bluuebunny/crossref_metadata_2025 huggingface dataset:
Fast axoplasmic transport in the fibres of chromatolysed neurones.
Authors: Ochs S
Published: December 2014

1. The rate of fast axoplasmic transport in cat sensory nerves was determined in sciatic nerves above transections made low in the popliteal fossa some 6‐165 days beforehand. The pattern and rate of movement of the crest of labelled components in the nerve fibres after injecting the L7 dorsal root with [3H]leucine was used to characterize fast axoplasmic transport. 2. The mean rate and S.D. found on the transected side was 424 + 33 mm/day compared with 432 +/‐ 34 mm/day for the control nerves. These rates were not significantly different and were similar to the rate of axoplasmic transport previously reported to be 410 +/‐ 50 mm/day. The results gave little support for the hypothesis that a speeding up of the rate of fast axoplasmic transport is the signal for the initiation of chromatolysis. 3. The amount of transport shown by the level of activity in the crests on the chromatolytic and control sides relative to the "pool" of radioactive materials remaining in the cell bodies of the ganglion were also similar. The significance of these findings was discussed with respect to changes in the cell bodies known to take place during chromatolysis and the stability of the axoplasmic transport mechanism in nerve fibres.
The membrane potential of rat diaphragm muscle fibres and the effect of denervation.
Authors: Bray J J , Hawken M J , Hubbard J I , Pockett S , Wilson L
Published: December 2014

1. Resting membrane potentials of rat diaphragm muscles were measured in vitro after previous denervation for 0‐10 days. In some experiments denervated muscles were incubated in vitro for 3 hr while in others they were cultured for 15‐24 hr to allow adequate exposure to drugs before recording. 2. It was found that resting membrane potentials, within 2‐5 mm of the site of nerve section were significantly lower, within 3 hr, than resting membrane potentials measured more than 9 mm away from site of nerve section. This difference could be reduced or abolished by bathing preparations in solutions containing adrenaline (10 muM), noradrenaline (10 muM) or isoprenaline (10 muM) or dibutyryl cyclic AMP (10 muM‐0‐25 mM in the presence of 2 mM theophylline). Cyclic AMP (0‐5 mM) was ineffective. 3. Application of solutions containing dibutyryl cyclic AMP for 3 hr also raised the resting membrane potential of muscles denervated 4‐5 days previously. Culture studies showed that this effect was sustained when the time of incubation was 24 hr. 4. Incubating freshly denervated preparations with cycloheximide (22 mug/ml.) or actinomycin D (1 mug/ml.) did not prevent the development of the early (3 hr) fall in resting membrane potential despite a concomitant inhibition of RNA or protein synthesis. Culturing freshly denervated muscles in solutions containing cycloheximide (10 or 25 mug/ml.) which blocked 93% of protein synthesis, did not prevent the expected drop in resting membrane potential after 15 or 24 hr. 5. It was found that exposure to ouabain (1 or 5 mM) produced a rapid (15 min) fall in resting membrane potential in innervated and denervated preparations treated with dibutyryl cyclic AMP but not denervated preparations. After 5 days denervation cyclic AMP levels in muscle were increased by about 40%. 6. It is suggested that upon denervation an electrogenic action of a NA+‐pump is blocked and that dibutyryl cyclic AMP and catecholamines are capable of stimulating this pump.
The preparation of human red cell ghosts containing calcium buffers.
Authors: Simons T J
Published: December 2014

1. Ca buffers may be introduced into human red cells by reversible haemolysis. The resealed ghosts retain Ca and chelating anions in the same ratio as in the haemolysing solution, enabling the intracellular Ca2+ concentration to be calculated simply. 2. The passive permeability of the ghosts to Na and Cl is unaffected by intracellular Ca2+ concentrations in the 10(‐8)‐10(‐4) M range, whereas the K permeability is greatly increased at concentrations above 10(‐7) M. 3. These preparations enable Ca‐dependent K movements to be studied under stable conditions. When the ghosts contain about 5 X 10(‐6) M‐Ca2+, over 96% of K transport occurs via the Ca‐sensitive route.
Short‐term adaptive changes in the human vestibulo‐ocular reflex arc
Authors: Gonshor A. , Jones G. Melvill
Published: December 2014

1. Two sets of experiments have examined the vestibulo‐ocular response (VOR) to repeated sinusoidal rotation (A) in the dark and (B) after attempting visual tracking of a mirror‐reversed image of the visual surround.

2. In both A and B a horizontal sinusoidal rotational stimulus of 1/6 Hz and 60°/sec angular velocity amplitude was employed, specifically chosen to lie within the presumed range of natural stimulation of the semicircular canals.

3. In A each of seven subjects underwent ten 2‐min runs of the standard stimulus in the dark on each of three consecutive days, with 3‐min rest periods between runs. Using d.c. electro‐oculography (EOG) the VOR gain was measured throughout as eye velocity/head velocity. Mental arousal was maintained by competitive mental arithmetic. Constancy of EOG gain was assured by 50 min dark adaptation before experimentation.

4. The results of A showed no consistent change of VOR gain over the three times scales of a run, a day and the 3‐day experiment.

5. In B the same subjects underwent a similar pattern of vestibular stimulation, but during eight of the 2‐min daily runs they attempted the reversed visual tracking task. VOR gain was measured during the 1st, 6th and last runs which were conducted in the dark for this purpose. Constancy of EOG gain was maintained by using red light throughout.

