bluuebunny/crossref_metadata_2025 huggingface dataset:
Three types of acetylcholine response in bivalve heart muscle cells
Authors: Elliott Ellen J.
Published: December 2014

1. The acetylcholine (ACh) responses of cardiac muscle cells from three species of bivalves were studied by intracellular recording and ACh ionophoresis. Heart muscle contraction was abolished by bathing in artificial sea water in which Mn2+ had been substituted for Ca2+.

2. Three different types of membrane potential changes were observed in response to ACh pulses: a slow hyperpolarization in the clam Mercenaria mercenaria, a rapid depolarization which was sometimes followed by a slower hyperpolarization in the muscle Mytilus edulis, and a biphasic response consisting of both a rapid depolarization and slower hyperpolarization in the oyster Crassostrea virginica. All responses were accompanied by an increase in membrane conductance, as measured by passing constant current pulses with an extracellular suction electrode.

3. The hyperpolarizing response in all three species was blocked most effectively by methylxylocholine and not very effectively by tubocurarine or hexamethonium. The depolarizing response in Mytilus was blocked preferentially by tubocurarine and hexamethonium, while the depolarizing response in Crassostrea was blocked effectively by tubocurarine only.

4. The hyperpolarizing response in all three species was not altered by Cl−‐free or Na+‐free sea water, but was affected by changes in external K+. The rate of change of the inversion potential of this response with change in [K+]o was 59 mV per tenfold concentration change. The depolarizing response of Mytilus was not altered by changes in external Cl− or K+, but was abolished in Na+‐free sea water. The depolarizing response of Crassostrea was insensitive to external Na+ or K+, inverted at ‐31 mV in normal sea‐water, and was altered by changes in [Cl−]o. Substituting for Cl− with sulphate shifted the inversion potential at a rate of 56‐61 mV per tenfold Cl− concentration change.

5. The three types of ACh response seen in bivalve heart muscle are similar with respect to time course, pharmacological sensitivity and ionic mechanism to the three types of ACh response described in Aplysia central neurones. Analogies can also be drawn with vertebrate ACh responses.
The density, distribution and topographical organization of spinocervical tract neurones in the cat
Authors: Brown A. G. , Fyffe R. E. W. , Noble R. , Rose P. K. , Snow P. J.
Published: December 2014

1. In acute experiments, detailed grids of micro‐electrode recordings were made from spinocervical tract (s.c.t.) cells in the lumbosacral cord of anaesthetized cats. These grids provided electrophysiological data on the location, distribution, density and somatotopic organization of s.c.t. neurones.

2. In acute experiments lasting up to 48 hr, retrograde labelling of s.c.t. cells was carried out by injecting horseradish peroxidase into the lateral cervical nucleus in anaesthetized cats. The aim was to flood the nucleus with the enzyme so that all s.c.t. neurones would be labelled in order to provide an independent check on the location, density and distribution data obtained in the electrophysiological experiments.

3. The electrophysiological and the anatomical experiments were sometimes performed on the same animal.

4. The electrophysiological and anatomical results were in excellent agreement. (a) S.c.t. cells are located mainly in ipsilateral laminae III, IV and V. About 25% are in lamina III, 60% in lamina IV and 10% in lamina V. There are a few cells in laminae I, II and VI making up the remaining 5%. (b) There are about 550‐800 s.c.t. cells in the lumbosacral enlargement (L4—S2 inclusive) on each side of the cord. Most cells are in L7—S1 where there are twenty to forty s.c.t. neurones in each millimetre length of cord.

5. Many marginal (lamina I) cells were labelled with the retrograde horseradish peroxidase method and a few cells on the contralateral side in laminae III—V and VII—VIII were also labelled. The marginal cells formed 12‐18% of labelled cells on the side of injection and, in addition, a similar absolute number of marginal cells was labelled on the side contralateral to the injection. The possible identity of these neurones is discussed.

6. S.c.t. cells form a sheet of neurones across the dorsal horn. The sheet is organized somatotopically in a way which resembles the representation of the hind limb dermatomes in the dorsal columns (Werner & Whitsel, 1967). There is a relative enlargement of the L6—S1 dermatomes which encroach upon their neighbouring cord segments. The gradient of the map is very steep in the mediolateral direction but gradual in the rostrocaudal direction. The detailed somatotopic maps generated in the present work have revealed that s.c.t. cells are arranged so that their receptive fields form longitudinal columns and cells within the columns have overlapping fields.
Effects of acetylcholine on ion fluxes and chlorotetracycline fluorescence in pancreatic islets
Authors: Gagerman E. , Sehlin J. , Täljedal I.-B.
Published: December 2014

1. Acetylcholine potentiated glucose‐stimulated insulin release from ob/ob‐mouse islets in salt‐balanced bicarbonate buffer and to a lesser extent in Tris buffer; basal insulin release at 3 m
M-D‐glucose was not affected. Potentiation required the presence of Ca2+.

2. In bicarbonate buffer, ACh stimulated the islet uptake of 45Ca2+ at 3 m
M‐glucose but not significantly at 11 m
M; no effect was seen in Tris buffer.

3. At 11 m
M‐glucose, ACh increased the fluorescence from Ca2+‐chlorotetracycline in dispersed islet cells; the effect was inhibited by atropine.

4. At both 3 and 11 m
M‐glucose, ACh stimulated the islet uptake of 22Na+ in 60 min. At 11 m
M‐glucose, 22Na+ uptake in 5 min was also enhanced significantly, and this effect was inhibited by atropine.

