bluuebunny/crossref_metadata_2025 huggingface dataset:
The role of vagal innervation in gastric and pancreatic responses to meals varying in pH
Authors: Dembiński A. , Konturek S. J. , Thor P.
Published: December 2014

In three dogs provided with chronic gastric and pancreatic fistulae, gastric acid response to a peptone meal was measured by a method of intragastric titration at pre‐selected pH values ranging from 6·0 to 2·0 or at a constant pH during intravenous infusion of secretin in graded doses ranging from 0·25 to 4·0 u./kg.hr. Simultaneously, pancreatic secretion was determined by the standard collection technique and serum gastrin response was measured by radio‐immunoassay. In this way the pH profile for the inhibition of gastric response and stimulation of pancreatic secretion as well as serum gastrin response to a peptone meal have been determined and compared with that obtained with exogenous secretin or feeding a liver meal. Truncal vagotomy resulted in a significant decrease of gastric acid response to the meal at all pH levels or at all doses of secretin but the inhibitory effect of gastric acidification or secretin on serum gastrin and gastric acid response to a meal remained unchanged. Vagotomy caused a decrease of pancreatic secretory response to meals at all pH levels and at all doses of secretin except the largest one. Pancreatic secretion stimulated by secretin alone was not affected by vagotomy, whereas that induced by feeding a liver meal was markedly decreased by this procedure. From these studies we have tentatively concluded that the vagus nerve facilitates the release of intestinal hormones and that vagotomy causes a decrease of gastric and pancreatic responses to endogenous but not to exogenous stimuli.
Synapse formation during embryogenesis on ganglion cells lacking a periphery
Authors: Landmesser Lynn , Pilar G.
Published: December 2014

1. The development of transmission was studied in chick ciliary ganglia that had been deprived of their periphery during early embryonic development.

2. Peripherally deprived neurones in the ganglion differentiate in normal numbers and send functional axons into the post‐ganglionic nerve.

3. Ganglion cells lacking a periphery follow the normal developmental sequence sending out transient dendrites at the time ganglion cell synapses are formed, and later retracting them when calyces appear.

4. Synapses, which appear functionally and ultrastructurally normal, form on all ganglion cells at the normal time and transmission is normal until Stage 34. Therefore information from the periphery is not required for ganglion cell synapse formation per se.

5. From Stages 35 to 38 most cells die, so that only 8% of the original number of cells remain in the operated ganglion. Transmission fails in many cells during this same time, but precedes cell loss by only a short time, so that deafferentation probably does not contribute substantially to cell death.

6. Both ciliary and choroid cells achieve full cytologic differentiation and are distinct from each other, indicating that the periphery is not required for the elaboration of the distinctive characteristics of these cells. Presynaptic fibres also differentiate into typical bouton as well as calyciform endings. Therefore, the type of preganglionic ending does not depend on ganglion cells establishing proper peripheral contacts.

7. It has not been possible to ascertain whether ganglion cell specificity is affected by the periphery.

8. Peripheral removal affects ganglion cell migration, so that two ganglia are formed. Approximately half of the cells migrate into the remnant optic cup forming a second misplaced ganglion. Ciliary and choroid cells occur in both ganglia and these cells go through the typical sequence of events described above.
Cellular specificity of serotonin storage and axonal transport in identified neurones of Aplysia californica
Authors: Goldman James E. , Schwartz James H.
Published: December 2014

1. [3H]
D,L‐5‐hydroxytryptophan ([3H]5HTP) was injected under pressure into cell bodies of identified cholinergic and serotonergic neurones in the central nervous system of the marine mollusc, Aplysia californica.

2. Both serotonergic and cholinergic neurones converted [3H]5HTP to [3H]5‐hydroxytryptamine ([3H]5HT).

3. The fate of [3H]5HT in the two types of neurones differed. In serotonergic cells, 5HT was present primarily in particulate form; the transmitter readily moved from cell bodies into nerves by selective transport. In contrast, 5HT remained free in the cytoplasm of the cholinergic neurone, and was not transported from the cell body.

4. Treatment of Aplysia with reserpine decreased the proportion of [3H]5HT associated with particulate material, and also decreased the amount of [3H]5HT recovered.

5. Serotonergic neurones possess specific mechanisms for the storage and axonal transport of 5HT which are absent in cholinergic cells.
Adaptation of the discharge of frog muscle spindles following a stretch
Authors: Brokensha G. , Westbury D. R.
Published: December 2014

1. Stretching a frog muscle spindle evoked a discharge of action potentials in its sensory axon. As the rate of this discharge decreased during the adaptation that followed the dynamic phase of a stretch, the variability of the interspike intervals of the impulse train increased.

2. Adaptation occurred in two phases. At first the impulse train was almost regular and adapted rapidly, but later this gave way to a phase of slower adaptation where the variability of the discharge was much increased. In the second phase of adaptation the interspike intervals increased in length less than half as quickly as in the first phase.

3. When the rate of adaptation changed from the more rapid to the slower phase there was often an abrupt change in the character of the discharge and the relationship between the mean interspike interval and the variability changed. The interspike interval at which this change‐over occurred was relatively constant in records of the discharge from one afferent fibre even though stretches of different amplitude were employed, though it differed from one afferent fibre to another.