6. The results of B showed a substantial (approx. 25%) and highly significant (P « 0·001) reduction of VOR gain attributable solely to the 16 min of reversed visual tracking attempted during the 50 min daily experiment. In addition the pre‐test control gain was lower on day 3 than on day 1 (approx. 10% attenuation, P < 0·01) indicating a small cumulative effect from beginning to end of the 3‐day experiment.

7. It is concluded (A) that the repeated vestibular stimulus did not itself cause significant attenuation of VOR gain, but (B) that superposition of a reversed visual tracking task did induce retained VOR attenuation which was solely due to the antagonistic visual stimulus.

8. In conjunction with other experimental evidence it is inferred that this attenuation probably represents an adaptive change in the VOR induced at least in part by retinal image slip.
Glycine‐mediated inhibitory transmission of group 1A‐excited inhibitory interneurones by Renshaw cells.
Authors: Belcher G , Davies J , Ryall R W
Published: December 2014

1. Electrophysiological and micro‐electrophoretic studies were carried out in anaesthetized cats on spinal interneurones which were monosynaptically activated from group 1 muscle afferents and recurrently inhibited by Renshaw cells. 2. The recurrent inhibition was blocked by the iontophoretic administration of strychnine, which also blocked the action of glycine. 3. The time course of the block of synaptic inhibition by strychnine was slower than the block of glycine evoked inhibition. The significance of this observation in terms of the location of the inhibitory synapses is discussed. 4. The observation that recurrent inhibition of motoneurones and of interneurones is blocked by strychnine whereas the mutual inhibition of Renshaw cells is not is discussed in relation to the proposal that the nature of the post‐synaptic inhibitory receptor is not determined solely by the innervating neurone, which is the Renshaw cell in all three instances. 5. The recurrent inhibition of the interneurones was not blocked by the iontophoretic administration of bicuculline, but difficulties were encountered in demonstrating that this agent consistently antagonized the inhibitory effects of GABA.
The renal blood flow and the glomerular filtration rate of anaesthetized dogs during acute changes in plasma sodium concentration
Authors: Nashat F. S. , Tappin J. W. , Wilcox C. S.
Published: December 2014

1. The effects of acute changes in plasma Na concentration (PNa) on renal blood flow (RBF) and glomerular filtration rate (GFR) were studied in anaesthetized greyhounds. Saline was infused at a constant rate (0·1 ml. kg−1 min−1) either into a renal artery or into a systemic vein. Plasma Na concentration was altered by varying the Na concentration of the infused saline from 0·154 to 0·077, 0·616 or 1·232
M.

2. Blood pressure (B.P.), packed cell volume (PCV), concentration of plasma solids (PS) and the plasma concentration of H+ and K (PK) ions were measured but no attempt was made to contain their fluctuation.

3. An infusion of hypertonic saline into a renal artery usually led to an ipsilateral increase in RBF for 5‐15 min, followed by a progressive fall. Over‐all, mean values of RBF fell with PNa throughout the range studied (120‐190 m‐mole l.−1). Glomerular filtration rate rose with PNa to reach maximal values at PNa levels of 140‐160 m‐mole l.−1, but fell thereafter. The combined fall in RBF and GFR, without change in filtration fraction, at PNa values above 160 m‐mole l.−1 is consistent with an alteration in afferent arteriolar resistance. The fall in GFR despite a rise in RBF noted when PNa was reduced below 140 m‐mole l.−1 requires an additional explanation.

4. Renal blood flow was independent of PK; it was inversely related to [H+] and directly related to PS. Glomerular filtration rate was independent of PCV and PK. It was also inversely related to [H+] and directly related to PS up to a value of 6 g 100 g−1 plasma, after which the relationship was reversed. These results suggest that the renal vascular responses to acute changes in PNa may be mediated in part, at least, by concurrent change in PS and [H+].
Histamine release by exocytosis from rat mast cells on reduction of extracellular sodium: a secretory response inhibited by calcium, strontium, barium or magnesium.
Authors: Cochrane D E , Douglas W W
Published: December 2014

1. Histamine release from peritoneal mast cells of the rat was stimulated when the cells were exposed for 10 min to sodium‐deficient media where all NaCl had been replaced by KC1, RbC1, glucose, sucrose, mannitol, or Tris, provided calcium was less than about 0‐5 mM. 2. Light and electron microscopy showed the response to be exocytosis. 3. The chelating agents, EDTA and EGTA, abolished the response to sodium lack and their inhibitory effects were reversed by re‐incubating cells with calcium but not magnesium. 4. The response was inhibited by dinitrophenol combined with glucose‐deprivation. 5. The response was inversely related to the concentrations of sodium and calcium below 137‐5 and 0‐5 mM respectively. 6. The related alkaline earth metals, barium, strontium, and magnesium, resembled calcium in inhibiting the response to sodium lack. 7. No secretory response was seen when the cells were exposed for 10 min to calcium‐free medium in which lithium replaced sodium. Exposure to this medium for 60 min, however, elicited secretion. 8. It is concluded that when extracellular calcium is low, a reduction in extracellular sodium induces a conventional exocytotic secretory response dependent on energy and cellular calcium. It is suggested that sodium lack may mobilize calcium from a cellular site possibly the inner aspect of the plasma membrane.
Desensitization to gamma‐aminobutyric acid in crustacean muscle fibres.
Authors: Sarne Y
Published: December 2014