5. At 3 m
M‐glucose, ACh probably stimulated the islet uptake of 86Rb+ in 10 min.

6. ACh had no effect on 36Cl− retention at 3 or 11 m
M‐glucose, or on the oxidation of
D‐[U‐14C]glucose (11 m
M).

7. The insulin secretory potentiator, ACh, does not act by accelerating glucose oxidation and does not induce the same ionic effects as the secretory initiator,
D‐glucose. Increased Na+ permeability and altered interaction of Ca2+ with the plasma membrane may play roles in the cholinergic depolarization of β‐cells and potentiation of insulin release.
The effcts of sodium fluoride on gastric acid and electrolyte output in the anaesthetized cat.
Authors: Reed J D , Smy J R
Published: December 2014

1. The possibility of a Na+/H+ exchange mechanism in the presence of NaF (Bond & Hunt, 1956) has been studied in acid secreting and non‐acid secreting stomachs of anaesthetized cats. 2. In non‐acid secreting stomachs, although H+ loss and Na+ gain were both pH related, there was no constant relationship between the two. 3. The H+ loss in non‐acid secreting stomachs could not account for the H+ loss in histamine stimulated stomachs. 4. In acid secreting stomachs the Na+ or neutral Cl‐ gain was only of the order of 50% of the H+ loss, and, in the presence of isosmolal NaNO3, NaF produced the same reduction in H+ but with a markedly suppressed gain in neutral chloride. 5. The NaF induced reduction in H+ output was accompanied by reductions in the total Cl‐ output, the K+ output and the mucosal blood flow. 6. It is concluded that the reduction in H+ output from histamine stimulated stomachs is largely a result of inhibition of secretion.
Post‐exercise ketosis.
Authors: Koeslag J H , Noakes T D , Sloan A W
Published: December 2014

1. The effect of exercise on blood ketone body concentrations was studied in trained athletes and in sedentary subjects pedalling a bicycle ergometer. 2. Although the untrained subjects had higher heart rates and blood lactate concentrations at the same work load as the athletes, neither group developed ketonaemia even after intense or prolonged exercise. 3. Older subjects developed post‐exercise ketonaemia, reaching maximum about 3 hr after exercise. 4. A high‐carbohydrate diet before the exercise could prevent the onset of post‐exercise ketonaemia and a low‐carbohydrate diet enhanced it. The highest post‐exercise blood ketone levels were recorded in marathon runners after a "glycogen‐stripping' regimen. 5. Concentrations of free fatty acids, glucose, growth hormone and insulin in blood after exercise followed different patterns from that of ketones. 6. Post‐exercise ketosis, when it occurs in untrained subjects, may be due to a lower carbohydrate intake than that of athletes.
Electrical excitability of outgrowing neurites of embryonic neurones in cultures of dissociated neural plate of Xenopus laevis.
Authors: Willard A L
Published: December 2014

1. I have studied the electrical excitability of outgrowing processes of individual neurones in cultures made from dissociated neural plates of embryos of Xenopus laevis prior to the time of neurite outgrowth in vivo. 2. The electrical excitability of neurites was tested by stimulating them extracellularly and recording responses with an intracellular electrode in their cell bodies; neurites were excitable at all times examined. 3. The ionic basis of the excitability of neurites was tested by recording from cells while changing the composition of the salines perfusing the cultures. 4. In cultures less than 10 hr old, all neurites tested made responses which depended on Ca2+. The action potentials of the cell bodies were also Ca2+‐dependent at these times. 5. Between 10 and 12 hr in culture, a time at which the cell bodies still made Ca2+‐dependent action potentials, neurites acquired the ability to make Na+‐dependent responses. At these times, two‐thirds of neurites tested retained the ability to produce divalent cation‐dependent action potentials when perfused with solutions of isotonic Ba2+. 6. After 12 hr in culture, no neurites were observed to make Ca2+‐or Ba2+‐dependent responses; only Na+‐dependent responses were observed. Cells continued to initiate and elongate new neurites until about 24 hr in culture. Thus neurites sent out at different times in culture differed in their development of excitability. 7. Cell bodies making exclusively Ca2+‐dependent action potentials could be found until about 15 hr in culture, after which time a Na+‐dependent component appeared. Cell bodies could then be observed to make action potentials which depended on both Ca2+ and Na+ until about 3 days in culture. After 3 days, most cell bodies made predominately Na+‐dependent action potentials. Unlike the neurites, cell bodies retained the ability to make action potentials in isotonic Ba2+ for as long as the cultures were maintained (up to 5 days). 8. The possibility that changes in the ionic basis of action potentials reflected the death of one population of cells and the simultaneous appearance of another population with different properties was eliminated by observing the fate of single cells while changes in the physiological properties were occurring. Such observations showed that the majority of cells in each culture were surviving throughout the period of study. 9. Thus the membranes of the neurites and cell bodies of neurones in these cultures appeared to undergo independently timed changes in the ionic basis of their action potentials.
Voltage‐dependent charge movement in frog slow muscle fibres.
Authors: Gilly W F , Hui C S
Published: December 2014