4. These features of the discharge during adaptation suggest that the two sections of the impulse trains were derived from different spike generators by a process of probabilistic mixing.
The release of histamine during gastric acid secretion in conscious rats
Authors: el Munshid H. A. , Lake H. J.
Published: December 2014

1. Conscious gastric‐cannulated rats were given [3H]histidine and aminoguanidine by dosage procedures intended to build up fast‐turnover and slow‐turnover pools of tissue [3H]histamine. Acid secretion was stimulated by I.V. infusion of pentagastrin, and the [3H]histamine content of gastric juice and excretion in urine were determined at 30 min intervals.

2. The amount of [3H]histamine in gastric juice derived from either a slow‐turnover or fast‐turnover pool was very low in unstimulated animals, and was not altered during pentagastrin‐stimulated acid secretion.

3. From a slow‐turnover pool pentagastrin caused increased urinary excretion of [3H]histamine. This was abolished by gastrectomy, so that the [3H]histamine liberated by pentagastrin from this pool appears to have been derived from the stomach. Evidence was not found for the existence of a slow‐turnover histamine pool in the glandular mucosa of the stomach, and the source within the stomach of this pentagastrin‐liberated histamine is thus uncertain.

4. From a fast‐turnover pool pentagastrin did not cause an increased urinary excretion of [3H]histamine. The amount of [3H]histamine excreted by gastrectomized rats was not different from that produced by gastric‐cannulated animals. This suggests that a high proportion of urinary histamine derived from a fast‐turnover pool was non‐gastric in origin.

5. Differences in the time scale of [3H]histamine release and acid secretion were not found. In some experiments the urinary output of [3H]histamine was prolonged beyond the end of pentagastrin administration and gastric acid secretion. However, the overall data do not suggest that urinary histamine output and gastric acid secretion take different time courses.
Effects of membrane potential, temperature and neostigmine on the conductance change caused by a quantum or acetylcholine at the toad neuromuscular junction.
Authors: Gage P W , McBurney R N
Published: December 2014

1. Miniature end‐plate currents were recorded at neuromuscular junctions of toads, either in voltage‐clamped fibres or with extracellular electrodes. The two methods gave similar results. 2. Two types of m.e.p.c.s, differing in their growth times (50–300 musec and 0–5–5 msec) were found. The more frequent had the shorter growth times. 3. The decay of m.e.p.c.s was exponential with a single time constant. The time constant was an exponential function of membrane potential, becoming less as the membrane was depolarized. In contrast, there was little change, or in some cases an increase, in growth times of m.e.p.c.s when the membrane was depolarized. 4. The decay time constant had a Q‐10 of 3–13 plus or minus 0–22 (mean plus or minus S.E. of mean) whereas the growth time had a significantly lower Q‐10 of about 1‐2. The change of decay time constant with temperature followed the Arrhenius equation giving an activation energy of 18 plus or minus 1‐0 kcal (mean plus or minus S.E. of mean). The amplitude of m.e.p.c.s increased with temperature and had a Q‐10 of 1‐5 plus or minus 0–14 (mean plus or minus S.E. of mean) in voltage‐clamped fibres. 5. Neostigmine prolonged the decay phase and increased the amplitude of m.e.p.c.s but had little effect on the growth phase. The changes in m.e.p.c.s caused by membrane potential and temperature were not affected by neostigmine. 6. The results show that the growth phase and decay phase of m.e.p.c.s are governed by processes with quite different characteristics. The reaction which limits the decay phase appears first‐order, is voltage sensitive and has a Q‐10 of about 3, whereas the reaction underlying the growth phase does not appear first‐order, is less voltage‐sensitive and has a Q‐10 of about 1‐2. It is suggested that diffusion of transmitter across the synaptic cleft may be the rate‐limiting step during the growth phase.
Eye movements due to linear accelerations in the rabbit.
Authors: Baarsma E A , Collewijn H
Published: December 2014

1. Compensatory vertical or torsional eye movements of rabbits caused by linear accelerations along the transverse or sagittal axis were measured. Sinusoidal accelerations (parallel swing) in a frequency range of 0–068‐‐1–22 Hz and acceleration steps (linear track) of 0–02‐‐0–11 g were applied. 2. On the parallel swing, properties of the maculo‐ocular reflexes were similar for transverse and sagittal acceleration. Gain (rotation of eye/rotation of the resultant linear vector) proved to be very low: about 0–1 for 0–3 Hz and smaller than 0–01 for frequencies above 1‐0 Hz. The decrease in gain was accompanied by an increase in phase lag to about 180degrees. No non‐linearity was revealed by the use of different amplitudes (10–−30 cm). 3. On the linear track, eye deviation after an acceleration step took many seconds to develop fully. Gain increased with time and was about 0–65 after 5 sec. 4. The results indicate that the responses of the otoliths, as reflected in maculo‐ocular reactions, are very slow. Fluctuations in the direction of gravity seem to be averaged over several seconds by the system. This may explain that erratic linear accelerations(frequency greater than 1 Hz) during locomotion or transport do not lead to eye movements or disorientation.
Receptive fields in cat superior colliculus after visual cortex lesions.
Authors: Berman N , Cynader M
Published: December 2014

