bluuebunny/crossref_metadata_2025 huggingface dataset:
Efferent desensitization of auditory nerve fibre responses in the cochlea of the turtle Pseudemys scripta elegans.
Authors: Art J J , Fettiplace R
Published: December 2014

Extracellular recordings were made from single auditory afferents in the isolated half‐head of the turtle, and changes in their acoustic sensitivity were examined following electrical stimulation of the efferent fibres to the basilar papilla. Short trains of efferent shocks caused a prolonged elevation of the pure tone thresholds of the auditory afferents and an abolition of their spontaneous activity. These changes could be demonstrated in a majority of recordings and without antidromic firing of the afferent. The amount of desensitization increased steeply with shock number and a train of ten closely spaced shocks could elevate the threshold at the most sensitive or characteristic frequency by four orders of magnitude. Desensitization also occurred with single efferent shocks at repetition frequencies exceeding 25/s. Discharge rate versus sound pressure functions were constructed for a number of afferents. The maximum slope of the functions, and the saturated firing rates were both reduced by efferent stimulation; there was also an over‐all shift of the rate‐intensity function to higher stimulus levels. Such effects would enable the afferent to signal a wider range of sound pressures. Efferent stimulation caused a broadening of the afferent frequency‐threshold curves by removal of the narrowly‐tuned region around the characteristic frequency. We suggest that the loss in tuning and concomitant improvement in temporal resolution may be a functionally important consequence of efferent action.
Inhibitory post‐synaptic currents in rat hippocampal CA1 neurones.
Authors: Collingridge G L , Gage P W , Robertson B
Published: December 2014

Spontaneous synaptic currents were recorded in voltage‐clamped CA1 neurones in rat hippocampal slices at room temperature (21‐25 degrees C). The currents, which could be seen at the resting membrane potential only when cells were loaded with chloride ions, were blocked by bicuculline. It was concluded that they were inhibitory post‐synaptic currents (i.p.s.c.s) generated by the opening of chloride‐selective channels activated by gamma‐aminobutyric acid (GABA). In twenty‐nine cells, ten to forty‐five i.p.s.c.s were recorded at a potential between ‐75 and ‐85 mV. In every cell, i.p.s.c.s varied widely in amplitude with an average coefficient of variation of 28.7%. The mean amplitude varied from 0.22 to 1.16 nA with an average of 0.52 nA. Reversed (outward) currents could be recorded from cells voltage clamped at positive potentials. Null potentials varied between ‐20 and +20 mV, the variability being attributed to differences in chloride loading. Most currents had a rapid growth phase with a mean growth time (20‐80% of peak) of 1.1 ms followed by a slower decay phase. The decay phase was exponential with a single time constant. The average decay time constant (tau D) ranged from 8.3 to 16.2 ms with a mean value of 11.0 ms. The rate of decay of currents was affected by membrane potential. tau D decreased exponentially with hyperpolarization in the range from +40 to ‐120 mV with an average volt constant (H value) of 146 +/‐ 9.6 mV (mean +/‐ 1 S.E. of mean, n = 17). The mean value of tau D at 0 mV was 19 ms. In some cells, growth times also decreased with hyperpolarization. The decay of currents was faster at higher temperatures but remained exponential. At 32 degrees C, the average tau D at 0 mV was 8.3 ms (n = 5) giving a Q10 value of 3.3 for the decay time constant at 0 mV. The frequency and mean amplitude of i.p.s.c.s were reduced by tetrodotoxin (TTX) or cadmium, indicating that many of the currents were generated by action potentials in presynaptic terminals. The spontaneous 'miniatures' remaining had the same time course and voltage sensitivity as currents recorded in normal solutions. Pentobarbitone (50‐100 microM) greatly prolonged the decay of i.p.s.c.s but had no discernible effect on their amplitude or growth phase.
Cardiac inotropic responses from changes in carbon dioxide tension in the cephalic circulation of anaesthetized dogs.
Authors: Hainsworth R , McGregor K H , Rankin A J , Soladoye A O
Published: December 2014

Experiments were performed on anaesthetized dogs to determine the effects of moderate changes in PCO2 in the cephalic circulation on the inotropic state of the heart and on the reflex inotropic responses from changes in carotid sinus pressure. The cephalic circulation was perfused, through the brachiocephalic and left subclavian arteries, with blood taken from the superior vena cava and equilibrated with various gas mixtures in a gas exchange unit. The carotid sinus regions were vascularly isolated and perfused with arterial blood at controlled pressures. Cardiac inotropic responses were assessed from the maximum rate of change of left ventricular pressure (dP/dtmax) with heart rate and mean aortic pressure held constant. An increase in cephalic blood PCO2 resulted in an increase in dP/dtmax and an increase in the unpaced heart rate. Small, graded changes in cephalic PCO2 resulted in graded responses of dP/dtmax. A change in carotid sinus pressure resulted in a significantly greater response of dP/dtmax when cephalic PCO2 was high. After interruption of the left cardiac sympathetic nerves, the responses of dP/dtmax to changes in cephalic PCO2 and carotid sinus pressure were nearly abolished. These results indicate that the tension of carbon dioxide in the cephalic circulation is likely to be of importance in the control of the inotropic state of the heart. They also imply that, in studies of cardiovascular reflex responses, it is important to control the carbon dioxide tension in the arterial blood.
The effects of the Anemonia sulcata toxin (ATX II) on membrane currents of isolated mammalian myocytes.
Authors: Isenberg G , Ravens U
Published: December 2014

