bluuebunny/crossref_metadata_2025 huggingface dataset:
Responses of carotid body chemosensory activity and blood flow to stimulation of sympathetic nerves in the cat.
Authors: O'Regan R G
Published: December 2014

1. The effects of electrical stimulation of sympathetic nerves on sinus nerve chemosensory activity and carotid body blood flow were investigated in anaesthetized cats. 2. Two categories, designated as types I and II, of excitatory responses of chemosensory discharges to sympathetic stimulation were distinguished. Type I responses displayed elevations in impulse frequencies which were usually maximal in the initial 10‐20 sec of stimulation, resisted alpha‐adrenoceptor antagonism induced by phentolamine or phenoxybenzamine and were enhanced after administration of the dopamine antagonist, haloperidol. Type II responses showed increases in impulse frequencies which became more pronounced as stimulation progressed. These responses were susceptible to alpha‐adrenoceptor blockade, were unaffected by haloperidol administration and were usually recorded during systemic hypotension. 3. Inhibitory changes due to activation of sympathetic fibres were recorded in 10% of chemosensory preparations. These effects were usually either abolished or replaced by type I excitatory responses after haloperidol administration. 4. Sympathetic stimulation caused reductions of carotid body blood flow during both natural and artificial perfusion of the organ. This effect was abolished or considerably attenuated by alpha‐adrenoceptor antagonism and was unaffected by haloperidol administration. 5. Possible mechanisms which could account for the influences of sympathetic stimulation on chemoreceptor activity and carotid body blood flow are discussed. It is concluded that inhibitory and type I excitatory responses probably arise from activation of sympathetic fibres with non‐vascular terminations within the carotid body. Type II excitatory responses are most likely due to blood flow changes.
The role of vesicles in the transport of ferritin through frog endothelium.
Authors: Clough G , Michel C C
Published: December 2014

1. The transport of ferritin molecules by endothelial cell vesicles has been quantitatively investigated by electron microscopy. Single mesenteric capillaries of pithed frogs were perfused with solutions containing 6.7 g ferritin 100 ml.‐1 for known periods before fixation in situ with osmium tetroxide. 2. Two series of experiments were carried out: in the first series the perfusate contained bovine serum albumin (1.0 g 100 ml.‐1); in the second series the perfusate contained no protein other than the ferritin. To assess the molecular radius of ferritin in solution, the free diffusion coefficient of ferritin was measured in the presence and absence of albumin. 3. The free diffusion coefficient of ferritin in saline solution (110 m‐mole 1.‐1) was found to be 0.35 X 10(‐6) cm2 sec‐1 at 21 degrees C and was not affected by the presence of bovine serum albumin. This indicates that there is no significant binding of albumin to ferritin in solution and yields a value for the Stokes‐Einstein radius of ferritin of 6.1 nm. 4. In all perfusion experiments the percentage of luminal vesicles containing ferritin exceeded the percentage of labelled cytoplasmic vesicles, which in turn exceeded the percentage of labelled abluminal vesicles. 5. Labelling of all vesicle populations was seen after perfusions lasting less than 1 sec. At this time luminal vesicles were more heavily labelled in the absence of albumin. 6. The labelling of luminal vesicles increased with lengthening perfusion times up to 30‐40 sec, after which steady levels of labelling were achieved. The rate of rise in luminal labelling and the steady‐state levels reached were both greater in the absence of albumin. By contrast cytoplasmic labelling increased above its initial value only after perfusions of longer than 10 sec. 7. In the steady state, labelled cytoplasmic vesicles contained, on average, fewer ferritin molecules than labelled luminal vesicles. This finding is inconsistent with translocation of labelled luminal vesicles across the cell. 8. It is suggested that the early constant labelling of cytoplasmic and abluminal vesicles is consistent with the existence of vesicular channels. Later cytoplasmic labelling may result from the transient fusion of cytoplasmic vesicles with labelled luminal vesicles for periods long enough to allow mixing of vesicular contents. Albumin may affect vesicular transport by its interaction with the endothelial glycocalyx.
Pentobarbitone interference with inhibitory synaptic transmission in crayfish stretch receptor neurones.
Authors: Aickin C C , Deisz R A
Published: December 2014

