bluuebunny/crossref_metadata_2025_split huggingface dataset:
The contribution of excitatory and inhibitory inputs to the length preference of hypercomplex cells in layers II and III of the cat's striate cortex
Authors: Sillito A. M. , Versiani Vera 
Published: December 2014

1. The GABA antagonist bicuculline has been applied to hypercomplex cells in layers II and III of the cat's striate cortex in an attempt to test the hypothesis that their length preference derives from the action of a GABA mediated post‐synaptic inhibitory input.2. Iontophoretic application of bicuculline to these cells resulted in a reduction but not an elimination of the length preference. The reduction in length preference was only observed in the case of slits extended to one side of the receptive field or to slits only partially covering what appeared to be inhibitory flanking regions either side of the field centre. In cells normally showing a clear and stable length preference it was never possible to produce by the application of bicuculline a significant response to a slit fully extended to cover both flanking regions.3. The orientation tuning was basically eliminated by the application of bicuculline. In contrast the directional specificity was relatively unaffected.4. The action of bicuculline on hypercomplex cell orientation tuning supports the view that GABA mediated inhibitory inputs were effectively blocked and suggests that the partial effect on length preference and lack of effect on directional specificity reflect the varying degree of involvement of a GABA mediated inhibitory input to these receptive field properties.5. These observations introduce the possibility that the excitatory input to the superficial layer hypercomplex cells exhibits directional specificity, length preference with respect to a slit extended to both sides of the field and a low degree of orientation selectivity. Evidence is presented indicating that certain layer V cells with hypercomplex type receptive field properties exhibit some of the characteristics required of this input.
Secretion of a potassium‐rich fluid by the secretory coil of the rat paw eccrine sweat gland
Authors: Sato Fusako , Sato Kenzo 
Published: December 2014

1. It is already known that the rat paw eccrine sweat contains high K+ (greater than 150 m
M) and low Na+ concentrations (less than 70 m
M). The present study was intended to clarify the site of K+ secretion within the sweat gland, namely, the duct or the secretory coil. In vivo paw sweat was first induced by systemic pilocarpine injection or nerve stimulation. Both K+ and Na+ concentrations were studied in relation to the sweat rate to determine indirectly whether there is ductal secretion or reabsorption.2. Both Na+ and K+ concentrations in paw sweat agreed with the previous studies but did not show any saturation‐type flow dependence at the high sweat rate range.3. A method has been developed to isolate a single segment of the secretory coil and induce sweat secretion directly from it in an in vitro condition.4. In the presence of fresh serum (30%, preincubated for 30 min at 56 °C) in the incubation medium, stable secretory activity due to 10−6
M‐Mecholyl could be maintained for 40 min or longer. The primary sweat thus induced contained low Na+ (30 m
M) and high K+ (160 m
M) concentrations.5. In the secretory coil sweat in vitro, K+ concentration decreased and Na+ concentration increased as the secretory rate fell either spontaneously or after addition of atropine or cyanide.6. It remains to be studied whether auxiliary ductal secretion or reabsorption is present at low rates of sweating in the rat sweat gland.7. It was concluded that the secretory coil of the rat paw sweat gland is the major, if not the sole, site of K+ secretion.
The renin‐angiotensin system and sodium appetite
Authors: Fitzsimons J. T. , Wirth J. B. 
Published: December 2014

1. Bilateral nephrectomy or bilateral ureteric ligation greatly reduced the intake and retention of sodium in sodium‐depleted adrenalectomized rats which were experienced at drinking aversive concentrations of saline and which otherwise would have drunk and retained substantial quantities of sodium.2. Pharmacological activation of the renin—angiotensin system with isoprenaline or phentolamine caused increased intake of water but did not stimulate sodium appetite in sodium‐replete adrenalectomized rats, and decreased sodium appetite in sodium‐depleted adrenalectomized animals.3. Neither
I.P. injections of renin nor intravenous infusions of angiotensin II stimulated sodium appetite in normal rats or sodium‐replete adrenalectomized rats.4. No differences were found in the saline preference—aversion curves of normal rats not maintained on saline given intracranial injections of angiotensin II or carbachol.5. Preoptic injections of renin, renin substrate or angiotensin II into sodium‐replete adrenalectomized rats which were maintained on water and 2·7% saline induced immediate thirst followed by some saline intake. The saline intake was markedly less than the spontaneous saline intake of the same rats when sodium depleted.6. Similar preoptic injections in sodium‐depleted adrenalectomized rats caused increased water intake but did not increase the saline intake any further.7. Intracranial injections of carbachol had little effect on saline intake in either sodium‐replete or sodium‐depleted adrenalectomized rats but caused increased water intake.8. In conclusion, peripheral activation of the renin—angiotensin system stimulates water intake but has no direct effect on sodium appetite. Secondly, central administration of components of the renin—angiotensin system causes thirst and does not inhibit sodium appetite whereas centrally administered carbachol causes thirst and inhibits sodium appetite. Therefore the renin—angiotensin system has only a minor role in sodium appetite.
Membrane currents in cat myocardium: separation of inward and outward components
Authors: McDonald T. F. , Trautwein W. 
Published: December 2014