1. Voltage‐clamp experiments on frog slow and twitch fibres were carried out using the three‐micro‐electrode technique. Potassium currents were blocked by tetraethylammonium. Contraction was blocked by 2 mM‐tetracaine. 2. After subtracting the linear capacitive and leakage currents, the delta V(test‐control) traces from slow fibres show ‘on’ and ‘off’ charge movements similar to those observed in twitch fibres. 3. The time integrals of the ‘on’ and ‘off’ transients, Qon and Qoff, in slow fibres are, as in twitch fibres, almost equal in magnitude but opposite in direction. 4. The charge‐voltage distribution is well fitted by a sigmoid curve given by (Formula: see text), which has been successfully applied to twitch fibres. Data from three fibres gave V = ‐25 mV, k = 13 mV, and Qmax = 7 nC/microF. Thus, intramembranous charge in slow fibres has the same steady‐state voltage distribution as that in twitch fibres, but the quantity of maximum movable charge is only 1/4 to 1/3 as large. 5. Charge movement in slow fibres does not inactivate completely when the fibres are held at ‐20 to 0 mV for durations as long as 30 min. 6. These results show that charge movement exists in slow fibres and may serve the same function in regulating contractile activation as that postulated for twitch fibres. The lack of complete inactivation may be consistent with the ability of slow fibres to maintain maximal tension during prolonged depolarizations.
Chest wall movements during fetal breathing in the sheep.
Authors: Poore E R , Walker D W
Published: December 2014

1. Movement of the chest wall and abdomen during episodes of breathing has been measured by an ultrasound technique in ten fetal lambs. 2. The fetal thoracic and abdominal walls move inwards and outwards respectively during inspiration. The position where this transition occurs is variable. 3. Movement of the lateral thoracic walls is reduced or reversed during breathing stimulated by hypercapnia while inward dorso‐ventral movement increases. 4. Deep inspiratory efforts were associated with large inward then outward movements of the lateral and large inward movements of the dorso‐ventral thoracic walls. 5. No relationship was found between the amplitude of the tracheal pressure deflexions and the extent of thoracic wall movements during fetal breathing.
The requirement for calcium ions and the effect of other ions on axoplasmic transport in mammalian nerve.
Authors: Chan S Y , Ochs S , Worth R M
Published: December 2014

1. Until recently it was believed that axoplasmic transport in vitro was not affected by Ca2+, transport being normal in Ca2+‐free medium. This was found due to the presence of the relatively impermeable perineurial sheath around the nerve trunks. Using a desheathed cat peroneal nerve preparation, axoplasmic transport was shown to require an adequate level of Ca2+ in the external medium. In a buffered Ca2+‐free medium, transport began to decline within 30 min and a complete block occurred in 2 . 6 hr. A concentration of 5 mM‐Ca2+ added to a buffered isotonic sucrose of NaCl solution was able to maintain transport. With lower concentrations of Ca2+ of 1 . 5‐3 . 0 mM, those usually present in the extracellular fluid or in a Ringer medium, some impairment of transport was seen but the addition of 4 mM‐K+ restored the normal pattern of axoplasmic transport. With Ca2+ concentrations below 0 . 75 mM, however, 4 mM‐K+ was unable to sustain transport. 2. Potassium by itself at a concentration of 4 mM when added to a buffered isotonic sucrose of NaCl medium was unable to prolong the time of transport block beyond that seen in buffered isotonic NaCl or sucrose solutions. In concentrations of K+ up to 25 mM, 1 . 5‐5 mM‐Ca2+ was required for normal transport. With moderately higher concentrations of K+ in the range of 50‐100 mM, normal appearing transport was seen with or without Ca2+. This was seen whether or not Na+ was present in the medium. At higher levels of K+, 120‐150 mM, decreased transport was seen, with or without the addition of either 15 mM‐Na+ or Ca2+ in concentrations of 1 . 5‐3 . 0 mM. 3. While Mg2+ could not substitute completely for Ca2+ in maintaining transport, it was able to prolong the time before block occurred. An extra 30‐60 min of downflow was seen when 5 mM‐Mg2+ was added to a buffered isotonic NaCl medium. Magnesium also acts synergistically with Ca2+. Concentration of Ca2+ as low as 0 . 25 mM was, with the addition of 1 . 5 mM‐Mg2+, able to maintain transport. 4. The results are interpreted in the light of studies of the mechanism of Ca2+ regulation known to occur in giant nerve fibres and other clls controlling the level of free Ca2+. The relationship of Ca2+ to the mechanism considered to underlie axoplasmic transport in nerve fibres is also discussed.
Some properties of spontaneous excitatory junction potentials recorded from arterioles of guinea‐pigs.
Authors: Hirst G D , Neild T O
Published: December 2014

1. Spontaneous excitatory junction potentials were recorded from electrically short segments of arterioles taken from the intestinal submucosa of guinea‐pigs. 2. Histograms of the amplitudes of these spontaneous potentials were unimodal; their amplitudes often corresponded with the amplitudes of the smallest evoked potentials recorded from the same preparation. 3. The time courses of both spontaneous and evoked potentials were very similar and it is suggested that evoked potentials are made up by the simultaneous occurrence of several spontaneous potentials. 4. The mean quantal content of evoked potentials was always far fewer than the number of varicosities present in the preparations. 5. It is suggested that during neuromuscular transmission, transmitter is released at relatively few sites throughout the ground plexus for each nerve impulse.
Characteristics of the release of adenosine from slices of rat cerebral cortex.
Authors: Hollins C , Stone T W
Published: December 2014

1. The characteristics of the release of adenosine have been examined from slices of rat cerebral cortex after incubation with [3H]adenine or [3H]adenosine. 2. Increasing the potassium concentration of the extracellular medium to 36 or 54 mM did not evoke any release, but release was observed in the first post‐potassium sample. This occurred whether potassium was present for 2 or 10 min. 3. Calcium‐free solutions or verapamil prevented the post‐potassium release of tritium. Tetraethylammonium bromide and 4‐aminopyridine had no effect. 4. Ouabain (100 microM) induced the release of tritium, and did not prevent an additional increment of release after potassium stimulation. Ouabain induced release did not occur in calcium‐free or sodium‐free media, but was increased in low calcium (0.1 mM) medium. 5. It is concluded that the characteristics of adenosine release are unlike those of conventional neurotransmitters. It is suggested that the release is associated with the influx of sodium and calcium ions through sodium channels.
A post‐natal decrease in acetylcholine channel open time at rat end‐plates.
Authors: Fischbach G D , Schuetze S M
Published: December 2014

