bluuebunny/crossref_metadata_2025 huggingface dataset:
Influence of stretch‐evoked synaptic potentials on firing probability of cat spinal motoneurones.
Authors: Gustafsson B , McCrea D
Published: December 2014

Shapes of post‐synaptic potentials (p.s.p.s) in cat motoneurones were compared with the time course of correlated changes in firing probability during repetitive firing. Excitatory and inhibitory post‐synaptic potentials (e.p.s.p.s. and i.p.s.p.s) were evoked by brief triangular stretches of the triceps surae‐plantaris muscles. Depolarizing current was injected through the recording micro‐electrode to evoke repetitive firing and the post‐stimulus time histogram of motoneurone spikes was obtained. E.p.s.p.s (n = 80) of different sizes (30‐1040 microV) and rise times (1.1‐8.2 ms) were investigated in fifty‐nine motoneurones. The majority of the e.p.s.p.s were recorded in triceps surae‐plantaris motoneurones with high levels of synaptic noise (estimated peak‐to‐peak fluctuations of 1.5‐3.5 mV). This noise was generated by keeping the triceps surae‐plantaris muscles stretched to a near maximal degree. The remaining e.p.s.p.s were recorded in motoneurones to other hind‐limb muscles with a low level of synaptic noise. The height of the primary peak of the correlogram with respect to base‐line firing rate increased in proportion to both amplitude and rising slope of the e.p.s.p.s. Using normalization procedures or using e.p.s.p.s of constant amplitude but different slopes and vice versa, the relative peak height increased with e.p.s.p. peak derivative with a slope of around 6/mV per millisecond and with e.p.s.p peak amplitude with a slope of about 1/mV. The shape of the correlogram (peak and trough) seemed well described by a linear combination of the shape of the e.p.s.p. derivative and that of the e.p.s.p. itself. The relative e.p.s.p. contribution (e.p.s.p.:e.p.s.p. derivative ratio) varied with e.p.s.p. amplitude and noise level, being largest (mostly 0.25‐1.0) for small e.p.s.p.s (100‐300 microV) in high levels of synaptic noise and smaller (0‐0.25) for larger e.p.s.p.s and for e.p.s.p.s in a low noise background. In conformity with the above finding, a leaky integration of the correlograms gave time courses that in most cases closely resembled the shape of the e.p.s.p.s. The time constant of the leaky circuit (= inverse value of e.p.s.p.:e.p.s.p. derivative ratio) varied with e.p.s.p. amplitude and noise level in the same manner as obtained by direct fitting of e.p.s.p. and e.p.s.p. derivative shape to correlogram shape. Stretch‐evoked i.p.s.p.s (n = 10) of small amplitude (90‐360 microV as measured close to firing level) were investigated in pre‐tibial flexor motoneurones with low levels of synaptic noise. These i.p.s.p.s generated correlogram troughs closely resembling, albeit somewhat wider than, the shape of the i.p.s.p. derivatives.(ABSTRACT TRUNCATED AT 400 WORDS)
Repression of inactive motor nerve terminals in partially denervated rat muscle after regeneration of active motor axons.
Authors: Ribchester R R , Taxt T
Published: December 2014

The fourth deep lumbrical muscle in the hind foot of adult rats was partially denervated by crushing the sural nerve (s.n.). The denervated muscle fibres became completely reinnervated by sprouts from lateral plantar nerve (l.p.n.) motor axons. By about 20 days after the nerve crush, s.n. motor axons started to reinnervate the muscle. In control muscles, a small proportion of the muscle fibres‐‐about 2.5% of the muscle per motor unit‐‐was reinnervated by s.n. motor axons over the following 20 days. Hence the regenerating terminals were able to re‐establish functional synapses, despite the fact that all the muscle fibres were functionally innervated by l.p.n. terminals. When nerve impulse conduction in the l.p.n. was blocked with tetrodotoxin for up to 2 weeks, starting from the time when s.n. axons returned to the muscle, s.n. motor axons retrieved a much larger proportion of the muscle fibres‐‐about 6.5% of the muscle per motor unit. There was a concomitant decrease in the tension produced by the sprouted l.p.n. motor axons. Intracellular recordings showed that many muscle fibres became innervated exclusively by regenerated s.n. motor nerve terminals. Measurements of end‐plate potentials suggested that l.p.n. sprouts and the original nerve terminals were eliminated non‐selectively. These results suggest that regenerating, active motor nerve terminals have an additional competitive advantage in reinnervating innervated muscles, if the intact terminals are inactive. When the l.p.n. was cut, rather than blocked, extensive reinnervation by the s.n. occurred‐about 30% of the muscle per motor unit. This suggests that the absence of an intact nerve terminal in the motor end‐plate provides a stronger stimulus than inactivity for synapse formation by regenerating motor axons.
Relation between the specific H reflex facilitation preceding a voluntary movement and movement parameters in man.
Authors: Eichenberger A , Rüegg D G
Published: December 2014