1. Desensitization to gamma‐aminobutyric acid (GABA) was demonstrated in crab muscle fibres by measurements to conductance changes induced by the drug. 2. In standard solutions (containing 34 mM‐Ca2+), complete desensitization occurred in the presence of 5 X 10(‐4) M‐GABA. In Ca2+‐free solutions, however, only partial (70‐80%) desensitization was observed after the application of the same concentration of GABA. 3. Complete recovery of the membrane sensitivity to GABA was achieved after less than 60 min of continuous washout with standard solution. Only partial (10%) recovery was observed after 1 hr of washout with Ca2+‐free solution. 4. The results support the 'receptor hypothesis' of desensitization which assumes transformation of the receptor from an effective to refractory state, as opposed to the 'ionophore hypothesis' which assumes direct inactivation of the synaptic current. 5. The possible mechanism by which Ca ions effect desensitization is discussed in terms of the 'cyclic model' of Katz & Thesleff (1957).
Respiratory frequency response to progressive isocapnic hypoxia.
Authors: Rebuck A S , Rigg J R , Saunders N A
Published: December 2014

1. Ventilatory, tidal volume and frequency responses to progressive isocapnic hypoxia have been measured in twenty‐nine healthy subjects by a rebreathing technique. 2. A strong correlation was found between ventilatory response to hypoxia (deltaVI/DELTASaO2) and frequency response to hypoxia (deltaf/deltaSaO2) (r=0‐82, P less than 0‐001). There was a lesser correlation between deltaV1/deltaSaO2 and tidal volume response (deltaVT/deltaSaO2) (r=0‐50, P less than 0‐01). These findings suggest that the wide range of ventilatory response to hypoxia among subjects is mainly determined by differences in frequency response and contrast with previous findings in studies of the response to progressive hypercapnia. 3. The breathing pattern during progressive hypoxia and hypercapnia was compared in ten subjects. Ventilation/tidal volume plots were constructed and patterns of response were further analysed in terms of inspiratory duration (TI), expiratory duration (TE) and mean inspiratory flow rate (VI). 4. Increments in ventilation during hypoxia were achieved with a greater respiratory frequency and a smaller tidal volume than during hypercapnia in eight of the ten subjects studied. In two subjects no difference in breathing pattern during hypoxia and hypercapnia was observed. 5. Changes in respiratory frequency during progressive hypoxia were achieved in all subjects by a progressive shortening of TI and TE. By contrast, TI remained constant during hypercapnia until VT had increased to 3‐5 times the eupnoeic value; during hypercapnia the increase in frequency was achieved mainly by a progressive shortening of TE. 6. It is concluded that different mechanisms may be involved in altering respiratory frequency when ventilation is driven progressively by these different chemical stimuli.
Direct and indirect activation of nerve cells by electrical pulses applied extracellularly.
Authors: Gustafsson B , Jankowska E
Published: December 2014

1. The mode of activation of nerve cells by extracellular stimuli was investigated while recording from a selected cell with one electrode, and applying current pulses around this cell with another electrode. The analysis was done on motoneurones and on spinal border cells from lower lumbar segments in the cat. 2. Directly evoked action potentials were defined by their appearance in an all‐or‐none fashion with stable latencies of less than 0‐5 ms. The lowest thresholds for their generation were 0‐15‐0‐20 muA in the spinal border cells and 0‐35‐0‐40 muA in the motoneurones. In the main series on motoneurones a correlation has been established between different positions of the extracellular stimulating electrode in relation to the cells and the thresholds for the direct excitation of these cells. The position of the electrode were defined on the basis of an analysis of the IS and SD components of the action potentials recorded extracellularly around the cell when evoked by current pulses applied through the intracellular electrode; both the amplitudes of these IS and SD components and their timing with the IS and SD spikes, which were simultaneously recorded with the intracellular electrode, were then taken into account. The lowest thresholds (less than 2 muA) for the direct activation of cells were found nearest the initial segment of the axon. Their values increased to about 5 mu A at near‐soma positions and to greater than 10 muA at near‐dendrites positions about 150 mum away. 3. Transsynaptically evoked action potentials which were clearly set up by the preceding e.p.s.p.s appeared with latencies greater than 0‐7 ms. When single current pulses were used, the lowest thresholds for transsynaptic spike activation were usually greater than 5‐10 muA but they considerably decreased with repetitive stimuli. These thresholds were higher than the thresholds for the direct activation of cells within the region of the initial segment, of the same order of magnitude near the soma, and lower when the stimulating electrode was nearer the dendrites than the soma and generally at all larger distances from the cells. 4. All the observations on direct excitation of cells by extracellular stimuli (generation of the IS spike before the SD spike, lowest thresholds near the region of the initial segment of the axon, similar rates of increase in these thresholds with distance as for fibres) lead to the conclusion that the effects of the extracellular stimuli are exerted primarily via spread of current to the initial segment of the axon and its depolarization. 5. Late extracellular negativities presumably related to dendritic activation were observed in a few cells. These negativities were synchronous with late components of the intracellulary recorded action potentials.
On the elementary conductance event produced by L‐glutamate and quanta of the natural transmitter at the neuromuscular junctions of Maia squinado.
Authors: Crawford A C , McBurney R N
Published: December 2014