1. The mean channel open time (tau) of ACh receptors in adult developing rat skeletal muscle was estimated by analysis of ACh current fluctuations. 2. At adult end‐plates, tau was 1.4 msec at 21 degrees C. Time constants of miniature end‐plate current decays (taus) were equally brief. 3. On the other hand, tau and taus were long (4.5 msec, 21 degrees C) at neonatal rat end‐plates. These estimates are comparable to values obtained at extrajunctional sites on embryonic rat myotubes grown in culture and on adult denervated muscle fibres. 4. Both tau and taus decreased to values characteristic of adult end‐plates during the first 2 weeks after birth. 5. Complex ACh power spectra were obtained at most end‐plates during the transition period and at some, miniature synaptic current decays were doubly exponential. End‐plates in transition might contain a mixture of slow, neonatal channels and fast, adult channels.
Modification of thermoregulatory responses in rabbits reared at elevated environmental temperatures.
Authors: Cooper K E , Ferguson A V , Veale W L
Published: December 2014

1. Pregnant New Zealand white rabbits were kept from 14 days pre‐partum at an environmental temperature of 33 degrees C, and their offspring were reared at this temperature. 2. In response to a 4 hr cold exposure, animals (aged 90‐180 days) raised in this way showed significant drops in colonic temperature (‐2.7 +/‐ 0.5 degrees C) while control animals reared at 20 degrees C did not (+0.05 +/‐ 0.1 degrees C). 3. A reduced, monophasic endotoxin fever was observed in animals reared at 33 degrees C, while a normal biphasic fever was seen in rabbits originally reared at 20 degrees C and subsequently acclimated to 33 degrees C. 4. A greatly reduced temperature response to intravenous infusion of noradrenaline was also found in animals raised at 33 degrees C. 5. It is proposed that thermal afferent input during early life may play an important role in the development of the thermoregulatory system.
Acetylcholine sensitivity of developing ectopic nerve‐muscle junctions in adult rat soleus muscles.
Authors: Lømo T , Slater C R
Published: December 2014

1. The development of junctional ACh sensitivity has been studied during the formation of ectopic nerve‐muscle junctions (n.m.j.s) between the superficial fibular nerve and the denervated soleus muscle of adult rats. 2. When the soleus nerve was cut 2 weeks or more after implanting the fibular nerve, spontaneous m.e.p.p.s and evoked e.p.p.s were first detected in the vicinity of the fibular nerve sprouts 2.5‐3 days later. At this time, peaks of local ACh sensitivity greater than the high level of extrajunctional sensitivity induced by denervation were found near the sprouts of the fibular nerve. 3. During the first week of foreign innervation, the extrajunctional sensitivity of the newly innervated muscle fibres fell, but the peaks of sensitivity in the region of the fibular nerve sprouts persisted. Many of these peaks occurred at sites of transmitter release from the fibular nerve terminals. Each innervated fibre had from 1‐8 such peaks. 4. When the fibular nerve was cut 2 days or more after cutting the soleus nerve peaks of ACh sensitivity persisted in the region of the degenerated foreign nerve terminals even if the extrajunctional sensitivity was abolished by direct electrical stimulation of the muscle starting soon after cutting the fibular nerve. 5. When the fibular nerve was left intact, more than half of the peaks of sensitivity formed initially in the region of the foreign nerve sprouts had disappeared 2‐3 weeks after cutting the soleus nerve. 6. We conclude that during the formation of ectopic n.m.j.s in adult rat muscle the foreign nerve terminals bring about two types of long‐lasting change in the distribution and stability of the underlying ACh sensitivity in the muscle fibre membrane; an increase and stabilization of sensitivity at sites of transmitter release which occurs by the time functional transmission at the newly formed n.m.j.s can be detected, and a loss of sensitivity at some of the sites which takes place about 1‐2 weeks later.
Temperature regulation and prostaglandin E1 fever in scorpions.
Authors: Cabanac M , Le Guelte L
Published: December 2014

1. Scorpions Buthus occitanus and Androctonus australis were placed in a temperature gradient where they could select their thermopreferendum. Intrathoracic temperature was recorded continuously. 2. Both species selected 24.8 +/‐ 1.0 degrees C as their preferred body temperature. No nycthemeral cycle of preference was observed in the experimental conditions. Saline injection did not modify this thermopreferendum. 3. Prostaglandin E1 (PGE1) produced a fever. Duration and magnitude of fevers were related to PGE1 doses in a bell‐shaped curve. The longest and highest fevers were obtained with 4 microgram . g‐1 PGE1. 4. These results show that there is an ability to produce fever and, thus, indirectly, that there is a set point in body temperature regulation in arthropods, among the oldest known terrestrial animals.
The course of post‐ganglionic sympathetic fibres distributed with the trigeminal nerve in the cat.
Authors: Matthews B , Robinson P P
Published: December 2014