1. The single sucrose gap method was used to control the membrane potential of cat ventricular fibres.2. Following the early rapid events (capacitive, Na and slow inward (si) current spikes) the membrane current on depolarization contained three time‐dependent components which appeared attributable to the inactivation of Isi and the activation of two outward currents labelled IK and Ix.3. Tail currents were analysed with a view to confirming these conductance changes. At ‐60 mV the tail progressed from being predominantly inward in direction after short (30‐50 msec) depolarizations to being predominantly outward after long (> 300 msec) depolarizations. Inward and outward components decayed exponentially with time constants independent of previous membrane history. The Q10s were about 3.4. Experiments with D600 and variations of the driving force identified the inward tail component (τ ≈ 55 msec at ‐60 mV) as Isi. The major outward tail component (τ ≈ 300 msec) appears to be carried primarily by potassium. A second outward tail component (τ ≈ 3 sec) of much smaller amplitude than IK was observed after long depolarizations and is tentatively labelled Ix.5. Membrane currents at 0 mV can be described as the sum of three exponential processes: Isi inactivation (τ ≈ 90 msec), IK activation (τ ≈ 370 msec) and Ix activation (τ ≈ 3 sec). Conductance measurements (envelops of Isi and IK tails) supported these time courses. Isi time constants increased from 50 msec at ‐40 mV to 120 msec at +40 mV. IK time constants increased from 400 msec at ‐40 to about 520 msec at ‐25 mV before declining to 300 msec at +40 mV.6. Isi amplitudes measured visually (difference between peak Isi and current level after 200‐500 msec) were compared with those measured graphically (semilog plots, subtraction of IK and Ix). As a consequence of the relative amplitudes and time courses of Isi and IK, the shapes of the Isi voltage relations were not markedly different: visual estimates at 200 msec were in agreement with graphic estimates, visual estimates at 300 or 500 msec exceeded these by 15‐30% between ‐20 and +20 mV.
Activation of the electrogenic sodium pump in guinea‐pig atria by external potassium ions
Authors: Glitsch H. G. , Grabowski W. , Thielen J. 
Published: December 2014

1. When cardiac preparations are rewarmed following prolonged hypothermia a transient hyperpolarization occurs in K‐containing media. This hyperpolarization is correlated with the active Na efflux. It might be due to electrogenic Na pumping or to extracellular K depletion brought about by the activity of an electroneutral Na—K exchange pump. In order to distinguish between these mechanisms the effect of various extracellular K concentrations ([K]o) on the membrane potential of guineapig atria was studied before and after hypothermia.2. The membrane potential increased with decreasing [K]o before cooling. It reached values of ‐64 and ‐92 mV at 10·8 and 0 m
M‐K, respectively.3. The membrane hyperpolarized transiently after hypothermia beyong the potential observed before cooling. Maximal values of about ‐94 mV were obtained during rewarming in solutions containing 0·4‐2·7 m
M‐K. The membrane potential was significantly lower (‐88 mV) in K‐free media. It was also diminished at [K]o higher than 2·7 m
M and was measured to be ‐74 mV at 10·8 m
M‐K.4. The hyperpolarization of the cell membrane during the first 20 min of rewarming was maximal at 2·7 m
M‐K and yielded 15·5 mV. The hyperpolarization amounted to 7·2 and 10 mV at 0·4 and 10·8 m
M‐K, respectively. No hyperpolarization occurred in K‐free solutions.5. The rate of decline of the transient hyperpolarization increased with [K]o.6. Variations of membrane input resistance after changes in [K]o were measured in rewarmed atrial trabecula. The measurements revealed an increase in membrane resistance in lower [K]o.7. It is concluded that the transient hyperpolarization of the cardiac cell membrane during rewarming is due to the activation of an electrogenic Na pump.8. The (relative) strength of the pump current at various [K]o was derived from the observed dependence of the hyperpolarization and of the membrane input resistance on [K]o. The current is estimated to be half‐maximal at about 1·5 m
M‐K.
The effect of ouabain on noradrenaline output from peripheral adrenergic neurones of isolated guinea‐pig vas deferens
Authors: Nakazato Y. , Ohga A. , Onoda Y. 
Published: December 2014