The effects of Anemonia sulcata toxin (ATX II) on action potentials and membrane currents were studied in single myocytes isolated from guinea‐pig or bovine ventricles. Addition of ATX II (2‐20 nM) prolonged the action potential duration without a significant change in resting membrane potential. Concentrations of 40 nM‐ATX II or more induced after‐depolarizations and triggered automaticity. The effects were reversible after washing or upon addition of 60 microM‐tetrodotoxin (TTX). 5 mM‐Ni did not modify the effects. The single patch‐electrode voltage‐clamp technique of Hamill, Marty, Neher, Sakmann & Sigworth (1981) was applied to record membrane currents in response to 8.4 S long depolarizations starting from a holding potential of ‐90 mV. Currents flowing later than 5 ms after the depolarizing step were analysed. The fast events could not be considered because of insufficient voltage homogeneity. After 2 min of exposure to ATX II (20 nM) the changes in net membrane currents were measured. The difference between the currents in the presence of ATX II and during control was defined as the 'ATX‐II‐induced current' (iATX). After 4 min of wash iATX disappeared. Within 10 S of exposure to 60 microM‐TTX, iATX was blocked completely. At potentials positive to ‐60 mV, iATX was inwardly directed and decayed slowly but incompletely during the 8.4 S long depolarizing pulse. The rate of decay was faster during clamp pulses to more positive potentials. A high amplitude noise was superimposed on the current trace; its amplitude decreased with more positive potentials. We analysed the voltage dependence of iATX with 'isochronous' current‐voltage relations. The 0.1 S isochrone of iATX was characterized by a 'threshold' for negative currents at ‐60 mV, a branch with a negative slope (k = ‐7 mV, potential of half‐maximal activation (V0.5) = ‐38 mV, bovine cells) leading to a maximum inward current at ‐20 mV, and an ascending branch which led to an apparent reversal potential (Erev) around +40 mV. The values measured in guinea‐pig myocytes were similar though not identical (k = ‐5.5 mV, V0.5 = ‐30 mV, maximum of inward current at ‐5 mV, Erev = +50 mV). Erev shifted to less positive potentials in later isochrones. Holding the membrane at ‐45 mV prevented the induction of extra current by ATX II. When the holding potential was then changed to ‐85 mV, iATX developed within some 2 min. Returning the holding potential to ‐45 mV blocked iATX with a similar slow time course.(ABSTRACT TRUNCATED AT 400 WORDS)
The effects of caffeine on the noradrenaline‐sensitive calcium store in rabbit aorta.
Authors: Leijten P A , van Breemen C
Published: December 2014

The effects of caffeine on the noradrenaline‐sensitive Ca store in rabbit aorta have been studied measuring tension development and stimulated 45Ca efflux in Ca‐free solution. In addition, the inhibitory effects of caffeine on transmembrane Ca movements and on intracellular Ca release have been investigated, again comparing contractile force and 45Ca fluxes. The maximally effective caffeine concentration fully depletes the noradrenaline‐sensitive Ca store as found from both contraction and 45Ca efflux experiments. Within the concentration ranges used in this study for either caffeine and noradrenaline, a linear relation exists between the amplitude of contraction and the amount of stimulated 45Ca efflux. The Ca content of the store (presumably sarcoplasmic reticulum, s.r.) is 74 mumol/kg aorta, corresponding to an s.r. Ca concentration of 5.3 mM. After exposure of the cells to a high‐K solution the s.r. Ca concentration reached a value of 8.5 mM. At 37 degrees C the Ca is lost from the store in Ca‐free solution with a half‐time of 34 min. Although a comparable amount of 45Ca is released by the maximal doses of caffeine and noradrenaline, the caffeine‐induced contraction is much smaller than the noradrenaline‐induced one. The increase in adenosine 3',5'‐cyclic monophosphate (cyclic AMP) after caffeine was less than after noradrenaline, so could not account for the small size of the caffeine‐induced contraction. Asynchrony in response to caffeine by successive layers of smooth muscle, and a separate inhibitory action of caffeine, may contribute to the small size of caffeine‐induced contractions in thick muscle preparations. Caffeine inhibits high‐K‐induced contractions by inhibition of Ca influx. Caffeine also inhibits the noradrenaline‐induced contractions in Ca‐free solution. These inhibitory actions could be dissociated from caffeine‐induced release of intracellular Ca.
Permeability changes induced by L‐glutamate in solitary retinal horizontal cells isolated from Carassius auratus.
Authors: Tachibana M
Published: December 2014

Solitary horizontal cells isolated from goldfish retinae are depolarized by L‐glutamate (Glu) (Ishida, Kaneko & Tachibana, 1984), a possible candidate for the transmitter of photoreceptors. The underlying mechanisms were analysed under voltage‐clamp conditions using 'giga‐seal' suction pipettes in the whole‐cell recording configuration. Glu induced an inward current at the resting membrane potential (ca. ‐57 mV). Membrane depolarization decreased the amplitude of Glu‐induced current and reversed its polarity to outward beyond approximately ‐3 mV. Membrane hyperpolarization below the resting potential decreased the amplitude of the Glu‐induced inward current. When a K current through the anomalous rectifier, which is activated by membrane hyperpolarization (Tachibana, 1983), was blocked by Cs ions, this phenomenon disappeared and the Glu‐induced current increased in amplitude with hyperpolarization. Mg ions had no effect on the reduction of the Glu‐induced current at hyperpolarized potentials. It was strongly suggested that Glu produced two types of conductance change; a conductance increase due to an activation of Glu channels and a conductance decrease due to a blockage of the K current through the anomalous rectifier. The latter effect is analysed in detail in the following paper (Kaneko & Tachibana, 1985b). The Glu‐activated channel was permeable to cations (Na, K, Ca, Mg, Tris and choline ions) with low selectivity, but not to anions. The least effective dose of Glu was less than 10 microM. The relation between the Glu‐induced current and the membrane potential curved upwards near the reversal potential, and this relation was not affected by Mg ions.
The selective innervation of guinea‐pig superior cervical ganglion cells by sprouts from intact preganglionic axons.
Authors: Henningsen I , Liestøl K , Maehlen J , Nja A
Published: December 2014