1. The membrane potential of giant muscle fibres of Maia squinado was measured with an intracellular wire electrode. On applying L‐glutamate to the fibre the cell deplorized and fluctuations of the membrane potential around its mean level‐‐glutamate noise‐‐were seen. 2. The variance of the glutamate voltage noise is proportional to the mean level of depolarization. The noise can be regarded as being caused by numerous exponentially decaying elementary voltage events about 5 X 10(‐10) V in amplitude. The miniature excitatory junctional potential (min.e.j.p.) is approximately 6000 times the amplitude of the elementary voltage event produced by L‐glutamate. 3. The power spectrum of glutamate voltage noise is a Lorentzian with a half‐power frequency of approximately 20 Hz. 4. Min. e.j.p.s. decay exponentially with a time constant that coincides with the average lifetime of the elementary glutamate voltage event. 5. When glutamate is applied locally to a spot where extracellular min. e.j.p.s. can be recorded with a focal glass pipette, extracellular glutamate noise is seen. Glutamate noise could not be detected from elsewhere on the fibre. 6. The variance of the extracellular noise is proportional to the mean extracellular potential, and its power spectrum is a Lorentzian with a half‐power frequency of about 110 Hz. 7. The extracellular min. e.j.p.s decay exponentially with a time constant that coincides with average lifetime of the elementary glutamate current event. 8. It is suggested that the decay of the quantal currents flowing at the excitatory junction is limited by the closure of the conductance channels in the post‐synaptic membrane and not by the relaxation of the transmitter concentration in the synaptic cleft.
Alterations in amounts and rates of serotonin transported in an axon of the giant cerebral neurone of Aplysia californica.
Authors: Goldberg D J , Goldman J E , Schwartz J H
Published: December 2014

1. The giant cerebral neurone of the sea hare, Aplysia californica, is a unipolar serotonergic cell. Its axon bifurcates, one branch travelling in the cerebrobuccal connective, the other in the posterior lip nerve. 2. I13H]serotonin was injected under pressure into the cell body of the giant cerebral neurone. We studied fast axonal transport of the radioactive transmitter substance along the lip nerve when the cerebrobuccal connective was cut close to the bifurcation. 3. When the connective was cut, more than twice as much [3H]serotonin was transported along the lip nerve compared to uncut control nervous systems. 4. The increased [3H]serotonin appearing in the nerve probably was originally destined to enter the connective, but was diverted from the cut stump which was occluded with backed‐up material. 5. The incremental [3H]serotonin in the lip nerve was not the result of increased export from the soma in response to injury. 6. Not only was more [3H]serotonin transported along the lip nerve, but also a far greater fraction of the transmitter moved at very fast transport rates, approaching 120 mm/day. In uncut control nerves only a small fraction of total [3H]serotin moved faster than 70 mm/day. 7. These results are interpreted with a model for fast axonal transport. We suggest that serotonergic vesicles move at a fixed, maximal speed when attached to essentially immobile tracks, but that the vesicles are only intermittently associated with the tracks. We presume that the rate‐limiting step in movement of vesicles is the concentration‐dependent and reversible binding to the tracks. Transport along axons may be considered analogous to those enzymatic reactions in which formation of the enzyme‐substrate complex limits the appearance of product. Translocation is here analogous to formation of product. The process may therefore be approached theoretically by modification of the Michaelis‐Menten formulation.
Inhibition of food intake in the rat following complete absorption of glucose delivered into the stomach, intestine or liver.
Authors: Booth D A , Jarman S P
Published: December 2014

1. Solutions of glucose or other carbohydrates were administered during the dark or light period of the circadian cycle to rats which had been only briefly deprived of food. 2. food was restored to the animals at various times after administration of a glucose load by stomach tube. With delays between loading and access to food of up to 3 hr by night and 2 hr by day, subsequent food intake was less than intake after non‐nutritive loads. 3. measurement of the glucose content of the gastrointestinal tract at various times after glucose loading showed that this depression of intake was still apparent even when the rat was offered food some time after complete absorption of the stomach load. 4. infusion of a glucose solution into the duodenum or the hepatic protal vein also inhibited subsequent food intake. 5. in all cases, the inhibition of food intake was expressed as a decrease in the size of the first meal after restoring access to food. 6. these results provide the first demonstration that the entry of normal amounts of carbohydrate into the body by the physiological route is followed by depression of food intake which lasts until after absorption is complete.
Respiratory and cardiovascular interactions in ducks: the effect of lung denervation on the initation of and recovery from some cardiovascular responses to submergence.
Authors: Bamford O S , Jones D R
Published: December 2014

Lung denervation in ducks, by sectioning all vagal branches to one lung following mid‐cervical vagotomy on the other side, resulted in immediate bradycardia and fall in breathing frequency. Some 3‐5 weeks after lung denervation breathing frequency was within the normal range but the lung inflation reflex, present in unilaterally vagotomized sham‐operated ducks, was abolished. During 2 min dives there were no significant differences between sham‐operated and denervated ducks in heart rate, arterial blood pressure, blood gas tensions and pH(a). However, during recovery from diving heart rate increased more slowly in denervates and breathing rate was significantly below that attained by shams, although tidal volume rose to a maximum increase of 139% to a maximum of 225% of the pre‐dive value in denervates in contrast to a maximum increase of 139% of pre‐dive in sham‐operated ducks. Both sham‐operated and denervated ducks exhibited a significant fall in diastolic blood pressure 60 sec after emergence...
Interaction between inhibitory and excitatory synaptic potentials at a peripheral neurone.
Authors: Edwards F R , Hirst G D , Silinsky E M
Published: December 2014