1. The effect of pentobarbitone (PB) on GABA‐ergic inhibition was investigated in the isolated crayfish stretch receptor. The soma of the slowly adapting neurone was impaled with two micro‐electrodes to give an accurate determination of membrane conductances. 2. Application of PB in concentrations from 10(‐6) to 10(‐3) M increased the rise time constant of the inhibitory post‐synaptic potential (i.p.s.p.). The i.p.s.p. percentage amplitude and decay time constant were also increased in eight out of twelve neurones. On prolonged exposure, the percentage amplitude declined at a rate dependent upon the dose and the frequency of stimulation until the i.p.s.p. became undetectable. 3. The response to ionophoretically applied GABA remained essentially unaltered in the presence of PB, but the falling phase was prolonged by up to 8% in four of the ten neurones tested. Resting membrane conductance, i.p.s.p. driving force (i.p.s.p. reversal potential minus resting membrane potential), and parameters of the anti‐ and orthodromic action potential were not significantly affected. 4. Removal of PB after prolonged exposure usually caused an immediate increase in i.p.s.p. percentage amplitude but the i.p.s.p. rising phase remained slowed. 5. Application of excess extracellular GABA only affected the i.p.s.p. percentage amplitude after it had been reduced by PB. It transiently increased the attenuated i.p.s.p. percentage amplitude in the presence of PB, and after the removal of PB permanently increased the amplitude to its original value. 6. Nipecotic acid and cis‐1,3‐aminocyclohexane carboxylic acid, inhibitors of GABA re‐uptake, slightly increased the i.p.s.p. percentage amplitude, and prolonged the falling phase but did not affect the rising phase. The percentage amplitude declined on prolonged exposure. 7. We conclude that PB has no electrophysiologically demonstrable post‐synaptic action in the crayfish stretch receptor neurone, but it inhibits the presynaptic release and re‐uptake of GABA.
Involvement of Na+‐K+‐ATPase in p‐aminohippurate transport by rabbit kidney tissue.
Authors: Maxild J , Møller J V , Iqbal Sheikh M
Published: December 2014

1. The relation between renal accumulation of p‐aminohippurate (PAH), Na+‐K+‐ATPase activity, and the transmembranal Na+ gradient has been investigated by the use of cortex slices of rabbit kidney. 2. A moderate stimulation of PAH uptake rate was observed under anaerobic conditions in the presence of an extracellular‐to‐intracellular directed gradient of Na+. 3. Inhibition of aerobic accumulation of PAH by ouabain was related to a decrease in Na+‐K+‐ATPase activity, as evidenced by changes in tissue concentrations of Na+ and K+ and by measurements of high‐affinity binding of ouabain to the slices. 4. Accumulation of PAH in media with various concentrations of Na+ and K+ resembled the effect of the cations on the ATPase activity of an isolated preparation of Na+‐K+‐ATPase. 5. Counteraction of the inhibitory effect of ouabain on PAH accumulation by a high concentration of K+ in the medium was related to retention of Na+‐K+‐ATPase activity, as evidenced by preservation of tissue‐‐medium gradients of Na+ and K+. 6. The present data provide strong evidence for the involvement of Na+‐K+‐ATPase in the energization of renal PAH accumulation. However, it appears probable that a metabolic (Na+‐gradient‐independent) component, in addition to a Na+ gradient, is essential for the attainment of high accumulation ratios of PAH by intact renal cells.
Osmosensitivity of the hepatic portal vein area and vasopressin release in rats.
Authors: Baertschi A J , Vallet P G
Published: December 2014

1. The role of intraperitoneal osmoreceptors in hypothalamo‐neurohypophyseal control was studied in urethane‐ or nembutal‐anaesthetized rats. Plasma samples were taken for radioimmunoassay of arginine vasopressin, and the electrical activity of single supraoptic endocrine neurones and of the hypothalamo‐neurohypophyseal tract were monitored during superfusion of the hepatic portal vein with hypo‐, iso‐ and hypertonic solutions. 2. Plasma arginine vasopressin increased within 1 min following superfusion with 0.3‐0.9 osmolal NaCl solutions in a dose‐related manner from basal levels of 30 pg/ml, to 170 pg/ml. Prior superfusion with xylocaine or intravenous infusions of 800 micrograms atropine‐methyl bromate abolished this response, although vasopressin was still released to nicotine in atropine‐blocked rats. 3. Portal vein superfusions had no significant effects on arterial blood pressure, plasma osmolality and plasma Na concentrations. 4. Forty supraoptic neurones were antidromically activated from the neural lobe/stalk region. Superfusions of the portal vein with NaCl solutions (0.33‐1.20 osmole/kg, 37 degrees C, 5‐120 sec) stimulated seven out of eight phasically firing and eight out of twenty‐four continuously firing neurones. One phasically active, ten continuously firing and four silent cells were not affected, and six continuously firing neurones were inhibited by the superfusions. 5. The amplitude decreases of antidromic compound action potentials in the hypothalamo‐neurohypophyseal tract, reflecting an increase of the orthodromic nerve impulse traffic, ranged from 17 to 22% for superfusions with 1.2 osmolal NaCl or LiCl solutions, from 8 to 11% for 1.2 osmolal Na isethionate or choline Cl and from 3 to 9% for 1.2 osmolal glucose; there was no effect when 1.2 osmolal urea and isotonic or hypotonic NaCl solutions were applied. 6. Responses of the amplitude of compound action potentials to superfusions with 1.2 osmolal NaCl solutions or with 0.1 mumole ACh, but not to electrical stimulation of the portal vein or its superfusion with 1.2 osmolal KCl, were abolished by prior application of 0.3 mumole atropine sulphate. Prior superfusions with xylocaine abolished the responses to all stimuli above. 7. These results suggest that within the hepatic portal vein area there are osmosensitive receptor cells and/or nerve terminals which activate the hypothalamoneurohypophyseal system through a peripheral cholinergic mechanism.
Alpha‐aminoisobutyric acid efflux from the cornea of the toad, Bufo marinus.
Authors: McGahan M C
Published: December 2014