1. The effect of ouabain on the noradrenaline output from peripheral adrenergic neurones has been studied using isolated guinea‐pig vasa deferentia.2. Exposure to ouabain (10−4
M) causes a gradual increase in the noradrenaline output. The effect occurs after a delay of 20 min and reaches a maximum during the period from 40‐60 min.3. In the absence of external Ca, exposure to ouabain fails to produce an increase in the noradrenaline output. However, the reintroduction of Ca (2·5 m
M) after a 1 hr exposure to ouabain in Ca‐free media causes a rapid rise in noradrenaline output which reaches a maximum within the first 20 min.4. After a 1 hr exposure to a low concentration of ouabain (10−5
M) the reintroduction of Ca is almost ineffective in increasing the noradrenaline output. When the concentration of ouabain is increased, the reintroduction of Ca becomes effective and causes a maximum effect with 10−4
M ouabain. In the presence of a constant amount of ouabain (10−4
M) the noradrenaline output induced by the reintroduction of Ca increases over the range 0·2‐2·5 m
M.5. In the presence of ouabain (10−4
M) the Ca‐induced noradrenaline output increases in a linear fashion with increasing Na concentrations from 25 to 143 m
M, as long as NaCl is replaced with equimolar choline chloride or isotonic sucrose.6. In the presence of the lowest effective concentration of sodium (25 m
M) the noradrenaline output induced by the reintroduction of Ca after a 1 hr exposure to ouabain is potentiated by LiCl. However, in the complete absence of Na+ ions, there is no Li‐dependent increase in the Ca‐induced noradrenaline output.7. It is suggested that ouabain may cause an increase in noradrenaline output by an effect on the Na‐dependent Ca influx system.
Endotoxin fever in the new‐born guinea‐pig and the modulating effects of indomethacin and p‐chlorophenylalanine
Authors: Székely M. 
Published: December 2014

1. At 30 °C ambient temperature E. coli endotoxin injected into the cerebral ventricles evokes a febrile response in 0‐3 day‐old guinea‐pigs. If the dose is sufficiently high, the fever is biphasic: two rising phases separated by a transient fall.2. At 20 °C ambient temperature the change in body temperature after the endotoxin is still biphasic, but the transient fall is more pronounced and, finally, hypothermia develops. The relatively large surface area of the new‐born cannot explain, by itself, the hypothermia.3. The phasic changes in body temperature following endotoxin administration are unlikely to be mediated by a single central factor, and a sequence of several factors could be postulated.4. Indomethacin prevents the first‐phase febrile rise in body temperature, and also the consequent fall, but not the second‐phase rise.5. p‐Chlorophenylalanine pre‐treatment prevents the transient fall only, it slightly increases the first‐phase rise and does not influence the second‐phase rise.6. Prostaglandins and/or other derivatives of endogenous arachidonic acid in the brain might be responsible for the first rising phase of the endotoxin fever, and might also initiate a central serotonergic mechanism which, in turn, could lead to the transient falling phase between the two rising phases of fever. The mechanism of the second‐phase febrile rise in body temperature awaits some other explanation.
The baroreceptor input to cardiac vagal motoneurones
Authors: McAllen R. M. , Spyer K. M. 
Published: December 2014