If the guinea‐pig superior cervical ganglion is partially denervated in a way which spares some preganglionic axons arising from each of the spinal cord segments which normally innervate this ganglion (C8‐T7), sprouting of the intact preganglionic axons occurs without a loss of selective end‐organ responses to stimulation of individual ventral roots (Maehlen & Njå, 1981). In the present work we examine the selective innervation of individual ganglion cells by ventral roots after sprouting and compare it to that in normal ganglia. After sprouting the pattern of ganglion cell innervation by the intact preganglionic axons shows some of the features typical of normal ganglia. Thus each ganglion cell is strongly innervated by one or two neighbouring spinal cord segments, with the adjacent segments contributing a synaptic influence which diminishes with distance from the dominant one. Acutely after the partial denervation there is a tendency for the rostral segments to innervate ganglion cells more strongly than do caudal segments, compared to the situation in normal ganglia. The same is true following sprouting. The pattern of ganglion cell innervation observed after sprouting can be explained if the affinities of ganglion cells for innervation from particular spinal levels are assumed to be unchanged and the shift in the relative availability of different preganglionic axons, caused by the partial denervation, is taken into account. This view was substantiated by statistical analysis based on a model of selective synapse formation in the guinea‐pig superior cervical ganglion. We conclude that the ability of individual ganglion cells to distinguish preganglionic axons arising from different spinal levels is maintained during sprouting. Moreover, the way in which selective recognition and the availability of different preganglionic axons combine to produce particular patterns of innervation appears to be similar in normal development and after partial denervation in maturity.
Post‐exercise ketosis in post‐prandial exercise: effect of glucose and alanine ingestion in humans.
Authors: Koeslag J H , Levinrad L I , Lochner J D , Sive A A
Published: December 2014

This study examined ketosis in response to 90 min of running before and after the ingestion of 50 g glucose or 50 g L‐alanine in thirty‐three athletes. Everyone ran 20 km at 07.30 h and then rested, while fasting, till 16.00 h. There were four test groups: 'glucose‐before', 'glucose‐after', 'alanine‐before' and 'alanine‐after' according to whether glucose or alanine was ingested at 07.00 h, or 09.00 h. Controls did not ingest either test substance. The control 3‐hydroxybutyrate concentration rose from 0.23 +/‐ 0.03 mmol/l (S.E. of mean) at 07.00 h to 0.74 +/‐ 0.27 mmol/l at 12.00 h, and 0.94 +/‐ 0.33 mmol/l at 16.00 h. Glucose ingestion before or after exercise did not influence post‐exercise ketosis significantly, despite high insulin: glucagon ratios, low free fatty acid concentrations and hyperglycaemia. Alanine significantly lowered the 3‐hydroxybutyrate levels, especially after exercise (to 0.14 +/‐ 0.07 mmol/l at 12.00 h; P less than 0.05) despite reversed insulin: glucagon ratios. This suggests that hepatic responsiveness to portal hyperglycaemia and the main hormones of metabolism is altered immediately after exercise, presumably to promote muscle glycogen synthesis in preference to liver glycogen synthesis.
Effect of cephalic carbon dioxide tension on the cardiac inotropic response to carotid chemoreceptor stimulation in dogs.
Authors: Hainsworth R , Rankin A J , Soladoye A O
Published: December 2014

Dogs were anaesthetized with chloralose and the cephalic circulation was perfused, through the brachiocephalic and left subclavian arteries, with blood equilibrated with various tensions of CO2. The vascularly isolated carotid bifurcations were perfused at a constant pressure with either arterial or venous blood. Inotropic responses were assessed by measuring the maximum rate of change of left ventricular pressure (dP/dt max) with heart rate and aortic pressure held constant. Stimulation of carotid chemoreceptors with venous blood, at all values of cephalic PCO2, always resulted in a decrease in dP/dt max. An increase in cephalic PCO2, during arterial perfusion of chemoreceptors, resulted in an increase in dP/dt max and the response to chemoreceptor stimulation was enhanced. Graded changes in cephalic PCO2 resulted in graded changes in dP/dt max during arterial perfusion of chemoreceptors. However, the value of dP/dt max during venous perfusion was not significantly affected by increases in cephalic PCO2 above normal but it did decrease significantly during cephalic hypocapnia. These results confirm that an increase in cephalic PCO2 and stimulation of carotid chemoreceptors result in opposite responses of the cardiac inotropic state. The responses to chemoreceptor stimulation were enhanced by cephalic hypercapnia but the responses to cephalic hypercapnia, although not to hypocapnia, were suppressed by chemoreceptor stimulation.
Structural and topographical influences on functional connectivity in spinal monosynaptic reflex arcs in the cat.
Authors: Clamann H P , Henneman E , Lüscher H R , Mathis J
Published: December 2014