1. Amino acids move into and out of the amphibian cornea across its inner aqueous, side only. Most alpha‐aminoisobutyric acid (AIB) accumulation takes place in the corneal epithelium; the endothelium and stroma do not limit exchanges with these cells. The apical, or tear, surface of the epithelium is an impermeable barrier to the transport of amino acids. There are several sites or mechanisms by which AIB enters and leaves the cornea. 2. The entry of AIB is not Na‐dependent; however, the exit site is very sensitive to changes in internal Na concentration. Any factor, such as ouabain or metabolic inhibitors, that increases internal Na, markedly stimulates AIB efflux. 3. Site are also present for the exchange of internal for external amino acids, and this process is Na‐dependent. There was no measurable movement of Na into or out of the cells with these amino acids. Exchange efflux was more specific than uptake, since both alanine and leucine inhibit AIB uptake, but only alanine stimulates AIB efflux. 4. Although the largest amount of AIB accumulated by the cornea was present in the epithelium, evidence is presented that the endothelium and stromal keratocytes may also concentrate and retain amino acids.
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.
Kinetics of the disappearance of endogenous plasma renin following nephrectomy in pregnant and non‐pregnant rats.
Authors: Bidani A K , Churchill P C
Published: December 2014

1. Plasma renin concentration was higher in pregnant rats than in non‐pregnant female controls (43 +/‐ 5 vs. 12 +/‐ 1 ng/ml. per hr); 24 hr post partum, it was 8 +/‐ 2 ng/ml. per hr. 2. Twenty‐four hours after bilateral nephrectomy, plasma renin concentrations in pregnant and non‐pregnant rats were not significantly different from zero; the uterine venous minus arterial value in nephrectomized pregnant rts was not significantly different from zero either, and was not increased by haemorrhage. These observations suggest that neither the pregnant uterus nor any other extrarenal site of renin storage contributes to the elevated plasma renin concentration. 3. The disappearance of plasma renin following bilateral nephrectomy was resolved into fast and slow components. The half‐time of the slow component, which is considered to reflect the metabolic clearance of renin was significantly higher in pregnant rats than in controls. It is concluded that the plasma renin concentration is elevated, at least in part, because of a decreased metabolic clearance of renin during pregnancy.
Reliability and efficacy of the long‐latency stretch reflex in the human thumb.
Authors: Marsden C D , Merton P A , Morton H B , Rothwell J C , Traub M M
Published: December 2014

1. The amount of positional compensation afforded by the long‐latency reflex in the flexor pollicis longus has been investigated in ten normal human subjects. 2. The interphalangeal joint of the thumb was extended by between 2 and 40 degrees at up to 900 deg/s by suddenly increasing the standing force applied to the lever against which the subject was pressing with the pad of the thumb. 3. Electromyographic (e.m.g.) responses at spinal‐latency were very small or absent for stretches of this magnitude. The long‐latency stretch reflex produced an average positional correction of about 50% for disturbances in the range of 5‐25 degrees. The response began to saturate for disturbances of greater than 25 degrees. 4. The e.m.g. response was pulsatile, lasting only some 50 ms, even during continuously increasing disturbances; frequently it terminated despite a remaining positional error. 5. There was a large variation from subject to subject in the average amount of positional correction provided by the stretch reflex. Examination of single responses to the same stretch in individual subjects showed an even greater variation from trial to trial. 6. Variation in the compensation produced by the long‐latency stretch reflex from trial to trial could not be explained by the slight variation in size or maximum velocity of the individual stretches.
Amplitude‐ and instruction‐dependent modulation of movement‐related electromyogram activity in humans.
Authors: Brown S H , Cooke J D
Published: December 2014