1. The course of post‐ganglionic sympathetic fibres to the jaws, face and eye was investigated in cats by observing the effects of nerve sections on responses evoked by stimulation of the cervical sympathetic trunk. 2. Sympathetic fibres were present in the infraorbital and inferior alveolar nerves. From the superior cervical ganglion, all of these fibres travelled in the internal carotid nerve and all but a few passed through the foramen lacerum and joined the trigeminal nerve at its ganglion. 3. Compound action potentials were recorded from sympathetic fibres in six out of twenty‐seven teeth. These fibres followed the route described above. 4. Sympathetic fibres to the pupil and levator palpebrae superioris passed from the internal carotid nerve to the eye via the foramen lacerum and the superior orbital fissure. Some fibres causing piloerection in front of the ear travelled by the same route and some travelled with the maxillary division of the trigeminal nerve. 5. Sympathetic fibres to the nictitating membrane followed a similar route to those supplying the pupil except that they entered the cranial vault through the pterygoid foramen. 6. The secretomotor fibres to the submandibular salivary gland and some vasoconstrictor fibres to the lip did not travel with the internal carotid nerve or major branches of the trigeminal nerve.
Fever and antipyresis in the crayfish Cambarus bartoni.
Authors: Casterlin M E , Reynolds W W
Published: December 2014

1. Normothermic Cambarus bartoni crayfish thermoregulating behaviourally in an electronic shuttlebox prefer a mean temperature of 22.1 degrees C +/‐ 0.5 S.E. of mean. 2. Injection of 1% saline, or addition of paracetamol to the ambient water, caused a statistically insignificant decrease in preferred temperature of 0.4 degrees C. 3. Injection of killed Aeromonas hydrophila bacteria into the abdomen caused a significant mean increase in preferred temperature of 1.8 degrees C (defined as a behavioural fever). 4. Injection of A. hydrophila, with paracetamol in the water, resulted in an insignificant increase of 0.1 degrees C above the normothermic temperature; thus paracetamol is antipyretic in crayfish, preventing fever but not altering afebrile thermoregulation. 5. These results suggest that similar mechanisms may be operating in the neuropharmacological mediation of fever in vertebrates and invertebrates.
Calcium spikes in toad rods.
Authors: Fain G L , Gerschenfeld H M , Quandt F N
Published: December 2014

1. When the retina of the toad, Bufo marinus, was superfused with 6‐12 mM‐tetraethylammonium chloride (TEA), intracellular recordings from rods showed large, depolarizing regenerative potentials. For brief exposures to TEA, these potentials occurred during the recovery phase of the light responses; whereas, during longer exposures, they were spontaneous in darkness but suppressed during illumination. Similar regenerative potentials were observed during perfusion with 3‐10 mM‐4‐aminopyridine and 1‐2 mM‐BaCl2. 2. The amplitude of the regenerative potentials depended upon the extracellular Ca concentration ([Ca2+]o). Lowering [Ca2+]o decreased their amplitude and in zero [Ca2+]o they were reversibly abolished. Increasing [Ca2+]o by 1.5‐2 times produced a small hyperpolarization of membrane potential and a large augmentation in regenerative response amplitude. However, larger increases in [Ca2+]o produced large membrane hyperpolarizations and reversibly suppressed the regenerative responses. 3. High concentrations of Sr2+ in TEA also enhanced regenerative activity but did not affect the rod resting membrane potential. The amplitude of regenerative potentials increased continuously with increasing [Sr2+]o, and in 28 mM‐Sr2+ the rods generated 60‐70 mV action potentials, even in the absence of extracellular Na+. 4. The regenerative potentials were blocked by 25 microM‐Cd2+, 50‐100 microM‐Co2+, 5mM‐Mg2+, and 100 microM‐D‐600. They were unaffected by 2 microM‐TTX or 2‐5 mM‐Na aspartate. 5. In Ringer containing 12 mM‐TEA, large anode break responses could be recorded from rods at the termination of inward current pulses. These anode break responses were also suppressed by Co2+ and unaffected by TTX or Na aspartate. 6. We conclude that the membrane of toad rods contains a conductance normally selective for Ca2+, which is activated by depolarization. In normal Ringer, the inward current through this conductance produces little effect, since it is balanced by a large outward current, probably carried by K+. TEA and other agents appear to block this outward current, permitting the Ca2+ current to become regenerative.
A comparative study of the kinetics of the Bohr effect in vertebrates.
Authors: Maren T H , Swenson E R
Published: December 2014

1. The kinetics of the Bohr effect and the role of carbonic anhydrase were studied in a series of representative vertebrates using a continuous flow rapid reaction apparatus. 2. The rates of the Bohr effect in vertebrates are very similar, and differences among classes are manifestations of the ambient temperature. 3. Complete carbonic anhydrase inhibition causes a fifteen to fortyfold reduction in the rate of the Bohr effect, sufficient to abolish its occurrence within capillary transit. 4. There is a twenty‐three‐fold (duck) to 360‐fold (man) excess of carbonic anhydrase activity in vertebrate red cells for the normal generation of the Bohr effect. 5. When carbonic anhydrase is inhibited and CO2 hydration becomes rate limiting, the stoichiometry of the Bohr effect (delta log pO2/delta pH) is revealed in the ratio of the rates of proton formation in red cells to O2 release from haemoglobin.
The effects of ambient temperature on urinary flow and composition in the fowl.
Authors: Azahan E , Sykes A H
Published: December 2014