In a reaction‐time situation, the monosynaptic spinal reflex (H reflex) is facilitated before the onset of an electromyographic (e.m.g.) response. The aim of the present investigation was to study aspects of this facilitation. Human subjects were required to perform isometric plantarflexions of the foot in response to a visual stimulus. The movement was always on the same side in the simple reaction‐time situation, and randomly with the right or left foot in the choice reaction‐time situation. Stimuli to evoke H reflexes were applied bilaterally 40‐400 ms after the onset of the visual stimulus. Pre‐motor time, i.e. the interval between the onset of the visual stimulus and the e.m.g. response, and reaction time, i.e. the interval between the onset of the visual stimulus and the response on the torque recording, were computed. In both reaction‐time situations, there was a significant facilitation of the ipsilateral H reflex 100‐160 ms before e.m.g. onset and, in some subjects, a small facilitation of the contralateral H reflex. The specific facilitation, i.e. the difference between the facilitation on the ipsi‐ and contralateral side relative to the movement, was not significantly different on the right and left side. Pre‐motor time was divided into the interval from the light onset until the onset of the specific facilitation, and the interval from the onset of the facilitation until the onset of the voluntary response. Both intervals increased, and the slope and the amplitude of the facilitation decreased with increasing pre‐motor time and reaction time. The specificity of the H reflex facilitation in a choice reaction‐time situation implies that the interval from light onset until the onset of the facilitation includes stimulus identification and response selection, and the interval from the onset of the facilitation until the e.m.g. response preparation of the motor system for the required movement. The present results suggest that the specific facilitation of the H reflex before a movement is caused by removal of presynaptic inhibition at I a terminals or by activation of interneurones intercalated in polysynaptic components of the H reflex rather than by a subthreshold activation of motoneurones.
Conductance properties of single inwardly rectifying potassium channels in ventricular cells from guinea‐pig heart.
Authors: Sakmann B , Trube G
Published: December 2014

Single ventricular cells were enzymatically isolated from adult guinea‐pig hearts (Isenberg & Klöckner, 1982). The patch‐clamp technique (Hamill, Marty, Neher, Sakmann & Sigworth, 1981) was used to examine the conductance properties of an inward‐rectifying K+ channel present in their sarcolemmal membrane. When the K+ concentration on the extracellular side of the patch was between 10.8 and 300 mM, inward current steps were observed at potentials more negative than the K+ equilibrium potential (EK). At more positive potentials no current steps were detectable, demonstrating the strong rectification of the channel. The zero‐current potential extrapolated from the voltage dependence of the inward currents depends on the external K4 concentration [K+]o in a fashion expected for a predominantly K+‐selective ion channel. It is shifted by 49 mV for a tenfold change in [K+]o. The conductance of the channel depends on the square root of [K+]o. In approximately symmetrical transmembrane K+ concentrations (145 mM‐external K+), the single‐channel conductance is 27 pS (at 19‐23 degrees C). In normal Tyrode solution (5.4 mM‐external K+) we calculate a single‐channel conductance of 3.6 pS. The size of inward current steps at a fixed negative membrane potential V increases with [K+]o. The relation between step size and [K+]o shows saturation. Assuming a Michaelis‐Menten scheme for binding of permeating K+ to the channel, an apparent binding constant of 210 mM is calculated for a membrane potential of ‐100 mV. For this potential the current at saturating [K+]o is estimated as 6.5 pA. The rectification of the single‐channel conductance at membrane potentials positive to EK occurs within 1.5 ms of stepping the membrane potential from a potential of high conductance to one of low conductance. In addition to the main conductance state, the channel can adopt several substates of conductance. The main state could be the result of the simultaneous opening of four conducting subunits, each of which has a conductance of about 7 pS in 145 mM‐external K+. The density of the inward‐rectifying K+ channels in the ventricular sarcolemma is 0‐10 channel/10 micron2 of surface membrane; the average of twenty‐eight patches was 1 channel/1.8 micron2. It is concluded that the inward‐rectifying K+ channels mediate the resting K+ conductance of ventricular heart muscle and the current termed IK1 in conventional voltage‐clamp experiments.
The relation between the endocochlear potential and spontaneous activity in auditory nerve fibres of the cat.
Authors: Sewell W F
Published: December 2014