1. Studies were made of the electromyogram (EMG) patterns associated with the performance of visually guided, step‐tracking arm movements by normal humans. Subjects were instructed to make movement either ‘accurately', ‘as fast as possible’ or ‘fast and accurately'. Movements of 16, 32, 48 and 64 deg of arc were made with each instruction. Movements had durations of approximately 250‐600 msec. 2. A ‘triphasic’ pattern of EMG activity was associated with all movements in this study. All bursts in this pattern were more clearly defined in faster movements whether the increased speed of movement was a result of increased movement amplitude or of the instruction‐related ‘intent’ of the subject. 3. The magnitudes of the two agonist EMG bursts showed identical linear dependencies on movement amplitude. The slope of this relation was instruction‐dependent, being greatest for ‘fast’ and least for ‘accurate’ movements. 4. The duration and time of onset of the initial agonist burst relative to the start of the movement were not dependent on movement amplitude or on instruction. In contrast, the time of onset of the second agonist burst depended on both movement amplitude and instruction, occurring earlier when movements were made faster. 5. The magnitude of the antagonist activity was instruction‐ but not amplitude‐dependent. Duration and onset of this burst varied with both instruction and movement amplitude.
Calcium and the α‐action of catecholamines on guinea‐pig taenia caeci
Authors: Hertog Adriaan Den
Published: December 2014

1. The involvement of calcium in the α‐action of adrenaline on guinea‐pig taenia caeci was studied by measuring the changes in membrane potential and muscle contraction, using the sucrose‐gap method, and by determining the 42K efflux, in the presence of a β‐blocker (propranolol, 1·8 × 10−6
m).

2. In the presence of extracellular calcium, the hyperpolarization caused by adrenaline (3 × 10−6
m) was sustained during the period of its application (5 min), both in active preparations (at 36 °C) and in quiescent muscle (22 °C). In the absence of calcium, adrenaline caused a transient hyperpolarization which was smaller at 36 °C than at 22 °C and passed off within 5 min, while adrenaline was present.

3. Both the sustained and the transient hyperpolarization were associated with an increase in 42K efflux which had a similar time course. 42K flux measurements were made in depolarized tissue (52·8 m
m‐potassium), in which the effect was consistent and more pronounced than in polarized muscle (2·8 m
m‐potassium).

4. The transient hyperpolarization which is resistant to calcium removal and EGTA (0·1‐2·0 m
m) could be evoked only once but, following a short exposure to calcium (2·5 m
m) for 20 sec and readmission of calcium‐free medium, it was restored.

5. The sustained and the transient hyperpolarization and the increase in 42K efflux were abolished by the α‐antagonist phentolamine (10−5
m); their amplitude was dependent on the adrenaline concentration in the range 10−7 to 3 × 10−6
m, and both responses persisted in the absence of sodium or chloride.

6. The hyperpolarization and the increase in 42K efflux were greater at higher external calcium concentrations (0·3‐2·5 m
m).

7. Cobalt (0·6 m
m), D600 (2·5 × 10−5
m) and the bee toxin apamin (10−7
m) reduced the α‐response.

8. In the presence of apamin, in calcium‐containing solution, the sustained hyperpolarization caused by adrenaline was preceded by, or converted to, depolarization, spike discharge and contraction.

9. The depolarizing effect of adrenaline in the presence of apamin persisted in sodium‐free or chloride‐free medium, but was blocked in the absence of calcium and diminished by cobalt and D600.

10. It is concluded that the α‐response of guinea‐pig taenia caeci consists of two components, both involving calcium. First, the activation of α‐receptors increases calcium entry, which leads to the opening of potassium channels, a sustained hyperpolarization and inhibition of muscle activity. Secondly, in the absence of external calcium, a transient hyperpolarization is revealed, presumably due to the release of bound calcium from a limited cellular store which can be replenished by addition of external calcium, and this leads to an increase in potassium permeability.
Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.
Authors: McCloskey D I , Potter E K
Published: December 2014