1. The interaction between inhibitory and excitatory synaptic potentials in neurones lying in the submucous plexus of guinea‐pig ileum has been examined. 2. It was found that during an inhibitory conductance change, electrotonic potentials were more depressed in amplitude than were excitatory synaptic potentials. 3. It is suggested that inhibitory conductance changes may have only a slight effect on the impedance seen by excitatory synaptic currents as much of the excitatory synaptic current flow is likely to be capacitive. 4. A part of the depression of excitatory synaptic potential amplitude was not associated with changes in electrical properties of neurones and it is suggested that inhibitory transmitter may reduce the release of excitatory transmitter.
The effect of lithium on the transport of sodium, potassium and chloride by the colon of normal and sodium‐depleted rats.
Authors: Dolman D E , Edmonds C J
Published: December 2014

1. The effect of Li, given systemically or placed in the gut lumen, on the transport of Na, K and C1 and on the transepithelial electrical potential difference (p.d.) was studied in vivo in the distal colon of normal and Na‐depleted rats. 2. The specific effect of Li appeared to be on the Na transport system with K and C1 transport affected only indirectly. Active Na absorption was impaired and p.d. reduced when either Li was in the lumen or given systemically. In addition with Li in the lumen, a considerable rise in the plasma‐to‐lumen Na flux was observed, the flux increasing progressively with rising intraluminal Li concentration. The effects were greater in Na‐depleted rats. 3. The greater part of Li absorption from the colon of the rat takes place by exchange for Na, the secretion of which is much enhanced while the p.d. is reduced. This contrasts with human colon in which potassium is the ion exchanged for Li with the p.d. increased.
Inotropic effect of cyclic AMP in calf ventricular muscle studied by a cut end method.
Authors: Tsien R W , Weingart R
Published: December 2014

1. Cyclic AMP was introduced into ventricular muscle by a cut‐end method. Trabecular bundles were pulled through a partition which divided the preparation into a loading region and a test region. The loading region was exposed to Ca‐free solution, cut transversely near the partition, and then briefly exposed to cyclic AMP. The test region was continually superfused with Tyrode soltuion. 2. In preliminary experiments, cell‐to‐cell movements were studied in long bundles by including [3H]cyclic AMP in the loading procedure and allowing redistribution to occur. After suitable test periods, the bundles were removed, frozen, and sliced into segments. Segment radioactivity was plotted against distance and fitted by a theoretical diffusion curve. 3. The results showed longitudinal redistribution of label over many cell lengths with an average effective diffusivity of 8 X 10(‐7) cm2/sec. This value did not appear sensitive to the length of the test period or to the presence of a phosphodiesterase inhibitor. 4. The metabolic fate of cyclic AMP introduced by the cut‐end method was determined by chromatographic separation of [3H]cyclic AMP and its break‐down products. Most of the cyclic AMP was metabolized, but the results suggest that cell‐to‐cell movements of cyclic AMP contribute to the overall redistribution of label. 5. The cut‐end method was used to study the influence of cyclic AMP on the contractile activity in the test region. Introduction of cyclic AMP evoked a delayed increase in twitch tension, about 25% above control. The inotropic effect peaked about 50 min after the end of the loading procedure, a delay which seemed compatible with slow longitudinal diffusion into the test region. 6. In control experiments, the cut‐end procedure was repeated with 5'AMP (the immediate break‐down product of cyclic AMP) instead of cyclic AMP. No delayed increase in twitch tension was observed. 7. Introduction of dibutyryl cyclic AMP increased twitch amplitude by 130%, with a delayed time course similar to that found for cyclic AMP. 8. The results using the cut‐end procedure provide new evidence that cyclic AMP helps mediate adrenergic effects on the strength of contraction.
Stimulation of the rabbit hypothalamus: caudal projections to respiratory and cardiovascular centres.
Authors: Evans M H
Published: December 2014

1. Electrical stimulation of a small area of the hypothalamus, lying about 2 mm dorsal to the lateral margin of the mammillary bodies, evoked a characteristic complex of effects in the anaesthetized rabbit. 2. The observed effects included apneusis followed by tachypnoea, increased arterial blood pressure, and vagally mediated bradycardia. Exophthalmost and pupillodilatation was commonly seen. The ears were erected and the vibrissae drawn forward. Somatic effects were weaker, but often included increased extensor tone, especially in the forelimbs. 3. The intensity of these effects was dependent upon the frequency of stimuli within the trains. Effects were weak or absent below 20 shocks/sec, and were near‐maximal above 60 shocks/sec, when employing constant‐current rectangular wave stimuli of 100‐300 muA, 1 msec pulse duration and 5‐9 sec train duration. 4. The effects were not dependent upon connexions with the cerebral cortex, but were mediated by pathways that projected ipsilaterally from each side of the hypothalamus through the mesencephalon. 5. The evidence suggests that this region of the rabbit hypothalamus is partly homologous with that hypothalamic area associated with the defence reaction in cat. However, the over‐all responses to stimulation in the anaesthetized rabbit differed considerably from those described in the anaesthetized carnivore, suggesting that their integrated physiological responses to emotional threat are dissimilar.
Joint sense, muscle sense, and their combination as position sense, measured at the distal interphalangeal joint of the middle finger.
Authors: Gandevia S C , McCloskey D I
Published: December 2014