1. The superior colliculus has been studied in intact cats and in cats with visual cortex lexions by recording the responses of single tectal units to visual stimuli. 2. Three classes of units have been identified in the superficial layers of the colliculus in these visually decorticate cats. 3. One class, comprising 5% of the units studied, has receptive fields organized concentrically in a manner similar to retinal ganglion cells. 4. The second class, comprising 12% of the units studied, responds to stimulus velocities over 300/sec, responds well to both small and large stimuli, and can be driven by strobe flashes at frequencies up to 35‐‐40/sec. These units are termed ‘flicker’ cells. 5. The third class comprising 83% of the units studied, responds best to stimuli which are not larger than the activating region of the receptive field, moving at relatively low velocities. These units show strong suppressive surrounds which are sensitive to higher velocities of stimulus movement than the central activating region. Responses from the activating region in these units are dramatically inhibited by flickering dhanges in the level of background illumination. 6. In intact cats few units are found which are strongly inhibited by background flicker. 7. It is suggested that a high‐velocity sensitive element such as the ‘flicker’ cell or phasic retinal ganglion cell is responsible for the flicker‐induced inhibition of collicular units in the visually decorticate cat.
Electrical characteristics of pancreatic islet cells.
Authors: Matthews E K , Sakamoto Y
Published: December 2014

1. The electrical properties of mouse pancreatic islet cells have been explored in vitro using a single intracellular micro‐electrode for both voltage recording and current injection. 2. The frequency of spontaneous electrical activity induced in islet cells by concentrations of D‐glucose greater than 2‐8 mM was enhanced by depolarizing, and reduced by hyperpolarizing, current injection. Post‐stimulus inhibition and facilitation were also observed. 3. Intracellular current injection evoked a spike potential in Krebs solution containing a low D‐glucose concentration (2–8mM), and in glucose‐free, but not Ca‐free solution. Evoked spikes were observed in approximately 10% of the cell population impaled. 4. The relationship between the rate of rise of an evoked spike and membrane potential displacement by intracellular current injection a sigmoid curve suggesting the presence of an inactivation process in spike potential genesis. 5. High [K]o, 30–50mM, induced electrical activity rarely, and then only transiently, thereafter blocking it; conditioning hyperpolarizing current tended to restore spike activity. 6. D‐600, 5 times 10‐minus 5M, blocked the electrical activity induced by D‐glucose, tolbutamide or current injection; these inhibitory effects were reversed by a threefold increase in [Ca]o to 7–68 mM. 7. From these results it is concluded that the electrical activity induced in islet cells by Dglucose, tolbutamide and current injection is due mainlu to Ca‐2+ influx and is dependent on the level of the membrane potential
Binocular interaction in the cat's superior colliculus.
Authors: Berman N , Blakemore C , Cynader M
Published: December 2014

1. Binocularly driven neurones with small receptive fields near the area centralis were recorded in the cat's superior colliculus. 2. Binocular interaction was tested by stimulating both eyes simultaneously with a single moving stimulus at various retinal disparities. 3. Collicular cells in general showed strong summation or even facilitation when the images of the stimulus were in exact correspondence on the receptive fields, sometimes with occlusion when they were out of register. The range of retinal disparity over which there was additive interaction could be as little as 1 or 2 deg, almost as narrow as for the most precisely tuned neurones in the visual cortex. Even cells with large receptive fields sometimes showed a narrow range of binocular interaction. 4. Non‐directional cells generally exhibited weaker summation and broader disparity selectivity than did direction‐selective cells. 5. Some neurones with virtually no response to a stimulus in one of the eyes can exhibit marked binocular interaction. Other apparently monocular cells show little or no binocular interaction. 6. The disparity of the centres of the receptive fields was measured after correcting for small eye movements, which were assessed by two different techniques. For 132 cells the measured distribution of horizontal disparity (range 4.5 deg; S.D. 0.93 deg) was significantly broader than that of vertical disparity (range 2.2 deg; S.D. 0.52 deg). Sources of error in these measurements are considered. 7. The results are discussed in relation to the known connexions between visual cortex and superior colliculus and the possible role of the latter in the regulation of eye movements.
A note of the mechanism by which inhibitors of the sodium pump accelerate spontaneous release of transmitter from motor nerve terminals.
Authors: Baker P F , Crawford A C
Published: December 2014