1. The carotid sinus nerve was electrically stimulated in dogs anaesthetized with chloralose. Stimuli (1 ms, 1‐10 V, less than or equal to 1 Hz) evoked responses in single cardiac efferent fibres dissected from the cervical part of the vagus nerve. The mean latencies of these responses varied, from fibre to fibre, between 30 and 120 ms. 2. Stimuli given during the expiratory phase of the respiratory cycle evoked vagal responses with a shorter latency than similar stimuli given only during the inspiratory phase of the respiratory cycle. 3. Following the vagal response to carotid sinus nerve stimulation a period of inhibition of vagal activity, lasting 100‐150 ms, occurred. Refractoriness of the responding vagal motoneurone following an action potential could not account for this post‐excitatory depression. 4. The inhibitory effects of electrical stimulation of the carotid sinus nerve were further studied by applying pairs of similar electrical stimuli to the carotid sinus nerve. The second stimulus of a pair had to be given 80‐100 ms after the first to evoke a second response. 5. Trains of electrical stimuli (30‐100 Hz) were also studied. At low frequencies the inhibitory effect of successive stimuli on vagal responses became less marked, but at higher frequencies only the first and last stimulus of the train reliably evoked responses. For trains of stimuli at both low and high frequencies, the last stimulus of the train evoked a vagal response, which was succeeded by a period of inhibition of vagal firing: this inhibition was then followed by further excitation before vagal discharge returned to resting levels.
Electrophysiological analysis of inhibitory synaptic mechanisms in the preoptic area of the rat.
Authors: Mayer M L
Published: December 2014

1. Extracellular recordings were made from single neurones in the medial preoptic‐anterior hypothalamus of rats anaesthetized with urethane or pentobarbitone 2. Stimulation of the arcuate‐‐ventromedial area evoked inhibition in 76% of neurones; inhibition occurred as the initial response in 26% of neurones, followed orthodromic excitation in 26% and antidromic excitation in 24%. Stimulation of the periaqueductal grey evoked inhibition as the initial response in 63% of neurones. 3. Stimulation of both the arcuate‐‐ventromedial area and the periaqueductal grey generated synaptically evoked high‐frequency discharges in a few neurones. 4. Short ionophoretic pulses of beta‐alanine, gamma‐aminobutyric acid (GABA), glycine and taurine inhibited the discharge of most preoptic‐anterior hypothalamic neurones. Bicuculline methochloride and picrotoxin antagonized both GABA responses and synaptic inhibition. Strychnine antagonized beta‐alanine, glycine and taurine responses without altering synaptic inhibition. 5. Reduction of hypothalamic serotonin (5‐HT) levels to about 40% of control values by micro‐injection of 5,7‐dihydroxytryptamine into the ventral tegmental area, or parenteral injection of parachlorophenylalanine, did not alter the profile of responses evoked by either arcuate‐ventromedial or periaqueductal grey stimulation. Micro‐injection of tetanus toxin (100‐200 MLD) into the preoptic‐anterior hypothalamus significantly reduced the frequency of occurrence of inhibition evoked from both sites. 6. Pentobarbitone administered acutely or as the sole anaesthetic increased both the duration and frequency of occurrence of inhibitory responses evoked from the arcuate‐ventromedial nuclei. 7. It is suggested that a GABA‐linked inhibitory synaptic mechanism, activated by arcuate‐ventromedial and periaqueductal grey stimulation, operates in the preoptic‐anterior hypothalamus. Such convergent inhibition may be a result of activity in local interneurone circuitry.
The renin—angiotensin system in drinking and cardiovascular responses to isoprenaline in the rat
Authors: Evered M. D. , Robinson M. M.
Published: December 2014

1. We investigated the role of the renin—angiotensin system in isoprenaline‐induced drinking in the rat. Captopril, an inhibitor of angiotensin‐converting enzyme, was used to block the synthesis of angiotensin II either in the circulation alone or in the brain as well.

2. Subcutaneous injections of isoprenaline (0·1 mg/kg) alone caused nine rats to drink 8·4 ± 0·9 ml water in 3 h.

3. Pre‐treatment with doses of captopril (0·1‐1·0 mg/kg,
s.c.), which inhibit conversion of angiotensin I to II in the circulation but not in the brain, dose‐dependently enhanced the drinking response to isoprenaline. Captopril alone did not cause drinking.

4. Higher doses of captopril (5·0‐100 mg/kg,
s.c.), which inhibit conversion of angiotensin I to II in the brain as well as in the blood, caused dose‐dependent inhibition of drinking elicited by isoprenaline.

5. The highest dose of captopril tested (100 mg/kg,
s.c.) completely blocked the drinking response to isoprenaline (0·1 or 0·33 mg/kg,
s.c.) for at least 45 min. This inhibition was not caused by general debility of the rats; animals deprived of water (12 h) and treated with both captopril and isoprenaline drank as much as water‐deprived controls.