1. An anatomical peculiarity allows the hand to be positioned so that the terminal phalanx of the middle finger cannot be moved by voluntary effort. When positioned in this way only joint and cutaneous mechanisms subserve position sense. By altering the position of the hand the muscles are again engaged and able to move the finger. Moving the joint then also excites muscular afferents. 2. The position sense of twelve subjects was assessed with and without engagement of the muscles at the joint. Three tests were used in which either angular displacement, angular velocity or duration of displacement were held constant. 3. When muscular attachment was restored, performance in all tests was greatly enhanced. As engagement of the muscles caused little change in the 'stiffness' of the joint, it is unlikely that the improved performance resulted from increased discharges from the joint receptors. Cutaneous mechanisms are unlikely to mediate this improvement as they are likely to have been unaffected by engagement of muscles. It is concluded that intramuscular receptors are partly responsible for normal position sense. 4. In seven of the twelve subjects the test finger was anaesthetized to isolate the contribution of intramuscular receptors. This muscle sense was variable. In some subjects it provided accurate kinaesthetic information but in others the information was crude. If with the test finger anaesthetized subjects exerted voluntary tension with the muscles that move the joint the muscle sense was improved.
Pepsin secretion in the anaesthetized cat and the effect of sympathetic nerve stimulation.
Authors: Hooper R , Reed J D , Sanders D J
Published: December 2014

1. Experiments were performed on chloralose anaesthetized cats and gastric mucosal blood flow, acid and pepsin secretions were measured. Gastric mucosal pepsin and protein contents were measured at the end of the experiments which were done in three groups: gastrin (A), vagal (B), vagal and sympathetic nerve (C) stimulations. 2. Vagal stimulation significantly reduced (76%) the pepsin content of gastric mucosa compared with gastrin stimulated animals, none of which secreted pepsin. 3. The sum of the secreted and extracted pepsins for all the three groups was not significantly different. There was no significant difference in the extracted protein from any of the groups. 4. Gastric mucosal blood flow, acid and pepsin outputs all had significant correlations with time during the first 70 min of vagal stimulation. During the period 80‐160 min of vagal stimulation acid secretion and mucosal blood flow were not correlated with time but pepsin output declined significantly. From 170 to 220 min of vagal stimulation, acid and pepsin outputs and mucosal blood flow were not correlated with time. 5. The assumed pepsin store during each period was calculated and after 40 min of vagal stimulation there is a constant percentage pepsin output from this assumed store. 6. There is some data to suggest that pepsinogen synthesis was occurring during the period 170‐220 min of vagal stimulation. 7. Sympathetic nerve stimulation which started at 160 min after the beginning of sustained vagal stimulation, significantly inhibited gastric acid secretion and mucosal blood flow, and in addition it significantly inhibited pepsin secretion. This is consistent with the hypothesis that sympathetic nerve inhibition of gastric mucosal function is mediated by a vasoconstrictor mechanism.
Stimulation‐induced factors which affect augmentation and potentiation of trasmitter release at the neuromuscular junction.
Authors: Magleby D L , Zengel J E
Published: December 2014

1. End‐plate potentials (e.p.p.s) were recorded from frog sartorius neuromuscular junctions under conditions of decreased transmitter release to study the effect of repetitive stimulation on augmentation and potentiation of transmitter release. 2. The magnitudes and time constants of decay of augmentation and potentiation were determined both following a primary conditioning train and following an identical secondary conditioning train applied from 30 to 170 sec after the primary conditioning train. 3. The magnitude of augmentation following the secondary conditioning trains was increased over that following the primary conditioning trains even though augmentation, with a time constant of decay of about 7 sec, had decayed to insignificant levels before the onset of the secondary trains. This increase in augmentation was not due to a change in its rate of decay during the secondary trains. 4. The increased magnitude of augmentation can be described as arising from an expression factor which, for conditioning trains of 200 impulses at 20/sec, has an initial magnitude of 1‐6 +/‐ 1‐2 (S.D. of observation) (the magnitude of augmentation is increased 2‐6 times) and decays approximately exponentially with a time constant of 90 +/‐ 50 (S.D. of observation) sec. The expression factor thus decays about ten times slower than augmentation. 5. Doubling the number of impulses in the primary conditioning train from 100 to 200 led to a 2‐8 +/‐ 1‐0 (S.D. of observation) times increase in the magnitude of the expression factor, estimated by placing a 200 impulse secondary conditioning train 40 sec after the primary conditioning train. 6. The expression factor, while increasing the magnitude of augmentation, had little or no effect on the magnitude of potentiation or on trasmitter release in the absence of augmentation. The expression factor decayed about twice as slowly as potentiation. 7. The time constants characterizing the decay of potentiation were greater following the secondary conditioning trains than following the primary conditioning trains. 8. The increased time constant for the decay of potentiation can be described as arising from a time constant factor which, for conditioning trains of 200 impulses at 20/sec, has an initial magnitude of 1‐2 +/‐ 0‐7 (S.D. of observation) (the time constant of potentiation is increased 2‐2 times) and decays approximately exponentially with a time constant of 130 +/‐ 45 (S.D. of observation) sec. The time constant factor decayed about three times slower than potentiation. 9. Doubling the number of impulses in the primary conditioning train from 100 to 200 led to a 1‐6 +/‐ 0‐8 (S.D. of observation) times increase in the magnitude of the time constant factor, estimated by placing a 200 impulse secondary conditioning train 40 sec after the primary conditioning train. 10...
Action of vinblastine on the spontaneous release of acetylcholine at the frog neuromuscular junction.
Authors: Pécot-Dechavassine M
Published: December 2014