A greatly expanded version of spike‐triggered averaging (Mendell & Henneman, 1971), performed off‐line on tape‐recorded signals, was utilized to determine the presence or absence of functional connexions between stretch‐afferent fibres and homonymous motoneurones. As many as 264 possible connexions between eleven Ia or spindle group II fibres and twenty‐four motoneurones were studied in each single, acute experiment. Morphological and topographical factors influencing functional connectivity were analysed with the aid of wiring diagrams and connectivity matrices. In all experiments the greater the conduction velocity (i.e. diameter) of a Ia or group II fibre, the higher was the probability of its having functional connexions with homonymous motoneurones. The greater the longitudinal distance between the spinal entry points of Ia fibres and the location of a motoneurone, the less was the same probability. The influence of axonal conduction velocity of motoneurones on functional connectivity was apparent in some experiments, but not in others. In pooled data large motoneurones received functional connexions from a higher percentage of group II fibres than did small cells. The projection percentage reached 100 only when both Ia fibres and motoneurones were large, suggesting that motoneurone size influences the probability of functional connexions from group Ia as well as group II fibres. On a cell‐to‐cell level, connectivity apparently does not follow strict, deterministic rules. The results raise the question of how probabilistic connexions between afferent fibres and motoneurones give rise to deterministic outputs from the whole pool.
Influence of luminance gradient reversal on complex cells in feline striate cortex.
Authors: Hammond P , MacKay D M
Published: December 2014

The effects of reversing the polarity of luminance contrast in adjacent segments of a bar stimulus have been investigated in complex cells of area 17 in cats lightly anaesthetized with nitrous oxide/oxygen halothane mixtures. On the basis of length summation behaviour, complex cells were classified as standard (length summating) or special (optimum response to a bar much shorter than the receptive field), after Gilbert (1977), and were further subdivided into groups lacking and possessing end‐stopping. For each type of complex cell, we measured the effects of adding short segments of one polarity of contrast (light or dark) to either end of a bar of fixed length and optimum orientation but of opposite contrast. In all cells the response to the central bar was depressed by short segments of reversed contrast to an extent greater than predicted from the cells' length summation characteristics. Responses were minimized or abolished at a critical segment length. Increases beyond the critical length elicited a progressive recovery in response to a plateau level. In end‐stopped cells this was followed by a further decline in response up to the limits of the cells' inhibitory end‐zones. Special and standard complex cells differed only in their susceptibility to reversed‐contrast segments above the critical length. In standard complex cells, the recovery of response matched the cells' length summation profiles in slope and cut‐off point. In special complex cells the recovery was flatter in slope and significantly more protracted than the length summation profile. Similar results were obtained for either direction of motion (orthogonal to a cell's optimum orientation) and for either polarity of contrast (dark centre, light ends or the reverse). As might be expected, all the effects were weighted in favour of the receptive field centre. Thus the upturn in response as reversed‐contrast segments were progressively extended was more rapid and achieved a higher limiting level when the central bar was short. Merely interrupting the contours of a bar by a central gap, rather than a segment of reversed contrast, gave rise to no more attenuation of response than that predictable from the length summation curve. The results are compared and contrasted with our comparable data for simple cells.
Passive water flows driven across the isolated rabbit ileum by osmotic, hydrostatic and electrical gradients.
Authors: Naftalin R J , Tripathi S
Published: December 2014

Water flows generated by osmotic and hydrostatic pressure and electrical currents were measured in sheets of isolated rabbit ileum at 20 degrees C. Flows across the mucosal and serosal surfaces were monitored continuously by simultaneous measurement of tissue volume change (with an optical lever) and net water flows across one surface of the tissue (with a capacitance transducer). Osmotic gradients were imposed across the mucosal and serosal surfaces of the tissue separately, using probe molecules of various sizes from ethanediol (68 Da) to dextrans (161 000 Da). Flows across each surface were elicited with very short delay. The magnitudes of the flows were proportional to the osmotic gradient and related to the size of the probe molecule. Osmotic flow across the mucosal surface was associated with streaming potentials which were due to electro‐osmotic water flow. The mucosal surface is a heteroporous barrier with narrow (0.7 nm radius, Lp (hydraulic conductivity) = (7.6 +/‐ 1.6) X 10(‐9) cm s‐1 cmH2O‐1) cation‐selective channels in parallel with wide neutral pores (ca. 6.5 nm radius, Lp = (2.3 +/‐ 0.2) X 10(‐7) cm s‐1 cmH2O‐1) which admit large pressure‐driven backflows from the submucosa to the lumen. There is additional evidence for a further set of narrow electroneutral pores less than 0.4 nm radius with Lp less than 7 X 10(‐9) cm s‐1 cmH2O‐1. The serosal surface has neutral pores of uniform radius (ca. 6.5 nm), Lp = (7.6 +/‐ 1.6) X 10(‐8) cm s‐1 cmH2O‐1. Hypertonic serosal solutions (100 mM‐sucrose) cause osmotic transfer of fluid from isotonic mucosal solutions into the submucosa, expand it, and elevate the tissue pressure to 19.6 +/‐ 3.2 cmH2O (n = 4). Conversely, hypertonic mucosal solutions (100 mM‐sucrose) draw fluid out of the submucosa in the presence of isotonic serosal solutions, collapse the submucosa, and lower the tissue pressure to ‐87.7 +/‐ 4.6 cmH2O (n = 5). Water flows coupled to cation movement could be generated across the mucosal surface in both directions by brief direct current pulses. The short latency of onset and cessation of flow (less than 2 s), absence of polarization potentials, and high electro‐osmotic coefficients (range 50‐520 mol water F‐1), together with the presence of streaming potentials during osmotically generated water flows indicate electro‐osmotic water flow through hydrated channels in the tight junctions and/or lateral intercellular spaces.(ABSTRACT TRUNCATED AT 400 WORDS)
Fusimotor after‐effects on responses of primary endings to test dynamic stimuli in cat muscle spindles.
Authors: Emonet-Dénand F , Hunt C C , Laporte Y
Published: December 2014