6. We found no evidence that blocking the renin—angiotensin system inhibits drinking because it exacerbates isoprenaline‐induced hypotension. After injection of isoprenaline the mean arterial pressure of nephrectomized rats or rats pre‐treated with the high dose (100 mg/kg,
s.c.) of captopril (which blocked drinking) was only slightly lower (5‐10 mmHg) than that of rats pre‐treated with the low dose (0·5 mg/kg,
s.c.) of captopril (which enhanced drinking).

7. Water deprivation, which caused rats treated with isoprenaline and captopril to drink, did not increase arterial pressure. Pitressin increased the arterial pressure of rats treated with isoprenaline and captopril but did not cause drinking.

We conclude that the renin—angiotensin system has a direct and essential role in the drinking response to isoprenaline.
Water reabsorption capacity of the proximal convoluted tubule: a microperfusion study on rat kidney.
Authors: Corman B , Roinel N , De Rouffignac C
Published: December 2014

1. The differences in the water reabsorption capacity observed from one proximal tubule to another were investigated in vivo by continuous microperfusion. 2. Two to seven loops were punctured along the same tubule. The [3H]inulin, 22Na, [14C]glucose, sodium, chloride and magnesium concentrations as well as the osmolality of the collected samples were studied as a function of the perfused length. 3. With Ringer bicarbonate solution perfused in Saclay Wistar rats, the water reabsorption capacity ranged from 0 to 3 nl . min‐1 . mm‐1 depending on the tubule. This reabsorption rate was closely correlated with the unidirectional reabsorption flux of sodium, and with the rise in tubular chloride and magnesium concentrations. 4. In Munich Wistar rats with glomeruli accessible at the kidney surface, tubule perfusion with a Ringer bicarbonate solution showed that the highest water reabsorption rates per mm of tubule were found for the perfusion sites closest to the glomerulus; water fluxes were also positively correlated with glucose transport. 5. In a second series of experiments on Saclay rats, perfusion of a Ringer solution containing a high chloride concentration (137 m‐equiv/l.) was unable to increase the water reabsorption rate compared to the control perfusion; here again, water fluxes were positively correlated with glucose transport.
Prostaglandins alter the relationship between gastric hydrogen ion concentration and flow: evidence for stimulation of non‐parietal secretion in the cat
Authors: Gascoigne A. D. , Hirst B. H.
Published: December 2014

1. The effect of
i.v. administration of prostaglandin (PG) E2 (10‐40 μg kg−1 h−1), 16,16‐dimethyl PGE2 (0·1‐0·5 μg kg−1 h−1), PGE1 (16‐20 μg kg−1 h−1), PGA1 (5‐11 μg kg−1 h−1) and PGF2α (40 μg kg−1 h−1) on the relationship between [H+] and flow of gastric juice during stimulation of gastric secretion by pentagastrin was investigated in conscious cats prepared with cannulated gastric fistulae.

2. A‐ and E‐type prostaglandins significantly reduced pentagastrin‐stimulated acid output. This inhibition was associated with a reduction of the [H+] of the gastric juice such that the [H+] observed at any flow rate tended to be lower than the normal range observed with pentagastrin alone. With the highest doses of these prostaglandins the mean [H+] values were well below the normal range with pentagastrin alone.

3. At the dose tested, PGF2α had little effect on acid output, and did not alter the relationship between [H+] and gastric flow.

4. There is a linear relationship between acid output and gastric flow and this relationship is similar during stimulation of gastric secretion by pentagastrin, histamine or insulin. Gastric acid inhibitory doses of cimetidine, atropine and somatostatin did not alter this relationship. In contrast the A‐ and E‐type prostaglandins displaced this relationship to the right of the normal line observed with the acid stimulants alone. A‐ and E‐type prostaglandins reduced the slope of the line relating acid output and gastric flow from ∼ 150‐170 μequiv/ml−1 to ∼ 100‐120 μequiv ml−1, this being taken as evidence of dilution of the parietal H+ secretion with a non‐parietal secretion.

5. The volume of non‐parietal gastric secretion was calculated as the gastric flow at zero acid output by extrapolation of linear plots of acid output versus gastric flow. Unstimulated gastric flow measured directly was 0·75 ml 15 min−1. The calculated non‐parietal flow was in the range 0·52‐0·90 ml 15 min−1 during stimulation of gastric secretion with pentagastrin, histamine and insulin, and inhibition of pentagastrin‐stimulated acid secretion with cimetidine, atropine and somatostatin. PGE2 (1·51 ml 15 min−1) and 16,16‐dimethyl PGE2 (1·20 ml 15 min−1) nearly doubled the calculated non‐parietal flow.