1. Urine flow and compositions were determined in normally hydrated, waterloaded and hypotonic saline infused hens under various ambient temperatures (Ta). 2. At Ta 29 and 32 degrees C normal urine flow was reduced and osmolality increased; at Ta 0 and ‐5 degrees C urine flow increased and osmolality decreased. 3. In hydrated hens at Ta 32 degrees C antidiuresis occurred within 10 min and persisted for 2 hr without any significant change in rectal temperature (Tr). 4. At Ta 40 degrees C there was no antidiuresis but a tendency for urine flow to increase; Tr also rose. The antidiuresis shown by water‐restricted hens at Ta 20 degrees C was abolished at Ta 40 degrees C. 5. An antidiuresis, similar to that seen at Ta 32 degrees C, could be produced at Ta 20 degrees C by moderate haemorrhage, exposure to infra‐red heating or by vasopressin or vasotocin. Adrenaline and noradrenaline provoked a diuresis. 6. Hypothalamic heating failed to elicit an antidiuresis but hypothalamic cooling increased urine flow at Ta 20 degrees C and abolished the antidiuretic response at Ta 32 degrees C. 7. It is concluded that the antidiuresis seen at warm ambient temperatures is caused by the release of antidiuretic hormone possibly as a response to a rise in skin temperature.
Effect of calcium antagonism or chelation on rabbit lacrimal gland secretion and membrane potentials
Authors: Botelho Stella Y. , Dartt Darlene A.
Published: December 2014

1. ACh‐induced secretion from the main excretory duct, as well as ACh‐induced hyperpolarizations and resting membrane potentials of superficial, probably acinar, cells were recorded from the rabbit lacrimal gland perfused in vivo with either control or test solutions.

2. During perfusion with test solution containing a Ca antagonist, verapamil (10−5 to 10−3
M), or a Ca chelator EGTA (10−4 or 10−3
M), ACh‐induced secretion was only 30% of the control value, whereas the magnitude of the ACh‐induced hyperpolarization was unchanged.

3. With 10−5
M‐verapamil, but not with 10−3
M‐verapamil or EGTA‐containing solutions, the inhibition of ACh‐induced flow was completely reversed either by replacing the test with control solution or by increasing the Ca concentration of the test solution twofold.

4. In addition, EGTA (10−4
M) solution containing the normal extracellular Ca2+ concentration inhibited secretion by 30%.

5. During perfusion with verapamil or EGTA test solutions the mean resting membrane potential of superficial, probably acinar, cells was depolarized by 15%.

6. It is concluded that although extracellular Ca is required for the major portion of ACh‐induced secretion, the magnitude of the ACh‐induced hyperpolarization of cells, which are most likely acinar, is independent of extracellular Ca.
Effect of D‐600 on inhibition of in vitro renin release in the rat by high extracellular potassium and angiotensin II.
Authors: Churchill P C
Published: December 2014

1. Renin was secreted by rat renal cortical slices incubated at 37 degrees C in a physiological saline solution. 2. Secretion was nearly abolished by incubation in a medium containing 60 mM‐K. Secretion could be restored to the control level by the addition of 5 X 10(‐7) M‐D‐600 (methoxy verapamil) to 60 mM‐K medium. 3. Angiotensin II inhibited renin secretion in a concentration‐dependent manner. Concentrations of D‐600 ranging from 1 to 3 X 10(‐6) M (two to sixfold higher than required to block the inhibitory effect of high K) failed to antagonize the inhibitory effect of angiotensin II. 4. Ca is required for the inhibitory effect of angiotensin II, however, as Ca‐depletion (incubation of slices in a medium with Na2EGTA and no added CaCl2)( progressively decreased and finally abolished any inhibitory effect. 5. These results confirm and extend previous observations suggesting that Ca plays an inhibitory coupling role in the control of renin secretion from the juxtaglomerular apparatus. Moreover, they suggest that although voltage‐sensitive channels exist on juxtaglomerular cells, angiotensin II activates an independent pathway for Ca mobilization.
Optical signals from early embryonic chick heart stained with potential sensitive dyes: evidence for electrical activity.
Authors: Fujii S , Hirota A , Kamino K
Published: December 2014

1. Using an optical method for monitoring membrane potential, spontaneous electrical activity in the very early embryonic chick heart at the 7‐9 somite stages was measured. 2. Spontaneous absorption signals from the 7‐8 somite embryonic chick hearts stained with a potential sensitive merocyanine‐oxazolone dye were demonstrated. The signals were observed also when a merocyanine‐rhodanine dye was used. These signals were identified as spontaneous electrical activity in the embryonic heart cells. 3. The action spectrum in absorption of the merocyanine‐oxazolone dye was triphasic in early embryonic chick heart with an increase in transmittance from 750 to 700, a decrease from 700 to 600, and an increase from 600 to 525 nm. 4. The magnitude of the signal was about 10(‐3) of the resting intensity at 675 nm, with the merocyanine‐oxazolone dye. The spontaneous absorption signals had a signal‐to‐noise ratio of about 10, respectively. 5. The absorption signals were markedly depressed by a higher external K+‐concentration, however, were not affected by tetrodotoxin (TTX). 6. The results indicate that spontaneous electrical activity is generated at the 7‐9 somite developmental stage before the initiation of heartbeat.
Neuromuscular transmission without sodium activation of the presynaptic nerve terminal in the lobster.
Authors: Kawai N , Niwa A
Published: December 2014

1. We studed Na‐independent synaptic transmission in the inhibitory synapse of the walking leg of the spiny lobster (Palinurus japonicus). 2. After loading the preparation with tetrodotoxin (TTX), brief depolarizing current injected in the inhibitory axon produced a small action potential, which propagated to the nerve terminal and gave rise to inhibitory post‐synaptic potentials (i.p.s.p.) 3. The presynaptic action potential, in the presence of TTX, failed to propagate after removing Na+ in the solution. The TTX‐resistant action potential was decreased, but not blocked by 30 mM‐CoCl2. 4. When 4‐aminopyridine (4‐AP) was added to low Na+ or Na‐free solution containing TTX synaptic transmission was restored. When the duration of the current pulse was increased, graded i.p.s.p. were evoked. 5. In high Ca2+ solutions containing K blockers, action potentials with prolonged duration were evoked. 6. The action potential of the presynaptic axon of the lobster neuromuscular junction depends on both Na+ and Ca2+.
Effects of dietary intake of sodium chloride on sugar and amino acid transport across isolated hen colon
Authors: Lind J. , Munck B. G. , Olsen O.
Published: December 2014

1. Using the isolated mucosa from the colon of the adult hen, transport of galactose, leucine and lysine was studied through measurements of influx across the brush‐border membrane, unidirectional transmucosal fluxes, and of steady‐state mucosal uptake.