Conditioning stimulation of individual dynamic fusimotor axons, either gamma or beta, leaves after‐effects which enhance the responses of primary endings to test stimulation of the same axon applied during slow ramp stretch. These after‐effects have a long duration, persisting well over 5 min, but are abolished by stretch of large amplitude. The dynamic after‐effects also enhance frequencygrams elicited by low‐frequency repetitive stimulation during slow ramp stretch, causing single stimuli to become much more effective. When several dynamic axons to the same spindle are isolated, conditioning stimulation of one leaves an after‐effect to test stimulation of itself and of all other dynamic axons. When two dynamic axons are used for conditioning stimulation, facilitation or occlusion can be demonstrated in their interaction, indicating that they converge on the same intrafusal element. Dynamic after‐effects persist during background static fusimotor activity of considerable amplitude, suggesting that static and dynamic actions are quite independent. Dynamic after‐effects appear to result from residual changes in the bag fibre, probably from a persistent increase in the number of cross‐bridges between thick and thin filaments. These after‐effects produce a large increase in the response of primary endings to dynamic fusimotor activity and probably have an important functional role.
Effects of stretch on dynamic fusimotor after‐effects in cat muscle spindles.
Authors: Emonet-Dénand F , Hunt C C , Laporte Y
Published: December 2014

Conditioning stimulation of dynamic fusimotor axons leaves persistent after‐effects which increase the responses of primary endings to test dynamic stimuli. Such after‐effects are abolished by muscle stretch. Destruction of these after‐effects depends on the following. (a) Amplitude of stretch: with symmetrical triangular stretches of moderate velocity, an extension of soleus by 4‐5 mm totally abolishes the after‐effects. Lesser stretches cause a graded reduction. (b) Velocity of relaxation: for a given amplitude of stretch there is greater destruction of after‐effects when it is followed by a slow rate of relaxation than after rapid relaxation. (c) After‐effects tested late in ramp stretch are more resistant to destruction by stretch than those increasing test dynamic responses early in ramp stretch. Stretch itself produces after‐effects which enhance test responses to dynamic but not to static fusimotor stimulation. Interactions between conditioning dynamic stimulation and stretch suggest that both these effects occur in the same intrafusal elements, the bag fibres.
Calcium‐dependent chloride secretion in rat colon epithelium.
Authors: Cuthbert A W
Published: December 2014

Epithelia, dissected from the descending rat colon, were studied under short‐circuit conditions in Ussing chambers. The latter were modified to accept flexible light guides, so that the tissue could be irradiated, with white light, normal to its surface. Irradiation alone had no effect on short‐circuit current (s.c.c.). In the presence of erythrosine B (which by itself had no effect on the s.c.c.) on the basolateral side of the tissue, irradiation produced a substantial increase in s.c.c.; this increase was sustained after irradiation had ceased and the dye had been washed away. The photodynamic effect of erythrosine B required the presence of oxygen in the bathing solution. Also calcium was essential for the s.c.c. response to occur. Thus, irradiation in the presence of the dye in the absence of calcium had no effect on s.c.c., but a s.c.c. increase could be revealed by subsequent addition of calcium after irradiation had ceased. Cobalt and magnesium ions antagonized the effect of calcium in the conditions described above. Ion flux measurements with 36Cl and 22Na showed that the photodynamic effect of erythrosine B abolished net sodium absorption and reversed net chloride absorption to secretion. The data are consistent with abolition of electroneutral sodium chloride absorption and the stimulation of electrogenic chloride secretion to an extent equivalent to the s.c.c. responses. Using calcium‐containing buffers it was possible to compare the s.c.c. responses at low, known ionized calcium concentrations with the maximal chloride secretory effect following photodynamic activation. Chloride secretion was half‐maximally activated when the basolateral bathing fluid contained 1 microM‐ionized calcium and after the basolateral face of the tissue had been permeabilized by the photodynamic action of erythrosine B. The relation between ionized calcium concentration in the basolateral fluid and the chloride secretory response was steep.
Membrane current noise in toad retinal rods exposed to low external calcium.
Authors: Matthews G
Published: December 2014