6. These data demonstrate that gastric acid inhibitory doses of A‐ and E‐type prostaglandins can reduce the [H+] in the bulk fluid of the gastric lumen during stimulation of acid secretion. The data provide evidence that these prostaglandins stimulate a non‐parietal component of gastric secretion. This might be gastric bicarbonate and mucus secretion.
Spinal cord collaterals from axons of type II slowly adapting units in the cat.
Authors: Brown A G , Fyffe R E , Rose P K , Snow P J
Published: December 2014

1. The morphology of single axons, and their collaterals, of Type II slowly adapting mechanoreceptors situated at the claw bases was studied. Intra‐axonal injections of horseradish peroxidase were made into the axons near their entrance to the lumbosacral spinal cord of anaesthetized cats. The morphology was revealed by subsequent histochemistry. 2. Nine Type II axons were stained. All but one bifurcated into ascending and descending branches upon entering the cord. Eighty‐nine collaterals arose from the axons at a mean spacing of about 570 micrometers. 3. The collaterals formed plate‐like arborizations usually about 500‐600 micrometers wide in the transverse plane but only 100‐300 micrometers thick in the longitudinal axis of the cord. The terminal arborizations were in laminae III‐VI. 4. Synaptic boutons in laminae III and IV were more numerous than in laminae V and VI. Boutons en passant were common in laminae III and IV and arranged in series of three to six, whereas in deeper laminae only two or three boutons formed a series de passage. 5. The morphology of the slowly adapting Type II collateral is discussed. 6. Some general principles of the organization of cutaneous afferent fibres in the lumbosacral cord are presented.
3‐O‐methylglucose transport in internally dialysed giant axons of Loligo.
Authors: Baker P F , Carruthers A
Published: December 2014

1. The transport of the non‐metabolized sugar, 3‐O‐methylglucose, has been studied in the squid axon under conditions where the intracellular environment of the axon is controlled by internal dialysis. 2. Sugar transport is passive, shows saturation kinetics and is asymmetric. At 15 degrees C, the Michaelis and velocity constants for exit are approximately four times those for uptake. The asymmetry of transport is increased by raising the temperature. 3. Sugar uptake is not affected by intracellular sugar levels as high as 100 mM. Sugar exit is, however, reduced by external sugars although the apparent Km for exit is unaffected. 4. The kinetics of sugar exit under exchange conditions are determined by the kinetics of sugar uptake. These results can be accounted for by the asymmetric mobile‐carrier and simultaneous‐carrier models for transport. 5. Both sugar uptake and exit are reduced in the absence of ATPi. Kinetic analysis of transport under these conditions show that the capacity of the system to transport sugar is unchanged but that the affinity of the system for sugar is reduced. Internal cyclic AMP, AMP, ADP or GTP (2 mM) do not mimic this action of ATP. The hydrolysable analogue of ATP, alpha, beta‐methylene‐5‐ATP (2 mM), (but not the nonhydrolysable analogue beta, gamma‐methylene‐5‐ATP, 2 mM) has an ATP‐like action on sugar transport. 6. Transport is unaffected by internal Ca2+ concentrations in the range 4 X 10(‐8)‐‐9 X 10(‐7) M.
Stimulated gastric prostaglandin output, and the effect of inhibition of prostaglandin synthetase, in the conscious cat.
Authors: Baker R , Jaffe B M , Shaw B , Venables C W
Published: December 2014

1. In the conscious gastric fistula cat there was no correlation between the outputs of gastric acid and PGE secreted in response to incremental doses of pentagastrin and histamine acid phosphate. 2. PGE secreted in response to pentagastrin and histamine was not dose dependent. 3. Flurbiprofen significantly inhibited the gastric output of PGE but did not influence acid or pepsin secretion. Inhibition of PGE secretion was accompanied by evidence of gastric mucosal haemorrhage. 4. It is concluded that gastric juice PGE is unlikely to be involved in the physiological control of acid secretion.
Cross‐correlation analysis of the maintained discharge of rabbit retinal ganglion cells.
Authors: Arnett D , Spraker T E
Published: December 2014