1. Vinblastine induces reversible changes of the spontaneous release of acetylcholine (ACh) at the frog neuromuscular junction as characterized by the appearance of giant potentials. These large potentials occur soon after soaking the muscle in vinblastine and are not consequent to a large increase in the frequency of spontaneous release. Their number, relative to the total number of spontaneous potentials, increases with the duration of soaking. 2. Large potentials appear even in the presence of tetrodotoxin or in low Ca2+‐high Mg2+ Ringer solution. 3. Following vinblastine treatment,the amplitude histogram of spontaneous potentials recorded from a number of fibres display an evident periodicity with peaks occurring regularly at simple multiples of the model amplitude of the unitary potentials. It is suggested that giant potentials are produced by the release of preformed pluriquantal packets of ACh. 4. Comparison of the amplitude distribution of spontaneous potentials and end‐plates potentials show that only an insignificant number of large quanta are released by nerve stimuli. The absolute frequency of giant potentials does not markedly change when spontaneous discharge is accelerated by hypertonic solution. 5. The mechanism by which vinblastine induces the appearance of giant potentials is discussed.
Changes in membrane currents in bullfrog atrium produced by acetylcholine.
Authors: Giles W , Noble S J
Published: December 2014

1. A double sucrose‐gap voltage‐clamp technique has been used to study the effects of acetylcholine on the membrane currents in atrial trabeculae of the bullfrog, Rana catesbeiana. 2. The second, or slow inward (Ca2+/Na+) current, was found to be markedly reduced by concentrations of acetylcholine greater than approximately 2‐0 X 10(‐8)M. The resulting decrease in net calcium entry provides a straightforward explanation for the negative inotropic action of acetylcholine in atrial muscle. 3. Measurements of membrane resistance near the resting potential showed that relatively high doses of acetylcholine (approximately 10(‐7) M) decrease membrane resistance by about twofold. This effect is shown to be the result of an increase in a time‐independent background current which appears to be carried mainly by potassium ions. 4. Using appropriate pharmacological techniques, it has been possible to demonstrate: (i) that the peak slow inward current is reduced to about half its initial value before any significant increase in background current occurs; (ii) that even when a sufficient dose of acetylcholine to produce an increase in background current is used, the background current shows inward‐going rectification and cannot account for the observed reduction in the slow inward current. 5. No consistent change was observed in the degree of activation of the time‐dependent outward membrane currents after application of concentrations of acetylcholine which produced large decreases in the peak slow inward current. 6. These results are discussed in relation to previous electro‐physiological and radioisotope studies of the mechanism of the negative inotropic effect of acetylcholine in cardiac muscle.
Calcium and the control of discrete wave latency in the ventral photoreceptor of Limulus.
Authors: Martinez J M , Srebro R
Published: December 2014

1. Discrete, transient depolarization (discrete waves) of the ventral photoreceptor of the horseshoe crab, Limulus, occur spontaneously in the dark adapted photoreceptor and are also evoked by light. They form the basic events which comprise the receptor potential. A brief, low energy flash of light evokes variable numbers of discrete waves which have variable latencies. Evidence suggesting that discrete wave latency reflects the kinetics of the chemical reactions of phototransduction is reviewed. 2. The concentration of extracellular Ca influences both the average discrete wave latency and its variability. Lowering extracellular Ca prolongs the latency and increases its variability. Increasing extracellular Ca has the opposite effect. 3. Changes in discrete wave latency caused by changes in extracellular Ca require 10‐‐15 min to become fully manifest, whereas when the concentration of extracellular K is increased the photoreceptor achieves a steady‐state depolarization in 10‐15 sec. 4. Iontophoresis of the Ca‐chelating agent EGTA into the photoreceptor increases both the average discrete wave latency and its variability. Iontophoresis of Ca‐EGTA mixtures may either increase or decrease discrete wave latency and its variability depending upon the proportion of Ca mixed with EGTA. 5. It is suggested that the concentration of intracellular rather than extracellular ionized Ca is the prime factor indicating discrete wave latency. The effects of changing extracellular Ca can be explained if the photoreceptor is permeable to Ca in the dark and if it maintains a low intracellular Ca concentration by virtue of active metabolic processes (a pump‐leak system). 6. Lowering the temperature of the photoreceptor also has the dual effect of increasing discrete wave latency and its variability. However, effects of lowering temperature and Ca simultaneously are greater than the sum of the two effects in individually. This suggests that Ca may be a reactant in the chemical process of phototransduction. 7. Changing the concentration of extracellular Ca does not change the quantum efficiency of discrete wave production. A previous study showed that quantum efficiency is not changed by temperature. Thus, once initiated by the absorption of light, the reactions that subserve phototransduction may be forced to completion. Ca probably exerts its influence by changing one or more rate constants in the reaction sequence.
Electrical properties of pig colonic mucosa measured during early post‐natal development.
Authors: Hénin S , Smith M W
Published: December 2014