1. The actions of 0–1 mM ouabain and of K‐free Ringer have been examined at the frog neuromuscular junction. 2. After a delay of more than 30 min, ouabain produces an increase in the miniature end‐plate potential (m.e.p.p.) frequency. This increase occurs unchanged in Ca‐free Ringer containing 1 mM‐EGTA and is therefore unlikely to be due to an entry of Ca into the motor nerve terminals. 3. If the nerve to the preparation is stimulated repetitively in Ca‐free Ringer containing 0–1 mM ouabain and 1 mM‐EGTA the response of the m.e.p.p. frequency depends on the timing of the tetanus relative to the beginning of the ouabain treatment. 4. During the first 30 min of exposure to ouabain, the tetanus produces a small, transient increase in the m.e.p.p. frequency similar to that which occurs before ouabain is present. After about 30 min the same tetanus produces large, irreversible increases in the m.e.p.p. frequency. 5. Superfusion of an end‐plate with K‐free Ringer causes an immediate exponential rise in the m.e.p.p. frequency that is unaffected by the presence of external Ca ions. On replacing the normal K of the Ringer (2 mM) the m.e.p.p. frequency recovers quickly to its original value. 6. Late in an exposure to 0–1 mM ouabain the m.e.p.p. frequency becomes extremely sensitive to changes in the external Na concentration, [Na]o. Reducing [Na]o increases the m.e.p.p. frequency. The sensitivity to [Na]o is independent of external Ca ions or whether the isotonic substitute for NaCl is LiCl or sucrose. 7. It is suggested that the spontaneous release of transmitter is facilitated, in some way, by the changes in the monovalent cation content of the nerve terminals that result from blocking the Na‐K exchange pump. The Na sensitivity of the m.e.p.p. frequency that develops simultaneously can be explained if a Na‐dependent Ca efflux system is present in the membrane of the presynaptic terminals.
Insulin‐stimulated entry of glucose into muscle in vivo as a major factor in the regulation of blood glucose.
Authors: Daniel P M , Love E R , Pratt O E
Published: December 2014

1. The entry of glucose into the pectoralis major muscle of living rats was measured over a wide range of plasma glucose concentrations. A technique was used by which steady concentrations of substances are maintained in the circulation throughout the experiments. 2. Raising the concentration of glucose in the plasma caused saturation of the mechanism by which it is transported into muscle. Estimates of the values of the kinetic constants for this transport system were: Kt, 34 mumole ml‐1 and V, 1‐2 mumole min‐1‐g‐1 muscle. 3. When the plasma glucose concentration was raised up to at least twelve times normal, there was no sign of saturation of the transport system in insulin‐treated animals. This finding could be explained if insulin increased greatly both V and Kt for glucose transport. 4. Insulin increased the rate of entry of glucose into muscle over the entire range of plasma glucose concentrations studied (4–8 mumole ml.−1). There was evidence that endogenous insulin produced a similar increase in entry rate some 10 min after the injection of glucose. Fasting, which is associated with a decrease in insulin level, depressed the rate of entry. In hyperglycaemia insulin caused a rise in the concentration of glucose within the muscle cells. 5. The insulin‐induced increase in the rate of glucose entry into muscle ensured that approximately 25% of an I.V. dose of glucose entered the muscle cells of insulin‐treated animals within one minute. This illustrates the quantitatively important regulatory role that skeletal muscle plays in these circumstances in limiting the extent of a rise in circulating glucose.
Effects of nerve growth factors from mouse salivary glands and snake venom on the sympathetic ganglia of neonatal and developing mice.
Authors: Banks B E , Charlwood K A , Edwards D C , Vernon C A , Walter S J
Published: December 2014

1. Quantitative histological analysis has been made of the effects of nerve growth factor (NGF) from mouse submaxillary gland and from the venom of Vipera russelli on superior cervical ganglia of neonatal mice. 2. The hypertrophic and hyperplastic effects reported by other workers have been confirmed. 3. The hypertrophic effect arises from an increase in the rate at which the sympathetic neurones attain their mature size. The size at maturity is never exceeded. 4. The hyperplastic effect arises from an increase in the rate of production of neurones from less differentiated cells. In the developmental period, the number of neurones can exceed that found at maturity. If injection of NGF is discontinued the excess neurones disappear. 5. If injection of NGF is continued to maturity, the excess number of neurones is maintained.
The control of retinal ganglion cell discharge by receptive field surrounds.
Authors: Enroth‐Cugell C , Lennie P
Published: December 2014

1. This paper describes the behaviour of the receptive field surround, and how surround signals combine with those from the centre to generate the discharge of the retinal ganglion cells of the cat. 2. A small test spot is flashed upon the middle of the receptive field of an on‐centre X‐cell, alone, or together with a concentric annulus of fixed luminance. The reduction in discharge brought about by the annulus is independent of spot luminance. From this it is inferred that centre and surround signals combine additively. 3. Knowing that the combination of signals is additive, the surround signal can be estimated by comparing the ganglion cell's response to diffuse illumination of its receptive field with that to an equiluminous spot which optimally stimulates the centre while encroaching minimally upon the periphery. 4. Application of this technique to X‐cells shows that although the surround seems to have a threshold, it is at its most sensitive in the dark‐adapted eye, and typically is only 0.3–0.5 log units less sensitive than the centre. 5. Centre and surround sensitivities are decreased from their dark‐adapted levels by increasing background illumination, but the decline of surround sensitivity is initially less rapid than that of the centre. Thus with increasing light‐adaptation the surround becomes relatively more sensitive. In the light‐adapted eye centre and surround are about equally sensitive to diffuse illumination. 6. Although, in the dark‐adapted eye, illumination of the receptive field periphery of an on‐centre unit depresses firing, removal of that illumination produces no off‐discharge. Off‐discharges appear only when background illumination exceeds about 104 quanta (507)/deg 2 sec. This confirms Barlow & Levick (1969b). 7. In the dark‐adapted eye surround latency is longer than that of the centre. With increasing background illumination the latency difference is reduced. 8. For X‐cells, the rate of the maintained discharge depends to some extent on the balance of centre‐surround antagonism. But this antagonism is not the major factor accounting for the relative constancy of mean rate at high background luminances, for the rate then can be almost independent of the size of a steady pot. 9. The mean rate of discharge of Y‐cells seems to depend even less upon the balance of centre‐surround antagonism. 10. Y‐cell surrounds could not properly be isolated with the optimal spot‐diffuse illumination technique, so detailed measurements of their behaviour were not made. However, the dark‐adapted surround appear to be as sensitive as those of X‐cells.
The antipyretic effect of indomethacin.
Authors: Clark W G , Cumby H R
Published: December 2014