2. In hens maintained on a NaCl rich diet influx of galactose, leucine and lysine were saturable processes with well defined values for Jmax and Kt. All three substances were actively transported across the epithelium and accumulated in the mucosal tissues to steady‐state concentrations several times higher than in the incubation media.

3. In hens maintained on a NaCl poor diet the Kt of the leucine influx was markedly increased and the Jmax moderately decreased, while the epithelium maintained the capability of active transepithelial transport and of establishing a steady‐state tissue/medium distribution ratio well above 1. Galactose and lysine could no longer be actively transported and in the steady state their tissue concentrations did not exceed those of the medium.

4. It is proposed that in the low NaCl colon the processes of galactose and lysine co‐transport with Na are abolished and that the transport of galactose proceeds via a phloretin sensitive system like that described for the enterocyte of the chicken small intestine.

5. In the high NaCl colon 1 m
M‐leucine increases the mucosa to serosa flux of lysine by a factor 2·8 without affecting the serosa to mucosa flux or the steady‐state mucosal accumulation of lysine. In the low NaCl colon 1 m
M‐leucine induces active transepithelial transport of lysine. Assuming that the active transport of leucine is secondary to the transport of Na, leucine‐induced active transport of lysine is described as a tertiary active transport.

6. In the high NaCl colon the mucosa to serosa flux and the steady‐state mucosal accumulation of leucine were inhibited by galactose which had no effect on leucine influx across the brush‐border membrane. Leucine did not affect any of the parameters of galactose transport.
The decay of end‐plate currents in neostigmine‐treated frog muscle blocked by acetylcholine or tubocurarine.
Authors: Guinan J J
Published: December 2014

1. The decay times of e.p.c.s. (with acetylcholinesterase inhibited by neostigmine) were measured with a view to inferring the extent of acetylcholine (ACh) binding. 2. E.p.c.s from muscles blocked by ACh decayed at less than half the rate of e.p.c.s. from muscles blocked by tubocurarine, and slightly more slowly than m.e.p.c.s. from unblocked muscles. 3. ACh prolonged e.p.c.s and reduced their amplitudes when added to muscles blocked by tubocurarine. 4. After treatment with alpha‐bungarotoxin, some e.p.c.s. from muscles blocked by ACh were prolonged relative to e.p.c.s from muscles blocked by tubocurarine. 5. These phenomena are interpreted as indicating that either (a) desensitized receptors bind ACh and prolong e.p.c.s by buffered diffusion or (b) in highly desensitized muscles there is a population of active receptors which bind ACh for many milliseconds.
Cerebral blood flow and oxidative metabolism during hypoxia and asphyxia in the new‐born calf and lamb.
Authors: Gardiner R M
Published: December 2014

1. The effects of hypoxia and asphyxia on cerebral blood flow and oxidative metabolism have been investigated in the calf and lamb under sodium pentobarbitone anaesthesia. 2. Cerebral blood flow was determined using a hydrogen clearance technique, and cerebral metabolism quantified by the simultaneous measurement of arteriocerebral venous concentration differences for oxygen, glucose and lactate. Continuous measurements were made of arterial and cerebral venous PO2 in vivo. 3. Both cerebral blood flow and oxygen consumption were less in animals anaesthetized with sodium pentobarbitone than in conscious animals. 4. In the calf, recovery from transient episodes of severe hypoxia and asphyxia was associated with a rapid recovery and overshoot of cerebral venous PO2. Evidence was obtained that rapid changes in blood pressure during severe asphyxia were associated with pressure‐passive cerebral blood flow. Prolonged hypoxia (Pa,O2:21 +/‐ 2 mmHg) with normocapnia was associated with an increase in cerebral blood flow, fall in cerebral oxygen consumption, and no change in the glucose‐oxygen index. 5. In the lamb, prolonged asphyxia (Pa,O2:30 +/‐ 1 mmHg; Pa,CO2:56 +/‐ 2 mmHg) was associated with an increase in cerebral blood flow. Cerebral glucose uptake did not change, but cerebral oxygen consumption was markedly depressed, and the glucose‐oxygen index increased. 6. In the lamb during normoxia, there was a linear correlation between cerebral blood flow and arterial PCO2 in the range 10‐95 mmHg (r = 0.92; P < 0.001), with a slope of 1.74 ml. 100g‐1 min‐1 . mmHg Pa,CO2‐1 . Hypoxia did not significantly increase the fall in cerebral vascular resistance associated with a rise in Pa,CO2 from 34 to 56 mmHg.
Control of repetitive firing in squid axon membrane as a model for a neuroneoscillator.
Authors: Guttman R , Lewis S , Rinzel J
Published: December 2014