Microvillar membrane (Vm) and transmural (Vt) potential differences were measured in proximal colon taken from pigs at birth and up to 10 days of age. 2. Vm remained independent of the age of the animal provided it was measured in the absence of methionine. The over‐all mean was ‐43‐3 mV. Adding methionine to fluid bathing the mucosal surface of new‐born pig colon caused a 9‐8 mV depolarization of Vm and a 6‐7 mV increase in Vt. These effects, which were Na+‐dependent, were not seen in the 10‐day‐old animal. 3. Substituting SO4(2‐) for Cl‐ in methionine‐free medium caused a hyperpolarization in Vm. Increasing the concentration of K+ caused corresponding depolarization. Substituting choline for Na+ had no effect on VmCl‐ and K+ movement across the microvillar membrane together account for the bulk of the measured membrane potential. These results apply to all stages of development. 4. Na+ uptake across the microvillar membrane of the new‐born pig colon was increased in the presence of methionine. This effect disappeared in older animals. Na+ uptake in the absence of methionine doubled during the first 24 h of post‐natal life. This increase was maintained using colons taken from older animals. 5. Methionine depolarization of Vm in the new‐born pig colon is probably caused by the electrogenic influx of Na+. The ability of the colon to actively concentrate methionine within tis mucosa disappears at the same time as methionine ceases to affect Vm and Vt. It is suggested that methionine and Na+ form a ternary complex with a carrier in the brush border of the new‐born pig colon and that this carrier is lost or modified during early post‐natal development.
The release of endogenous amino acids from the rat visual cortex.
Authors: Clark R M , Collins G G
Published: December 2014

The release of endogenous taurine, GABA, glycine, aspartate, glutamate, glutamine and alanine from the rat visual cortex was measured using a cortical cup technique. The electrocorticogram (ECoG) was monitored throughout most experiments. 2. Spreading depression, evoked by the dropwise placement of 10% KCl solution on to the brain outside the cup was associated with a significant increase in the release of GABA and glutamine but a marked fall in that of glutamate. The evoked release of GABA and glutamate but not of glutamine was Ca2+ dependent. 3. A solution containing 50 mM‐K+ placed within the cup elicited a significant increase in the release of taurine and GABA, whereas 100 mM‐K+ additionally released aspartate and glutamate. The K+‐evoked release of these amino acids with the exceptions of taurine and glutamine was Ca2+‐dependent. 4. Three series of experiments were carried out in which the preparations were stimulated electrically. Bipolar stimulation (100 Hz, 1 msec pulse width, 2‐5 mA for 5 min) with the electrode within the cup was followed by significant increases in taurine, GABA and glutamate release; using a 5 mA current, there was an additional release of aspartate and alanine. Only the evoked release of GABA and glutamate was Ca2+ dependent. 5. In the second and third series of experiments, the electrode was sited adjacent to the cup or on the contralateral cortex respectively. Following stimulation (100 Hz, 1 msec pulse width, 2‐5 mA for 5 min) there was a significant increase in taurine and GABA release and a significant fall in the release of aspartate and glutamate. With the exception of taurine, these changes in release were Ca2+ dependent. Reducing the stimulus current to 1‐5 mA or the period of stimulation to 2‐5 min initiated similar but statistically insignificant changes in release. A range (10‐100 Hz) of stimulation frequencies was examined: the evoked release of GABA was linearly related to frequency whereas that of taurine was frequency‐independent. The fall in aspartate and glutamate release was maximal at a frequency of about 50 Hz. 6. The results are discussed in relation to (a) the possible sites of release of the amino acids and (b) the proposed neurotransmitter roles of the physiologically active amino acids.
Chloride transport in human erythrocytes and ghosts: a quantitative comparison.
Authors: Funder J , Wieth J O
Published: December 2014

1. Homogeneous preparations of resealed ghosts with intracellular KCl concentrations between 15 and 900 mM could be prepared. Virtually all ghosts sealed to chloride. The chloride transport system was found not to be damaged: a quantitative comparison of the self‐exchange of 36Cl‐ across intact and resealed membranes showed that both the transport capacity and a number of characteristic properties were identical (saturation kinetics, temperature dependence and the effect of inhibitors). 2. Due to the absence of intracellular titratable buffers intracellular chloride concentration in ghosts vary only slightly between pH5 and 11. The unidirectional exchange flux was constant between pH 7 and 11, showing that the transport system does not have a functionally important titratable group in the alkaline range, as previously assumed. The decrease of transport below pH 7 is similar in intact erythrocytes and ghosts. 3. Mean cellular volume of the resealed ghosts was a function of the amount of KCl added at 'reversal', before the ghosts are sealed. The ghosts shrank by osmosis when KCl was added to the suspension of 'unsealed' ghosts. The reflexion coefficient of sucrose (and therefore the osmotic effect) is larger than that of KCl. It was, therefore, possible to demonstrate that volume changes do not affect the chloride transport across the human red cell membrane. Unidirectional chloride fluxes at a KCl concentration of 165 mM were independent of ghost volume (100‐40 mum3).