1. Several possible mechanisms of the antipyretic action of indomethacin administered cat. 2. Indomethacin did not decrease bacterial endotoxin‐induced release of endogenous pyrogen in vivo. 3. Indomethacin (5–40 mug/kg) inhibited the pyrogenic effect of peripherally or centrally administered leucocytic progen. A dose of 10 mug/kg caused a parallel shift to the right of the log dose‐response curve for I.V. leucocytic pyrogen and reduced the potency of the pyrogen at least 50%. 4. Incubation of leucocytic pyrogen with indomethacin did not alter its pyrogenic potency. 5. Indomethacin exerted only a slight non‐dose‐related hypothermic effect in afebrile animals. 6. Indomethacin (up to 1 mg/kg) did not diminish the hyperthermic response to intraventricular administration of prostaglandin E1. 7. This pattern of activity indicates that indomethacin acts centrally to inhibit an effect of leucocytic pyrogen.
The amplitude and the time course of the end‐plate current at various pH levels in the frog sartorius muscle.
Authors: Scuka M
Published: December 2014

1. The amplitude and the time course of the end‐plate current are dependent on the pH of the bathing solution. 2. When pH is changed from 5.4 to 9.4 the amplitude of the end‐plate current is increased and its decay is speeded up. 3. The change in the amplitude seems to be a result of a variation of quantal content. 4. The change in the time course of the end‐plate current is explained by assuming that the rate constants which determine the dissociation of the receptor‐mediator complex are affected by a change in pH. 5. This speculation is supported by the finding that the effect of membrane potential on amplitude and time course of the end‐plate current are dependent on pH of the bathing solution.
The effects of extracellular pH and buffer concentration on the efflux of lactate from frog sartorius muscle
Authors: Mainwood G. W. , Worsley‐Brown Pauline
Published: December 2014

1. The rate of efflux of lactate from isolated frog sartorius muscles is measured with a superfusion technique. Efflux curves are followed after raising the internal lactate level of the muscles by repetitive electrical stimulation over a 200 sec period.

2. With an external pH of 7·0 or below the measured efflux rates following stimulation reach 100–150 n‐mole/g.min. Increasing the pH of the superfusion fluid to 8·0 results in a two or threefold increase in the peak efflux rate. The effect is independent of the buffer system used and occurs fairly rapidly when the pH of the superfusion fluid is changed. This suggests that the effect of pH on lactate efflux is extracellular.

3. The increase in efflux rate due to an increase in pH is dependent on buffer concentration. This fact together with measurements of surface pH changes in muscles following arrest of superfusion indicates that a pH gradient exists through the muscle thickness during lactate efflux.

4. The low lactate efflux rate seen at a low buffer concentration (1 m
M) is reduced to an even lower level by depolarization with potassium sulphate suggesting a membrane potential dependent component. At pH 8·0 with a high buffer concentration (25 m
M) potassium sulphate only reduces efflux rate slightly.

The observations are interpreted as indicating that a fraction of lactate lost is in the form of undissociated acid and that this fraction increases with increasing external pH.

5. Conditions which favour loss of hydrogen ions and lactate from muscle are also associated with improved recovery of twitch tension.
Effects of stimulating the acetylcholine receptor on the current‐voltage relationships of the smooth muscle membrane studied by voltage clamp of potential recorded by micro‐electrode.
Authors: Bolton T B
Published: December 2014

1. A double sucrose‐gap voltage‐clamp technique is described for use on smooth muscle strips longer than about 2 mm. It involves intracellular recording by microelectrode of the membrane potential of a narrow region of the strip (“node”) sandwiched between two streams of deionized sucrose solution. Current was passed into the node across one or both sucrose streams. 2. Preliminary experiments in which potential was recorded intracellularly at two points during polarization of a “short cable” preparation, formed by folding over a strip of smooth muscle, suggested that a node width of less than 0–15 mm was needed to achieve uniform potential during inward current flow. However, when node width between sucrose‐gaps was reduced to 0–5 mm, spontaneous electrical activity was lost, and below 0–5 mm spike threshold was raised and the regenerative spike became graded. The currents flowing during the application of rectangular voltage‐clamp command potentials were described. 3. Using taenia smooth muscle it was shown by recording with a second, independent micro‐electrode that potential was not uniform for up to 200 ms or more following a step change in potential under voltage‐clamp in nodes 0‐4‐0‐5 mm wide where current was passed across both sucrose gaps. However, reasonably uniform nodal potentials were obtained using ramps with relatively slow rates of rise (25 mV/s). 4. Using such slow ramp commands under voltage clamp, the effects of carbachol on the current‐voltage relationship of longitudinal muscle of ileum and taenia were studied in hypertonic solution. 5. In the presence of carbachol (10(−6) to 10(−5) g/ml.) additional inward current flowed across the membrane (in some experiments an equilibrium potential was observed at which this current reversed direction). The magnitude of this additional current was linearly related to potential at potentials negative to the resting potential. At potentials positive to the resting membrane potential, this additional current increased with depolarization over the range −40 to −10 mV; in ileum the effect of this additional inward current on the current‐voltage relationship was to produce a region of net inward current where before, in the absence of carbachol, a net outward current existed. In taenia the additional inward current flowing in the presence of carbachol was too small to produce a region of net inward current; thus carbachol produced regenerative slow oscillations of potential (slow waves) in ileum but not in taenia. 6. These results support a previous suggestion that activation of the acetylcholine receptor of ileal smooth muscle produces an additional inward current in the membrane which increases with depolarization and is responsible for the regenerative slow waves seen when muscarinic stimulants are applied. A similar effect apparently operates in taenia but the additional inward current is too small to produce regenerative slow waves.
Lipid A fever in cats.
Authors: Dey P K , Feldberg W , Gupta K P , Wendlandt S
Published: December 2014