1. A study has been made of twenty‐three cardiac vagal motoneurones (c.v.m.s) in the nucleus ambiguus of chloralose‐anaesthetized cats.2. C.v.m.s were identified as described previously (McAllen & Spyer, 1978). They were either spontaneously active (five units) or induced to fire by the ionophoresis of
DL‐homocysteic acid (DLH). Evidence is presented that above threshold, the DLH dose is not critical for the ability to show a baroreceptor influence.3. The influence of the baroreceptors was determined by plotting pulse‐triggered histograms of c.v.m. activity. If the aortic baroreceptors were denervated, the pulse synchronous activity disappeared reversibly on carotid occlusion (eight out of eight cases). In five out of fifteen cells studied, when aortic baroreceptor pathways were intact, a small degree of cardiac modulation survived carotid occlusion.4. Estimates of the central delay of the baroreceptor‐vagal reflex were made by timing the c.v.m. response to both electrical stimulation of the sinus nerve and natural baroreceptor stimulation. When both methods were used on individual units, electrical stimulation invariably gave shorter values. Natural stimulation gave values that fell into two ranges (20‐60 msec and 70‐110 msec), suggesting the involvement of two pathways.5. Using higher currents, four c.v.m.s were induced to fire tonically during inspiration. Their activity in this phase showed a cardiac rhythm just as during expiration. Similarly, they responded to sinus nerve stimulation throughout the respiratory cycle.6. This result is discussed in relation to the observation of others that the baroreceptor‐cardiac reflex is ineffective during inspiration. It is proposed that there is no need to invoke a ‘gate’ early in the pathway but that this phenomenon and the present observations are best explained by summation of influences at the c.v.m. cell membrane.
Ballistic contractions in fast or slow human muscles; discharge patterns of single motor units
Authors: Desmedt John E. , Godaux Emile 
Published: December 2014

1. Single motor units were recorded from the masseter, soleus and first dorsal interosseous muscles of normal adult man. An analysis of discharge patterns was carried out either during slow ramp voluntary contractions, or during self‐initiated isolated ballistic voluntary contractions. The isometric myogram was simultaneously recorded.2. Each motor unit was only recruited when the peak force of a brisk contraction exceeded a certain value and a ‘ballistic force threshold’ (in kg) was estimated for the unit from a large series of brisk contractions of different strengths. For each muscle, the ranking order for recruitment of different motor units recorded from one electrode position was virtually identical in slow ramp versus brisk ballistic contractions of different force (Kendall rank correlation coefficient = 0·91‐1·0). There was no evidence for any consistent selective activation of fast twitch motor units in ballistic contractions.3. The ballistic force threshold is considerably reduced with respect to the slow ramp force threshold for the motor units of the soleus muscle. This drop is also marked for the units of the first interosseous and tibialis anterior muscles, whereas it is only small for the units of the masseter muscle. These data have been validated after consideration of the complicating factor related to the possible differential involvement of synergic muscles in ramp or ballistic contractions.4. In the masseter and first interosseous muscles, the time to peak is about 80 msec in small ballistic voluntary contractions and it increases to about 150 msec in strong contractions. This effect appears related to repetitive discharges of single motor units when their force threshold is exceeded. By contrast, in the soleus muscle, the time to peak remains at about 150 msec both in small and in strong ballistic contractions and most soleus motor units fire only one spike in the ballistic burst.5. Brisk ballistic contractions are graded in force by the recruitment of additional motor units according to their usual rank order. The importance of rate gradation through the repetitive firing of motor units varies in the different human muscles investigated, being quite significant in isometric brisk contractions of the masseter and first interosseous muscles but much less so in the soleus muscle in which little repetitive firing of single motor units was observed over the range of ballistic forces studied.
Noradrenaline as a possible mediator of the actions of angiotensin on fluid transport by rat rejunum in vivo
Authors: Levens N. R. , Munday K. A. , Parsons B. J. , Poat Judith A. , Stewart C. P. 
Published: December 2014