Outer segment membrane current of single rod photoreceptors from toad retina was recorded with a suction electrode, and extracellular calcium concentration was manipulated by transferring the recorded cell from one pool of saline to another or by locally perfusing the outer segment. The large increase in dark current that resulted from exposure to low‐calcium saline was accompanied by an increase in dark noise in the band 1‐800 Hz. This noise was suppressed by bright light, and its power spectrum could be described by a single Lorentzian equation with average corner frequency of 40.1 +/‐ 9.5 Hz (mean +/‐ S.D., n = 11). In low‐calcium saline, saturating flash responses were often followed by a transient increase in the dark current lasting 30‐100 s. During this rebound period of increased dark current, increased dark noise similar to that described in 2 was observed. The power spectrum of this noise was also fitted by a single Lorentzian equation, with corner frequency averaging 29.7 +/‐ 6.6 Hz (mean +/‐ S.D., n = 27). To examine the possible role of intracellular voltage fluctuations in generating the noise, suction electrodes were filled with calcium‐free saline and recordings were made from outer segments of rods attached to pieces of retina. In this recording configuration, the electrical coupling among the rods in the piece should attenuate voltage fluctuations associated with the post‐light rebound period of increased dark current. In this situation, the rebound increase in dark current was still observed, but the noise was reduced or absent. Using the same recording configuration, isolated rods showed pronounced noise during the rebound. The result in 4 suggests that the noise resulted from fluctuations in intracellular voltage, not directly from fluctuations in the light‐sensitive channels. In this view, the corner frequency of the noise power spectrum probably reflects the membrane time constant of the isolated rod.
Effects of readmission of substrate on the membrane potential in glycogen‐depleted guinea‐pig taenia coli.
Authors: Takai A , Tokuno H , Tomita T
Published: December 2014

In the glycogen‐depleted smooth muscle of the guinea‐pig taenia coli, application of glucose or beta‐hydroxybutyrate (beta‐HB) in the presence of 20 mM‐K or carbachol (5 microM) produced a transient hyperpolarization for about 1 min followed by a sustained depolarization accompanied by spike activity. The early hyperpolarization was highly temperature dependent, so that below 30 degrees C, substrate application produced the depolarization with a delay of approximately 2 min, without a clear preceding hyperpolarization. The responses to substrate were not affected by ouabain (10 microM). Readmission of K after a treatment with K‐free solution for 10 min caused a transient hyperpolarization only in the presence of substrate. This hyperpolarization was abolished by ouabain. Verapamil (0.1 microM) blocked the substrate‐induced depolarization, revealing an underlying slow hyperpolarization. Removal of Ca abolished both the hyperpolarization and depolarization caused by substrate application, but the hyperpolarization disappeared much more slowly than the depolarization. Removal of the external K had little effect on the substrate‐induced hyperpolarization, but the hyperpolarization induced by substrate application was increased when the external K was increased up to approximately 20 mM. Both the hyperpolarization and the depolarization were not clearly affected by completely replacing Na with choline. The results suggest that ATP supplied by the addition of substrate activates some electrogenic pump, probably a Ca pump, causing hyperpolarization, and that ATP also removes the inactivation of Ca conductance with some delay, resulting in an increased depolarization.
Ionic conductance associated with electrical activity of guinea‐pig red nucleus neurones in vitro.
Authors: Kubota M , Nakamura M , Tsukahara N
Published: December 2014

Intracellular recordings were made from red nucleus (r.n.) neurones in guinea‐pig slice preparations in vitro. In the control solution, a fast action potential was elicited by a depolarizing current pulse. This fast action potential was abolished by tetrodotoxin (TTX). When tetraethylammonium (TEA) was added to the perfusing solution, a TTX‐resistant slow action potential was elicited by a large depolarizing current pulse. This TTX‐resistant slow action potential was abolished by Co2+ or Mn2+. In the control solution, the action potential was followed by a fast and a slow after‐hyperpolarization (a.h.p.). The fast a.h.p. was abolished by TEA. The amplitude of the fast a.h.p. was dependent on the extracellular K+ concentration. The slow a.h.p. was reversibly abolished by Co2+ or Mn2+. The reversal potential of the slow a.h.p. was dependent on the extracellular K+ concentration. When the membrane potential was hyperpolarized, a time‐dependent inward rectification was observed. This inward rectification was inhibited by Cs+ but not by Ba2+, TTX, TEA or Co2+. It is concluded that the fast action potential is produced by a voltage‐dependent Na+ conductance, the TTX‐resistant slow action potential is produced by a voltage‐dependent Ca2+ conductance, the fast a.h.p. is produced by a voltage‐dependent K+ conductance, the slow a.h.p. is produced by a Ca2+‐activated K+ conductance and the inward rectification is produced by a time‐dependent inward rectifier in r.n. neurones.
The physiological effects of hydrostatic pressure are not equivalent to those of helium pressure on Rana pipiens.
Authors: Dodson B A , Furmaniuk Z W , Miller K W
Published: December 2014

The effects of helium pressure and hydrostatic pressure on Rana pipiens were compared. Both agents caused paralysis at pressures greater than 135 atmospheres (1 atm = 101.325 kPa), but the median pressure for hydrostatic‐pressure‐induced paralysis was 35 atm less than that for helium pressure. When the ability of both pressurizing agents to reverse urethane‐induced anaesthesia was compared, it was found that hydrostatic pressure raised the median dose for anaesthesia 2.2‐fold more per atmosphere than did helium pressure. Animals that were lightly anaesthetized by urethane at 110 atm hydrostatic pressure became more deeply anaesthetized when helium was admitted isobarically into the pressure chamber. This difference in depth of anaesthesia between hydrostatic pressure and helium pressure is consistent with helium possessing an inherent anaesthetic effect. The abilities of other gases to pressure‐reverse urethane anaesthesia were also determined. The degree of attenuation of the full pressure reversal effect observed with hydrostatic pressure was proportional to the lipid solubility of the gases, increasing in the order helium, neon, hydrogen, nitrogen and argon. Our data on the difference between hydrostatic and helium pressure are consistent with the critical volume hypothesis.
Effect of ventricular tonicity upon cerebrospinal fluid production in rabbits.
Authors: Pullen R G
Published: December 2014