In unanaesthetized cats the effect of lipid A on rectal temperature and on prostaglandin E2 (PGE2) activity in cisternal cerebrospinal fluid (c.s.f.) was examined. Lipid A was injected either intravenously or into the cerebral ventricles. 2. Lipid A injected intravenously in a dose of 1‐‐4 mug/kg produced longlasting fever which was more often biphasic than monophasic. With a second injection a much shorter but usually hither monophasic response was produced. The cat was then for a time insensitive to I.V. lipid A but when the injections were repeated at 24 hr intervals brisk monophasic fevers were again produced. The threshold dose of I.V. lipid A lay between 0‐1 and 0‐3 mug/kg. 3. Lipid A injected into the cerebral ventricles in a dose of 100 ng or 1 mug produced long‐lasting monophasic fever. No tolerance developed; the same or only slightly diminished responses occurred on repeated injections. The threshold dose was between 5 and 20 ng. 4. A cat rendered insensitive to I.V. lipid A gave its normal fever response to injection of lipid A into the cerebral ventricles. 5. The fever produced by lipid A injected I.V. or into the cerebral ventricles was associated with the appearance of, or a rise in PGE2 activity in c.s.f. 6. Both the fever and the PGE2 activity in c.s.f. produced by lipid A injected intravenously or into the cerebral ventricles were brought down and prevented by I.P. injections of aspirin, paracetamol, or indomethacin.
The release of pancreatic glucagon and inhibition of insulin in response to stimulation of the sympathetic innervation.
Authors: Bloom S R , Edwards A V
Published: December 2014

The changes in the concentration of glucagon and insulin in arterial plasma which occur in response to splanchnic nerve stimulation have been investigated in adrenalectomized dogs, cats and sheep. 2. In dogs, stimulation of both splanchnic nerves at a low frequency (2‐0 c/s) for 10 min produced a small but statistically significant increase in plasma glucagon concentration and appeared to inhibit the release of insulin. Stimulation at a higher frequency (10‐0 c/s) produced a much greater increase in plasma glucagon concentration, which was normally accompanied by a rise in plasma glucose concentration. 3. Qualitatively similar changes in plasma glucagon and insulin concentration were observed in both sheep and cats in response to adrenergic stimulation. 4. Intramesenteric infusions of glucagon at a dose of 5‐0 ng kg‐1 min‐1 in dogs produced a comparable rise in plasma glucagon concentration to that elicited by splanchnic nerve stimulation at high frequency (10‐0 c/s) and invariably caused a rise in plasma glucose concentration. 5. In dogs given exogenous glucose, release of glucagon in response to splanchnic nerve stimulation was unaffected by induced hyperglycaemia. Secretion of insulin was partially inhibited by stimulation at 2‐0 c/s and completely suppressed at higher frequency (10‐0c/s). 6. It is concluded that stimulation of the sympathetic innervation to the pancreatic islets, at frequencies within thephysiological range, stimulates the release of glucagon and inhibits that of insulin in each of these species.
Changes in statistical release parameters during prolonged stimulation of preganglionic nerve terminals.
Authors: McLachlan E M
Published: December 2014

1. An analysis has been made of the release of acetylcholine (ACh) from the preganglionic nerve terminals of the isolated superior cervical ganglion of the guinea‐pig during prolonged repetitive stimulation (10 Hz), using the amplitude of the excitatory post‐synaptic potential (e.p.s.p.) as a measure of the amount of ACh released. 2. The decline in the mean amount of ACh released by each impulse over 20 min of continuous stimulation was accompanied by a small decrease in the mean miniature (min.) e.p.s.p. amplitude (less than 20%), both in the presence and absence of supplementary choline (3 x 10(‐5) M). During stimulation in the presence of hemicholinium‐3 (HC‐3) (2 x 10(‐5) M), the fall in min.e.p.s.p. amplitude was significantly larger. 3. Amplitude‐frequency histograms of e.p.s.p.s evoked at different times after the beginning of stimulation were usually well predicted by binomial statistics, using the min.e.p.s.p.s released during each sample period as a measure of the quantal unit. In the other cases, histograms could be predicted using Poisson's Law. 4. A decline in quantal content, m, occurred in all experiments. In the presence of synthesis, with or without added choline, this was always associated with a decrease in the binomial parameter, n, and, in many cases, with a decrease in the binomial parameter, p. During stimulation in the presence of HC‐3, a larger fall in p was observed in all experiments. 5. The results suggest that depletion of the ACh stored in the terminal decreases both the size and number of quanta available for release, and that the decrease in the amount of ACh in each quantum reduces the probability of its release.
Plasma sodium concentration and sodium excretion in the anaesthetized dog.
Authors: Nashat F S , Tappin J W , Wilcox C S
Published: December 2014