1. Net fluid absorption and transmural potential difference were measured in the rat jejunum in vivo.2. Increased rates of net fluid transport were observed following infusions of angiotensin or noradrenaline. There was a small, but significant, fall in transmural p.d. associated with noradrenaline but not with angiotensin infusions.3. The α‐adrenergic antagonists phentolamine and dihydroergotamine abolished both the angiotensin and the noradrenaline stimulations of transport and the noradrenaline‐induced fall in p.d., whereas the β‐adrenergic antagonist propranolol did not significantly affect these responses.4. Phentolamine did not alter the rise in p.d. following administration of the cholinergic agonist pilocarpine.5. The protein synthesis inhibitor cycloheximide abolished both the angiotensin and the noradrenaline‐induced stimulation of fluid transport.6. Neither angiotensin nor noradrenaline significantly altered jejunal cyclic AMP levels.7. Bilateral nephrectomy had no apparent effect upon the increase in fluid transport following noradrenaline infusions.8. The noradrenaline‐induced stimulation of transport was unaffected, and the fall in p.d. potentiated in rats pre‐treated with reserpine, but a marked inhibition of transport was observed following angiotensin infusions.9. The results are consistent with the view that noradrenaline may mediate the actions of angiotensin upon intestinal fluid absorption in the rat.
Pancreatic acinar cells: effects of microionophoretic polypeptide application on membrane potential and resistance
Authors: Petersen O. H. , Philpott H. G. 
Published: December 2014

1. Acinar cell membrane potential and resistance were measured from superfused segments of mouse pancreas, in vitro, using intracellular glass micro‐electrodes. One or two extracellular micropipettes containing caerulein, bombesin nonapeptide (Bn) or acetylcholine (ACh) were placed near to the surface of the impaled acinus. The secretagogues were ejected rapidly from the micropipettes by ionophoresis.2. Each secretagogue evoked a similar electrical response from the impaled acinar cell: membrane depolarization and a simultaneous reduction in input resistance. The duration of cell activation from caerulein ionophoresis was longer than that observed for ACh and Bn. The cell response to the peptide hormone applications could be repeated in the presence of atropine.3. The minimum interval before the onset of cell depolarization after caerulein ionophoresis was determined. Values ranged between 500 and 1000 msec. The minimum latencies after Bn ionophoresis were 500‐1400 msec.4. With two electrodes inserted into electrically coupled acinar cells, direct measurements of the caerulein and Bn null potentials were made. At high negative membrane potentials an enhanced depolarization was evoked by caerulein ionophoresis. At low negative membrane potentials the caerulein stimulation produced a diminished depolarization, and at membrane potentials less than — 10 mV acinar cell hyperpolarizations were observed. A similar series of responses was obtained in experiments where Bn ionophoresis was used. The caerulein and the Bn null potentials were always contained within — 10 to — 15 mV.5. The results describe the almost identical electrical response of acinar cells to stimulation by ACh, caerulein and bombesin. All three secretagogues have similar null potentials and latencies of activation on acinar cells. The bombesin latency responses appear as short as those measured for caerulein and provide electro‐physiological evidence that Bn acts directly on acinar cells. The findings support the hypothesis that ACh, caerulein and Bn, though acting on different receptors, evoke the observed changes in electrical properties of acinar cell membranes, through a common pathway.
Dependence of motoneurone properties on the length of immobilized muscle
Authors: Gallego R. , Kuno M. , Núñez R. , Snider W. D. 
Published: December 2014

1. The soleus muscle of adult cats was fixed in a shortened or lengthened position for 2 weeks by immobilizing the leg with a plaster cast. To eliminate the effects of reflex activity arising from the muscle, the lumbosacral dorsal roots were sectioned on the side of leg immobilization.2. The soleus muscle showed a significant decrease in weight after immobilization in a shortened position. Immobilization of the muscle in a lengthened position produced no significant changes in its weight.3. Two weeks after transection of the throacic spinal cord, the soleus muscle showed a significant decrease in weight. This decrease was prevented by immobilization of the muscle in a lengthened position. Immobilization in a shortened position caused no further muscle atrophy in cord‐transected animals.4. Soleus motoneurones showed a significant decrease in the duration of after‐hyperpolarization (a.h.p.) 2 weeks after immobilization of the muscle in a shortened position, whereas immobilization of the muscle in a lengthened position caused no significant changes in the duration of a.h.p.5. A decrease in the duration of a.h.p. of soleus motoneurones induced by cord transection was significantly prevented by immobilization of the muscle in a lengthened position but not by immobilization in a shortened position.6. In a variety of experimental conditions, the mean duration of a.h.p. of soleus motoneurones was significantly correlated with the soleus muscle: body wt. ratio.7. It is concluded that certain motoneurone properties depend upon the condition of the innervated muscle and that the primary factor responsible for the trophic influence is metabolic change in the muscle rather than contractile activity itself.