1. Repetitive firing in space‐clamped squid axons bathed in low Ca and stimulated by a just suprathreshold step of current can be annihilated by a brief depolarizing or hyperpolarizing pulse of the proper magnitude applied at the proper phase. 2. In response to such perturbations, membrane potential and ionic currents show damped oscillations toward a steady state. 3. For other, non‐annihilating, perturbations repetitive firing resumes with unaltered frequency but with phase resetting. 4. Experimental findings are compared with calculations for the space‐and current‐clamped Hodgkin‐Huxley equations. Annihilation of repetitive firing to a steady state corresponds to a solution trajectory perturbed off a stable limit cycle and into the domain of attraction of a coexistent stable singular point. 5. Experimentally and theoretically the nerve exhibits hysteresis with two different stable modes of operation for a just suprathreshold range of bias current: the oscillatory repetitive firing state and the time‐independent steady state. 6. Analogy is made to a brief synaptic input (excitatory or inhibitory) which may start or stop a biological pace‐maker.
Mechanism of the noradrenergic motor control on the lower oesophageal sphincter in the cat.
Authors: Gonella J , Niel J P , Roman C
Published: December 2014

1. The release of labelled acetylcholine has been measured on lower oesophageal sphincter (l.o.s.) muscular strips previously loaded with tritiated choline. 2. This release was greatly increased by noradrenaline 10(‐5) g/ml. and unaffected by atropine 10(‐6) g/ml., but it was practically abolished if hemicholinium 5.2 X 10(‐4) M was added to the incubating bath containing the tritiated choline. 3. A radioautographic study of sections of l.o.s. strips loaded with tritiated choline showed that the radioactivity was mainly located in the nervous cells of the enteric plexuses and that the muscular cells were very poorly labelled. 4. The increased release of acetylcholine induced by noradrenaline did not occur in a Ca2+‐free or in a hypermagnesic Tyrode (12 mM). 5. Tetrodotoxin 10(‐6) G/ml. had no effect on the increased release of acetylcholine induced by noradrenaline. In addition, sucrose gap recordings showed that the depolarizing effect of noradrenaline on l.o.s. muscular strips was unaffected by tetrodotoxin 10(‐6) g/ml. 6. It is concluded that acetylcholine released in the l.o.s. under the action of noradrenaline originated from the synaptic endings of the cholinergic intramural neurones.
Chloride‐bicarbonate exchange in human red cells measured using a stopped flow apparatus.
Authors: Lambert A , Lowe A G
Published: December 2014

1. A new stopped‐flow apparatus has been used to measure the exchange of intracellular chloride and extracellular bicarbonate across the human erythrocyte membrane at 37 degrees C. 2. The concentration dependence of the activation of the anion exchange system by extracellular bicarbonate was consistent with the existence of a saturable membrane‐carrier. Analysis of the results assuming Michaelis‐‐Menten kinetics indicated a Vmax for chloride‐‐bicarbonate exchange of 73 . 4 +/‐ 14 . 4 mol. (3 x 10(13) cells.min)‐1 and Km for bicarbonate of 11 . 1 +/‐ 2 . 8 mM at 37 degrees C (pH 7 . 1). 3. Correction of the directly computed values of Vmax for incomplete saturation of the carrier by intracellular chloride and the inhibitory effects of intracellular bicarbonate and extracellular chloride gave a Vmax of 157 +/‐ 43 . 8 mol (3 x 10(13) cells.min)‐1 and a Km of 15 . 5 +/‐ 5 . 2 mM‐bicarbonate at 37 degrees C. 4. Comparison of Vmax obtained at 37 and 10 degrees C indicates that the activation energy for chloride‐‐bicarbonate exchange in this temperature range is 18 . 7 ‐‐19 . 6 kcal.mol‐1 depending on whether corrected or uncorrected values are used. 5. Extracellular furosemide inhibited chloride‐‐bicarbonate exchange with a KI of 0 . 12 microM assuming competition between furosemide and bicarbonate and 0 . 17 microM assuming non‐competitive inhibition. 6. Extracellular chloride also inhibited chloride‐‐bicarbonate exchange but the kinetics of inhibition were complex.
Atropine does not abolish cephalic vagal stimulation of gastrin release in dogs
Authors: Dockray G. J. , Tracy Hilda J.
Published: December 2014

1. The effect of atropine was studied on serum gastrin responses to feeding in conscious gastric fistula dogs. Intragastric pH was monitored and could be maintained at pH 6·0 by infusion of sodium bicarbonate into the gastric fistula.

2. A standard liquid meal was consumed by the dogs in less than a minute. Serum gastrin increased from a basal concentration of 8 pmol/l to a peak of 27 pmol/1 at 4‐7 min, and intragastric pH fell to less than 3·0 after 20 min. Since vagotomy abolished the early gastrin response to feeding, and instillation of the meal directly into the fistula produced only a modest and delayed increase in serum gastrin, we conclude that cephalic vagal stimulation played a major part in mediating the gastrin responses. When intragastric pH was maintained at 6·0 serum gastrin was significantly higher at all times from 4 to 50 min after feeding, indicating the importance of acid inhibition in the control of gastrin secretion.

3. After atropine (25 or 100 μg/kg), acid secretion was abolished and intragastric pH was about 6·0 at all times. The low dose of atropine enhanced the gastrin response to feeding, but the time course and magnitude of the response closely resembled that to normal meals pH‐stated to 6·0. The high dose of atropine decreased, but did not abolish serum gastrin responses to feeding.

4. When the meal was allowed to drain freely from the gastric fistula (virtually eliminating stimulation of gastrin release by luminal mechanisms) serum gastrin again reached a peak after 4‐7 min, and neither dose of atropine significantly changed the response.

5. It is concluded that cephalic vagal stimulation of gastrin release is atropine resistant and so unlikely to be mediated by muscarinic receptors. The enhanced gastrin response to feeding caused by moderate doses of atropine can be attributed to the loss of acid inhibition of gastrin release. The neuropeptide bombesin is a candidate neurotransmitter for the action of post‐ganglionic vagal nerves on gastrin cells.