1. The effect of acute alterations of plasma sodium concentration (PNa) on renal sodium excretion (UNaV) was investigated by three types of experiments on anaesthetized dogs: (a) A local increase in PNa at one kidney was produced by infusion of hypertonic saline directly into its artery while systemic levels of PNa were stabilized by haemodialysis. (b) Systemic levels of PNa were lowered by exchange transfusion of blood for an equal volume of salt‐free dextran‐in‐dextrose solution. The results were contrasted with those observed after similar exchanges, but using dextran‐in‐saline solution. (c) The level of PNa was altered by varying the sodium concentration of a saline solution infused at a fixed rate either intravenously or into one renal artery. 2. All three types of experiment suggest a dependence of UNaV on PNa Analysis demonstrated that this relationship was not due to contemporary changes in: packed cell volume; plasma solids concentration; plasma potassium concentration; blood pressure or plasma hydrogen ion concentration. The distribution of these variables did not change with PNa except for plasma hydrogen ion concentration. Moreover, the relationship persisted when data were selected to exclude clearance periods in which the value for any variable had shifted past the group mean obtained before PNa was altered. 3. The fall in UNaV at low levels of PNa could be attributed to a fall in glomerular filtration rate (GFR), but the progressive rise in UNaV seen as PNa exceeded 150 m‐mole 1(‐1) occurred despite a fall in GFR and no apparent change in the mean filtered load of sodium. These results suggest that the increased sodium excretion accompanying raised levels of PNa is due to reduced tubular re‐absorption of sodium.
Involvement of uptake2 in the termination of activity of neurogenic noradrenaline in the rat isolated atrium.
Authors: Bell C , Grabsch B
Published: December 2014

1. An examination has been made of the relative effect of drugs which affect Uptake1 and Uptake2 on the mechanical responses to adrenergic nervous stimulation (0‐5‐5 Hz for 5 sec) in rat isolated atrium. 2. Inhibition of Uptake1 with desmethylimipramine (2 muM) prolonged by 50‐90% the time taken for recovery of normal heart rate after a five sec train of nervous stimulation. Inhibition of Uptake2 with metanephrine (4 muM) prolonged by 20‐40% the time taken for recovery of normal heart rate. 3. Neither desmethylimipramine nor metanephrine had any consistent effect on the time course of the inotropic response to stimulation or on the amplitudes of either inotropic or chronotropic responses. 4. After administration of desmethylimipramine, metanephrine had a somewhat greater effect on chronotropic responses than when given alone. After administration of metanephrine, desmethylimipramine still further prolonged chronotropic responses to low frequency stimulation (0‐5, 1 Hz) but had no effect at 5 Hz. These results agree with the known affinities of each uptake process for different concentrations of noradrenaline in the rat heart. 5. It is concluded that both Uptake1 and Uptake2 participate in the termination of physiological activity of neurogenic noradrenaline in rat isolated atrium even at low frequencies of nervous activation. 6. No evidence was obtained to indicate that manipulation of circulating oestrogen levels by oöphorectomy and oestrogen‐priming of female rats had any effect of the efficiency of the cardiac Uptake2 process.
The effect of hypercapnia on a blood‐brain barrier mechanism in foetal and new‐born sheep.
Authors: Evans C A , Reynolds J M , Reynolds M L , Saunders N R
Published: December 2014

1. The effect of marked hypercapnia (arterial PCO2 100 mmHg), nonrespiratory acidosis (pH 6‐95‐7‐15) or hypoxia (arterial PO2 10‐15 mmHg) upon penetration of labelled sucrose from blood into brain and c.s.f. has been investigated in exteriorized foetal sheep and new‐born lambs. 2. In hypercapnia there was a consistent increase in c.s.f./plasma sucrose ratio after 90 min I.V. sucrose to four to five times control. Brain/plasma sucrose ratios were more variable. Usually there was an increase (up to three‐and‐a‐half‐times control); sometimes there was no change or even a decrease. The effect of hypercapnia on sucrose penetration was reversible. 3. Hypercapnia reduced c.s.f. secretion rate to approximately half the control value. Hypercapnia also caused a decrease in brain extracellular space. 4. Non‐respiratory acidosis did not affect sucrose penetration. Hypoxia caused a decrease in brain/plasma sucrose ratio. 5. It is concluded that hypercapnia can cuase an increase in cerebral vascular permeability to sucrose in foetal and new‐born sheep. Some possible mechanisms are discussed.
Kittens reared in a unidirectional environment: evidence for a critical period.
Authors: Daw N W , Wyatt H J
Published: December 2014