Ventriculo‐cisternal perfusion in rabbits has been employed to examine steady‐state relations between ventricular sodium and water fluxes and ventricular osmolality. These fluxes have been determined in individual rabbits when the ventricular fluid was either similar to normal cerebrospinal fluid (c.s.f.) or when its osmolality was changed to one value within the range of about 150‐300 mosmol/l. The ventricular osmolality was changed by perfusing the ventricles with sucrose solutions of different concentrations that were either ion free, contained a low concentration of sodium, or contained both sodium and furosemide to inhibit the active production of c.s.f. Results suggest that this experimental range of ventricular osmolality is without significant effect upon a constant active sodium‐coupled water movement into the ventricles, whereas a passive osmotic water flux into the ventricles increases with ventricular osmolality.
Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.
Authors: Denton D A , Nelson J F , Tarjan E
Published: December 2014

Wild rabbits trapped in their natural habitat and adapted to laboratory conditions were studied. Food, water and electrolyte (0.5 M‐NaCl, 0.5 M‐KCl, 0.25 M‐MgCl2 and 0.25 M‐CaCl2) consumption, urinary volume and sodium losses were monitored daily following stimuli which were found dipsogenic in other species. Water drinking was observed immediately after the intravenous injection of 1 M‐NaCl (3 ml/kg), and following withdrawal of a mean of 13.9% of calculated blood volume. Daily intake of water decreased during intracerebroventricular (I.C.V.) infusion of 0.3 M‐NaCl in artificial cerebrospinal fluid (c.s.f.), during I.C.V. infusion of 0.9 M‐mannitol c.s.f., both at a rate of 17 microliters/h, following peritoneal dialysis with 5% (w/v) glucose solution, and during food restriction. Water intake was not affected following intravenous administration of acetazolamide (10 mg/kg). Daily intake of 0.5 M‐NaCl solution was increased following peritoneal dialysis with 5% (w/v) glucose solution, which caused hyponatraemia, but not after haemorrhage which caused about the same sodium deficit as peritoneal dialysis, but as an isosmotic loss. Administration of two different angiotensin II analogues, systemically or I.C.V., failed to induce water drinking. However, urinary sodium excretion and intake of 0.5 M‐NaCl were increased during the 5 days of I.C.V. infusion of angiotensin II (10 pmol/h). Infusion for 1 day of angiotensin II (500 pmol/h) led to increased urinary sodium excretion which was followed by increased intake. The intake of other electrolyte solutions was not significantly affected by any of the treatments detailed above. The mechanisms participating in initiation of thirst in wild rabbits are very sensitive to decrease in blood volume, in contrast to other species studied in laboratories. Angiotensin II at the doses and routes administered was not dipsogenic in wild rabbits. The increased intake of 0.5 M‐NaCl solution observed during and after the long‐term intraventricular administration of angiotensin II in the wild rabbit appears predominantly a response to sodium deficit caused by natriuresis. The persistence of appetite after the cessation of infusion is indicative of a residual effect on central mechanisms of salt appetite.
Lack of nicotinic supersensitivity in frog sympathetic neurones following denervation.
Authors: Dunn P M , Marshall L M
Published: December 2014

The sensitivity of bull‐frog sympathetic neurones to nicotinic, cholinergic agonists has been studied in both normal (control) and surgically denervated ganglia. Using gross extracellular recording, the sensitivity to acetylcholine (ACh) increased 18‐fold following denervation, while that to carbachol (CCh) was unchanged. Normal ganglia showed a similar sensitivity increase after inhibition of cholinesterase. This suggests that the rise in ACh sensitivity is due to reduced cholinesterase activity, not to true supersensitivity. There was no significant difference in resting membrane potential or input resistance between normal and denervated neurones. Neurones denervated for 7‐50 days showed no significant change in sensitivity to ACh or CCh applied iontophoretically at a distance of 10 micron from the cell surface. In control ganglia, localized iontophoretic application of ACh revealed an uneven distribution of sensitivity which is attributed to the localization of receptors to synaptic areas. Fourteen days after denervation, the geometric mean sensitivity to focally applied ACh was not significantly different from that found in control ganglia. The variation in sensitivity to focally applied ACh at randomly chosen sites on denervated neurones was as great as that found in control ganglia. It is concluded that denervation does not cause frog sympathetic neurones to become supersensitive to ACh. The apparent increase in nicotinic ACh sensitivity observed using extracellular recording from whole ganglia is due not to a change in the number or distribution of ACh receptors, but to a decrease in cholinesterase activity.
Hypothalamic thermosensitivity in capsaicin‐desensitized rats.
Authors: Cormarèche-Leydier M , Shimada S G , Stitt J T
Published: December 2014

In rats, we tested the hypothesis that capsaicin desensitization reduces hypothalamic warm thermosensitivity. We locally heated and cooled the hypothalamus using water‐perfused thermodes while observing thermoregulatory variables. In untreated rats, a small dose of capsaicin had profound effects on thermoregulation. However, desensitizing rats to capsaicin had no effect on hypothalamic thermosensitivity for metabolic rate or changes in body temperature due to displacements of hypothalamic temperature. Contrary to current opinion, we conclude that capsaicin desensitization does not alter hypothalamic thermosensitivity to warm or cold.
Modulation of slow response excitability by calcium in rabbit atrial trabeculae.
Authors: Cukierman S
Published: December 2014

