independent current passing and voltage sensing micro‐electrodes. Pulses of current produced time‐varying potentials having relaxation and rebound phases. Current—voltage measurements showed a strong outward‐going rectification. Input resistances at the resting potential ranged up to 96 MΩ.8. Square grid and hexagonal lattice models of ohmic electrical coupling were applied to the results. Using the measured values for the length constants and input resistances of single rods, we calculate that the plasma membrane resistance of each rod is approximately 1000 MΩ at the resting potential and that the coupling resistances are 272 and 444 MΩ for the square grid and hexagonal models, respectively.9. The time‐varying and voltage‐dependent properties observed at the input and in the coupling between rods appear to reflect characteristics of the rod's plasma membrane and not of the coupling pathways between the rods. Both the outward‐going rectification and relaxation phase of the response appear to involve voltage‐dependent conductance increases in the rod's plasma membrane.
Effects of bleaching and backgrounds on the flash response of the cone system
Authors: Geisler Wilson S. 
Published: December 2014

1. Increment‐threshold functions for flashed backgrounds were measured in the human fovea under several conditions: (1) during dark adaptation following full bleaches, (2) in the presence of steady adapting backgrounds and (3) 500 msec following extinction of adapting backgrounds.2. To prevent the intense flashed backgrounds from interfering with the course of dark adaptation the inter‐trial interval was continuously increased during dark adaptation. This technique may prove generally useful for presenting suprathreshold stimuli during dark adaptation.3. All the increment‐threshold functions measured during dark adaptation were found to be roughly shape invariant and continuously accelerating when plotted in log—log co‐ordinates. Furthermore, in order to translate a function obtained at any given time into coincidence with a function obtained at any other time, it had to be translated vertically and horizontally the same number of log units. This is equivalent to adding or removing neutral density filters from in front of the eye.4. The increment‐threshold functions obtained with steady adapting backgrounds were also continuously accelerating, but could not be brought into coincidence by equal vertical and horizontal translation. However, this became possible again if the adapting background was extinguished during presentation of the flashed background.5. These results contradict the equivalent‐background hypothesis. None the less, they suggest that under present conditions the effects of bleaches and backgrounds may be similar except that steady backgrounds provide additional quanta which drive the visual system part of the way up its intensity—response function.6. The conclusions above were supported by applying a simple model based on the equation R = Rmax. In / (In + I1n), which has frequently been used to describe the peak responses of retinal neurones to flashed stimuli. Virtually all of the data reported here were fitted by this simple model with Rmax held constant.7. The parameters estimated from the model imply that the flash responses measured in the present experiments differ in at least one fundamental way from receptor responses. Even after taking into account changes in the half saturation constant I1, steady backgrounds were found to be much less effective than flashed backgrounds in driving the visual system up its intensity—response function. A subtractive inhibitory network prior to the non‐linear stages responsible for threshold saturation could explain this result.
Neuromuscular transmission and smooth muscle membrane properties in the guinea‐pig ear artery
Authors: Kajiwara Makoto , Kitamura Kenji , Kuriyama Hirosi 
Published: December 2014

Effects of noradrenaline and α‐adrenoceptor blocking agents on neuromuscular transmission of the guinea‐pig ear artery were assessed using the micro‐electrode method.1. The mean membrane potential, and length and time constants of the longitudinally oriented muscle cells were ‐64.5 ± 5 mV (n = 150), 1.03 ± 0.16 mm (n = 15) and 410 ± 40 msec (n = 7) respectively. From the current—voltage relationship, weak outward current pulses produced an anomalous rectification of the membrane while stronger intensities produced a normal rectification of the membrane with a depolarization over 10‐15 mV.2. Brief stimulation (0.1‐0.5 msec) of the tissue produced an excitatory junction potential (e.j.p.). Facilitation produced by repetitive stimulation was evident only on very rare occasions. Higher stimulus intensities caused a stepwise increase of the amplitude of e.j.p.s.3. Spontaneously generated miniature excitatory junction potentials (m.e.j.p.s) were recorded from the muscle membrane. In many cells, the interval and amplitude histograms of m.e.j.p.s showed skew curves. On rare occasions, a bell‐shaped amplitude distribution (quantal release of packeted noradrenaline (NA)) was observed.4. NA (> 3 × 10−7
m) depolarized the membrane and increased the membrane resistance, as measured from the amplitude of the electrotonic potential. Phentolamine suppressed the NA‐induced depolarization. However, high concentrations of phentolamine (> 10−5
m) depolarized the membrane and increased the membrane resistance.5. NA (10−8
m) caused no change in membrane potential though it suppressed the amplitude of an e.j.p. produced by a single stimulus, but did not suppress the amplitude of the subsequent e.j.p.s evoked by repetitive stimulation (0.2‐2.0 Hz). A higher concentration of NA (3 × 10−7
m) depolarized the membrane and markedly suppressed the amplitude of e.j.p.s. On the other hand, NA (10−8 or 2 × 10−8
m) generated burst discharges of m.e.j.p.s between silent periods or random generation.6. Phentolamine (10−6
m) markedly enhanced the amplitude of e.j.p.s and caused a smooth facilitation in response to a train of stimuli with no effect on the membrane potential. A stepwise change in the amplitude of e.j.p.s was no longer observed at any given stimulus frequency and intensity.7. Phenoxybenzamine (10−7
m) suppressed the amplitude of e.j.p.s with no change in the membrane potential.8. The results led to the conclusion that, at a concentration which has no effect on the post‐junctional muscle membrane, NA and phentolamine seemed to be more effective on prejunctional adrenoceptors, while phenoxybenzamine seemed to have a greater effect on post‐junctional adrenoceptors. NA depresses adrenergic transmission by negative feed‐back, while the enhancing action of phentolamine can be explained partly by blocking of prejunctional adrenoceptors and, in addition, by an increase of NA release.
Non‐linearities in the responses of turtle hair cells
Authors: Crawford A. C. , Fettiplace R. 
Published: December 2014