1. Kittens were reared in the dark from birth except for a period each day when they were put inside a stationary transparent cylinder, around which a drum with vertical black and white stripes on the inside, rotated in one direction. After the end of the period of exposure, we recorded a sample of single cells from their visual cortices, and analysed each cell for direction and orientation sensitivity and other properties. 2. Two kittens were placed inside the drum, rotating rightward, for 2 hr each seekday from 3 1/2 to 7 weeks of age. A greater proportion of the directionally sensitive cells in their cortices showed a preference for rightward movement. 3. Six other kittens were placed inside the drug for 1 hr each weekday from 2 to 12 weeks of age with the drum rotating leftward up to a particular changeover age, then rightward until 12 weeks. The changeover point occurred at 21, 26, 28, 33, 35 and 51 days for different kittens. A changeover earlier than 4 weeks of age led to a preponderance of cells preferring rightward movement. A changeover later than 5 weeks of age led to a preponderance of cells preferring leftward movement. Comparison of these results with others on monocular deprivation suggests that the peak of the critical period for directional deprivation may occur earlier than the peak of the critical period for monocular deprivation. 4. None of the samples of cells showed a preponderance of cells specific for vertical orientations. It is unclear whether this negative effect resulted from the presence of some horizontal contours during exposure, or some more fundamental cause.
Measurement of potassium and chloride ion concentrations in the cupulae of the lateral lines of Xenopus laevis.
Authors: Russell I J , Sellick P M
Published: December 2014

1. Potential measurements were made with double barrel ion selective electrodes from the cupulae of lateral line organs in the aquatic toad Xenopus laevis. 2. A positive endocupular potential (ECP) of 15‐50 mV was recorded within the cupula, immediately above the hair cells. 3. Increases in the Cl‐ and K+ potentials were recorded when the ion selective electrodes touched the cupula. Cupular Cl‐ and K+ varied between 35 and 70 mM and 24 and 100 mM respectively. This variation existed between, rather than within, different animals. 4. Subcutaneous injections of 0‐4 ml. 2 mM ouabain greatly reduced the ECP and cupular K+, whereas 0‐4 ml. of Xenopus Ringer had no effect. 5. Changing the bath Cl‐ a hundredfold had no effect on the ECP. It was concluded that the ECP was produced by an electrogenic K+ pump which maintained high K+ levels within the cupula.
Relationships between the spike components and the delayed depolarization in cat spinal neurones.
Authors: Baldissera F
Published: December 2014

1. Changes in the delayed depolarization (DD) following composite (IS‐SD) intracellular spikes in motoneurones and neurones of the ventral spinocerebellar tract were recorded in a variety of experimental conditions. Cell activation was either antidromic or by direct intracellular stimulation. 2. It was observed that under all conditions in which IS‐SD coupling changes took place (as a consequence of spontaneous fluctuations, membrane conductance variations, variations of direct‐stimulation parameters, changes in steady membrane polarization), SD spike delays were always accompanied by a progressive concomitant reduction of the DD depolarizing hump amplitude. 3. Under the same conditions the latency of the DD peak from the stimulus artifact remained constant. Accordingly, any increase of the SD delay was accompanied by a reciprocal reduction of the time interval between the SD spike and the DD peak. This variability of temporal relationships between SD spike and DD would appear to contradict the hypothesis that the DD might represent the image of the excitation spreading from the soma to the dendrites (Kernell, 1964; Nelson & Burke, 1967). 4. as the gradual reduction of the DD hump progressed, the time course of the decay phase of the afterhyperpotential more and more closely approximated the decay phase of the IS spike. As an alternative hypothesis it is suggested that the DD might originate from the current which generates the IS spike.
Stretch reflex and servo action in a variety of human muscles.
Authors: Marsden C D , Merton P A , Morton H B
Published: December 2014

1. In the long flexor of the thumb the latency of the stretch reflex and of other manifestations of servo action is some 45 msec, roughly double the latency of a finger jerk. 2. Tendon jerks are feeble or absent in the long flexor of the thumb even in subjects with brisk long‐latency stretch reflexes in this muscle. This, and other facts, suggests that the nervous mechanism of the tendon jerk is different from that of the stretch reflex. 3. A muscle that has feeble tendon jerks may show a late component in the response to a tendon tap, with a latency similar to that of the long‐latency stretch reflex. 4. On the hypothesis that the excess latency of the stretch reflex over that of a tendon jerk is because the stretch reflex employs a cortical rather than a spinal arc, the excess would be expected to be larger in magnitude for the long flexor of the big toe and smaller for the jaw closing muscles. This is confirmed, 5. An alternative hypothesis that the long latency of stretch reflexes in thumb and toe is because they are excited by slow‐conducting afferents is made improbable by the finding that stretch reflexes with an equal or greater excess latency are also found in proximal arm muscles. 6. The long‐latency stretch reflex in proximal muscles was seen most distinctly in a healthy subject who happened to have feeble or absent tendon jerks. In ordinary subjects there is often a large, short‐latency, presumably spinal component of the stretch reflex in proximal muscles; and short‐latency responses to halt and release are also seen, The significance of this spinal latency servo action in proximal muscles remains to be explored. 7. The Discussion argues that the available data on conduction time to and from the cerebral cortex are compatible with the hypothesis that the long‐latency component of the stretch reflex uses a transcortical reflex arc, and that none of the experiments described in the present paper are inimical to this view.