Slow responses were induced in rabbit isolated left atrial trabeculae in a modified Tyrode solution containing 15 mM‐KCl and 1 mM‐BaCl2. Conventional electrophysiological techniques were employed for stimulating and recording membrane potentials. Under these conditions, the excitability of the slow response depends on the past excitatory history of the preparation. As the stimulation frequency increases (range: 0.08‐1 Hz) for a conditioning period of stimulation, the excitability of the slow response increases. This can be demonstrated by a decrease in stimulus requirement necessary to maintain slow response excitation following the conditioning period of stimulation. It is shown that when extracellular Ca2+ concentration is reduced to 0.5 mM, that phenomenon of frequency‐dependent slow response excitability disappears but slow responses can still be elicited. Also, the addition of D‐600 to 2.7 mM‐Ca2+ solutions depresses both the slow response and its frequency‐dependent excitability. The absence of frequency‐dependent slow response excitability is not related to the depression of the slow response upstroke caused by low‐Ca2+ solutions. Increasing intracellular Ca2+ concentration by exposing the preparation to low‐Na+ solutions or to ouabain did not revert the observed effects in low‐Ca2+ solutions. The addition of substances (5 mM‐caffeine or 0.35 microM‐adrenaline) that potentiate the influx of Ca2+ in low‐Ca2+ solutions was found to be effective in restoring the dependence of slow response excitability on the frequency of stimulation. The increase in extracellular Ca2+ above 4 mM depressed the excitation of the slow response. Above 5.4 mM‐Ca2+, the excitation of the slow response was completely inhibited while the preparation displayed continuous oscillations in transmembrane potential. The presence of a subthreshold response (subliminal response) that precedes and triggers slow response excitation is accompanied by tension development. Since the subliminal response is responsible for the changes in slow response excitability it is proposed that the Ca2+ inflow during slow response electrogenesis modulates the excitability of the slow response. Two possible physiological implications for this finding are discussed.
The possible relation between mastication and parotid secretion in the rabbit.
Authors: Anderson D J , Hector M P , Linden R W
Published: December 2014

Salivary flow has been recorded from conscious rabbits during 1 min periods whilst continuously chewing standard laboratory dry pellets or pieces of carrot and, in some animals, a mash of pellets with water. Flow was measured using contact drop recorders or a continuous flow recorder via Polythene tubes permanently inserted into one or both parotid ducts. Large variations in flow were obtained with unilateral recordings particularly during dry pellet chewing. Bilateral recordings showed that the flow was always greater on one side than on the other and that dominant secretion alternated from side to side in an apparently random manner. Rabbits chew unilaterally. Videotaped recordings of chewing movements showed that the greater secretion was always produced on the chewing side. To test the possibility that drying of the oral mucosa, or the prolonged hardness of the pellets may result in higher flow rates in animals with cannulated ducts than would normally be seen in intact animals, water was injected downstream into the mouth through a third cannula. This was inserted in an anterograde direction in the parotid duct on one side. Significant reductions in flow were recorded during dry pellet eating, but not during carrot eating. When animals were fed a soft pellet mash, salivary flow was significantly lower than with dry pellets. Recordings have been made from strain gauges attached to the ascending ramus of the mandible. Previous findings that dry pellets produce greater strain than carrots have been confirmed. It has also been shown that less strain is produced with soft pellet mash. The strain gauge data suggested that a relation exists between masticatory force and parotid salivary flow. The results are compatible with the hypothesis that intra‐oral mechanoreceptors may be involved in a masticatory‐salivary reflex.
Activation of enteric nerve pathways in the guinea‐pig duodenum by cholecystokinin octapeptide and pentagastrin.
Authors: Ngu M C
Published: December 2014

The action and mechanism of action of cholecystokinin octapeptide (CCK‐8) and pentagastrin on isolated segments of guinea‐pig duodenum were examined using contractility studies and by intracellular recordings made from smooth muscle cells. Both CCK‐8 and pentagastrin caused an excitatory contractile response. The threshold concentration ranged from 5 X 10(‐11) to 10(‐9) M for CCK‐8 and 5 X 10(‐10) to 10(‐8) M for pentagastrin. The excitatory response was abolished by tetrodotoxin (3.1 X 10(‐6) M) and atropine (1.5 X 10(‐6) M) and inhibited by d‐tubocurarine (up to 2.9 X 10(‐5) M). In the presence of atropine a proportion of preparations relaxed in response to CCK‐8 (nineteen of thirty‐one) and pentagastrin (thirteen of seventeen). This response was only seen at high concentrations of the peptides (10(‐8)‐10(‐7) M) and was abolished by tetrodotoxin (3 X 10(‐6) M). Intracellular recordings from duodenal smooth muscle revealed multiple excitatory junction potentials (e.j.p.s) in response to CCK‐8 and to pentagastrin. These e.j.p.s were identical to those evoked by transmural nerve stimulation and were abolished by atropine (1.5 X 10(‐7) M) and by tetrodotoxin (3 X 10(‐6) M). Inhibitory junction potentials (i.j.p.s) were not recorded in response to the peptides except on one occasion. It is suggested that CCK‐8 and pentagastrin cause an increase in duodenal motility by the selective activation of excitatory pathways in the enteric nervous system.