1. Intracellular recordings were made from single cochlear hair cells in the isolated half‐head of the turtle. Receptor potentials were recorded while the ear was stimulated with high‐intensity tones in order to examine the cochlear non‐linearities which shape the hair cell responses.2. The size of a hair cell's voltage response to a tone burst was reduced, abolished and then reversed by steady depolarizing currents of increasing strength. The average current needed to produce reversal was about 0.3 nA, the reversal potential being close to zero with respect to the scala tympani.3. Short current pulses injected on the peaks and dips of the receptor potential showed that the membrane resistance and time constant were decreased on the depolarizing phase of the receptor potential. These changes were not due to non‐linearity in the hair cell's current—voltage curve in the absence of acoustic stimulation. The results are consistent with the idea that the transducer causes the cell to depolarize by increasing the membrane conductance to ions with an equilibrium potential close to zero.4. Saturated receptor potentials from poorly tuned cells exhibited a pronounced asymmetry, with the maximum depolarizing excursion being several times the maximum hyperpolarizing excursion. This asymmetry was not seen in sharply tuned cells. It is proposed that the asymmetry is present in the transducer conductance change and in sharply tuned cells is reduced in the receptor potential by subsequent filtering.5. For high sound pressures which produced close to a saturated response, the hair cell voltage wave form displayed a number of non‐linear features dependent upon the frequency of stimulation relative to the characteristic frequency (c.f.). The most prominent feature occurred at very low frequencies where the potential exhibited damped oscillations on the depolarizations and hyperpolarizations; these ‘ringing frequencies’ lay above and below the c.f. of the cell respectively.6. The ‘ringing frequencies’ varied with the c.f. of the cell but for a given cell were largely independent of the frequency of stimulation. The ‘ringing frequencies’ could be changed by injecting steady currents into the cell during acoustic stimulation; depolarizing currents increased the ringing frequencies and hyperpolarizing currents decreased the frequencies.7. The hair cell's response to a continuous test tone at the c.f. of the cell could be suppressed by simultaneous addition of a second tone whose sound presure was comparable to, or greater than, the test tone. The degree of suppression varied with the intensity and frequency of the second tone, and was maximal close to the c.f. of the cell. The sound pressure required to produce a constant suppression as a function of frequency was sharply tuned, and the tuning of the suppression showed similarities to the frequency selectivity of two‐tone suppression described in the auditory nerve.8. An attempt was made to reconstruct the main features of the receptor potential at high intensities.
Role of a renal arginylesterpeptidase in the production of a renotrophic factor in unilaterally nephrectomized rats
Authors: Dicker S. E. , Morris Christine A. , Pearce F. L. 
Published: December 2014

1. Renal cortical slices incubated for 4 hr in culture medium in the presence of either dibutyrylguanosine‐3′: 5′‐cyclic monophosphate (dibutyryl cyclic GMP, 10−6
m) or freeze‐dried normal rat plasma (35 μg mg−1 wet wt. tissue) did not show any change in dry weight or protein content. However, addition of freeze‐dried normal plasma together with dibutyryl cyclic GMP led to an increase in both parameters.2. Unilateral nephrectomy produced a marked increase in the level of arginylesteropeptidase in the renal cortex of the remaining kidney. A similar increase was observed in renal cortical slices incubated with dibutyryl cyclic GMP in vitro.3. The renal cortical esteropeptidase was inhibited by phenylmethylsulphonyl fluoride (PMSF, 2 m
m). The inhibitor did not, however, prevent the normal increase of dry weight and protein content of renal cortical slices incubated with plasma from unilaterally nephrectomized rats. Similarly, control normal plasma incubated with cortical slices from a kidney removed 10 min after unilateral nephrectomy became endowed with renotrophic activity (Dicker & Morris, 1980b) but this activation was abolished by PMSF.4. Control plasma treated with a purified arginylesteropeptidase and incubated for 4 hr with renal cortical slices produced a hypertrophy of the slices similar to that evoked by plasma from a unilaterally nephrectomized rat.5. Since following unilateral nephrectomy there is a rapid increase in the level of cyclic GMP in the renal cortical tissue of the remaining kidney (Dicker & Greenbaum, 1977) it is suggested that this increase leads to the induction of a specific arginylesteropeptidase. The possibility that the enzyme then cleaves a renotrophic precursor normally present in the plasma, so converting it to an active form, is discussed.