1. Simultaneous recordings were made from pairs of rabbit retinal ganglion cells. Physiological tests were used to classify the receptive field properties of each cell and the receptive field locations were mapped. 2. The statistical dependence between simultaneously recorded retinal ganglion cells was assessed by cross‐correlating the maintained discharge of the simultaneously recorded cells. Cross‐correlations from cell pairs in which the constituent cells had non‐overlapping receptive field centres were statistically flat, reflecting no statistical dependence. 3. Most cell pairs consisting of transient and sustained concentric cells and having overlapping receptive field centres exhibited a correlated maintained discharge indicative of statistical dependence. The strength of the statistical dependence varied approximately inversely with the degree of overlap between the two cells comprising the cell pair. 4. Cell pairs consisting of two ON‐centre cells or two OFF‐centre cells and having overlapping receptive field centres possessed incremental cross‐correlations which were characterized by a peak centred near zero. Cell pairs consisting of an ON‐centre cell with an OFF‐centre and having overlapping receptive field centres possessed decremental cross‐correlations which were characterized by a valley centred near zero. 5. The results are consistent with the hypothesis that a noise source provides shared input to two or more retinal ganglion cells. Bipolar and photoreceptors are the most likely sources of noise responsible for the statistical dependency between retinal ganglion cells.
Immobilization of membrane charge in frog skeletal muscle by prolonged depolarization.
Authors: Rakowski R F
Published: December 2014

1. Inactivation ('immobilization') of the non‐linear component of capacitive current in semitendinosus muscles of Rana pipiens was studied using the three‐micro‐electrode voltage‐clamp technique (Adrian, Chandler & Hodgkin, 1970). 2. The steady‐state voltage dependence of non‐linear charge immobilization was determined by changing the holding potential. The data were fitted to an equation analogous to that used to describe the charge activation process (Schneider & Chandler, 1973). The steepness parameter, k, is the same for charge activation and immobilization, but the mid‐point voltage of charge immobilization is 8.9 +/‐ 2.6 mV (n = 9) more negative than the mid‐point of the non‐linear charge activation curve. The charge relaxation rate constants are unaffected by changes in holding potential. 3. The time course of non‐linear charge immobilization was studied using a protocol that measures the change in capacitive current required for a voltage step of a fixed magnitude determined before and after an intervening period of depolarization. The sum of the non‐linear charge that is immobilized and the non‐linear charge that remains mobile after a prolonged (greater than 1 s) depolarization is equal to the total non‐linear charge measured by a normally polarized holding potential (‐80 mV). The determination of the quantity of charge immobilized does not require the assumption of linearity of the control capacity transient. 4. The exponential time constant of the charge immobilization was found to be steeply voltage dependent. The charge immobilization time constant was 4.4 s at ‐40 mV, 1.5 s at ‐20 mV and 0.28 s at +20 mV. Temperature was 5 degrees C. 5. In addition to a decrease in the magnitude of non‐linear capacitive charge during prolonged depolarization muscle fibres generally showed showed an apparent decrease in linear effective capacity. It is suggested that this apparent change and the increase previously reported to occur when chronically depolarized fibres are hyperpolarized (Rakowski, 1978a) are artifactual results of incorrect current scaling rather than changes that result from alteration of a conductance pathway from the transverse tubular system into the sarcoplasmic reticulum.
Acetylcholine receptors in singly and multiply innervated skeletal muscle fibres of the chicken during development.
Authors: Harvey A L , van Helden D
Published: December 2014

1. The properties of acetylcholine (ACh) receptors of the singly innervated posterior latissimus dorsi (PLD) and the multiply innervated anterior latissimus dorsi (ALD) muscles of the chicken were investigated. Studies were made on chicks from 17 days in ovo to 14 weeks after hatching. Focal extracellular recordings and intracellular recordings in voltage clamped fibres were made. 2. Peak amplitudes of miniature end‐plate currents (m.e.p.c.s) of the two muscles were not significantly different. The time constants of decay (tau D) were similar in both muscles, although tau D in the PLD was generally smaller than in the ALD (usually by less than 25%). M.e.p.c. decays in both muscles were well described by a single exponential. 3. The conductance (gamma) and average lifetime (tau N) of end‐plate channels activated by ionophoretically applied ACh were calculated from records of current fluctuations. Noise spectra were well fitted by a single Lorentzian function. Values obtained in PLD did not differ significantly from those obtained in the ALD. There was not difference in the ACh null potential. 4. The voltage and temperature sensitivities of the ACh‐activated channels in both muscle types were very similar. 5. With age there was a slight decrease in tau D: from about 6 to 5 msec in the PLD and from about 7 to 5 msec in the ALD (at ‐40 mV). The change in tau N with age was even less marked. However, during development, gamma almost doubled in both muscles, increasing from about 20 to 35 pS. 6. The results provide no evidence for the hypothesis that the different pattern of innervation causes marked differences in the ACh‐activated channels of singly and multiply innervated muscles.