The relation between the endocochlear potential and spontaneous discharge rate in auditory nerve fibres was determined following intravenous injections of furosemide in anaesthetized cats. Following furosemide administration, both the endocochlear potential and the spontaneous discharge rates of auditory nerve fibres decreased synchronously. The logarithm of the spontaneous discharge rate was proportional to the endocochlear potential. The slope of the logarithmic relation increased as a function of the characteristic frequency of the fibre. The slope of the logarithmic relation is steeper for fibres with 'medium' spontaneous discharge rates (0.5‐12 spikes/s) than for fibres with 'high' spontaneous discharge rates (greater than 18 spikes/s). Among high spontaneous rate fibres, the slope does not appear to vary systematically with the spontaneous rate of the fibre. The decrease in spontaneous discharge rate in auditory nerve fibres is interpreted as follows: (1) the injection of furosemide causes a decrease in the endocochlear potential, (2) a decrease in the endocochlear potential produces a linearly related hyperpolarization of the membrane potential of the hair cell by altering the standing current which flows through the transducer membrane, and (3) the logarithm of the rate of release of transmitter quanta decreases with the hyperpolarization of the membrane potential of the hair cell, which decreases the rate of occurrence of action potentials at the hair cell afferent junction.
Compartmental models of electrotonic structure and synaptic integration in an identified neurone.
Authors: Edwards D H , Mulloney B
Published: December 2014

A three‐compartment model of the electrotonic structure of an identified motoneurone, the median gastric (m.g.) neurone of the stomatogastric ganglion of the spiny lobster (Panulirus interruptus) was constructed, based on the passive response of the cell to a step of injected current. While its structure is only remotely related to that of the cell, the model is able to predict the passive response of the cell to any wave form of injected current. The shape of the m.g. neurone provided the basis for the development of a multicompartment model of the cell from the simple compartment model. Unlike the three‐compartment model, the multicompartment model has a structure that corresponds closely to that of the cell while it retains the ability to predict the passive response of the cell to any wave form of injected current. The multicompartment model was used to analyse the electrotonic structure and synaptic integration of the cell. The axon acts as a current sink, causing steady‐state voltage attenuation between the tips of different dendrites and the integrating segment to range between 26 and 89%. Steady‐state voltage attenuation in the distal direction is 2% or less. Synaptic inhibition of m.g. by Interneurone 1 was simulated with simultaneously activated conductance‐increase synapses located on all dendritic end‐compartments of the model. Inhibitory post‐synaptic potential (i.p.s.p.) wave forms recorded in the cell soma were duplicated in the soma compartment when the synaptic conductance change in each of the twenty‐eight end‐compartments was set equal to 5 nS for 8 ms. I.p.s.p. wave forms in dendritic end‐compartments were 30% larger than the soma compartment i.p.s.p., while i.p.s.p.s in the integrating segment compartment were intermediate in size. Charge from a 92 mV, 1 ms action potential in the model axon was passively conducted from axonal compartments to the soma compartment of the model, where it reproduced the attenuated, broadened voltage wave forms of action potentials recorded in the cell soma. Passive spread of charge from an axonal action potentials to terminal dendritic compartments evoked potentials there that were 30% larger and faster than the corresponding soma compartment potential.
Calcium current activation kinetics in neurones of the snail Lymnaea stagnalis.
Authors: Byerly L , Chase P B , Stimers J R
Published: December 2014

Both the activation kinetics and the magnitude of the Ca current in Lymnaea are strongly dependent on temperature. The Q10 for the reciprocal of the activation time constant is 4.9 +/‐ 0.2 and the Q10 for the maximum current is 2.3 +/‐ 0.1. By lowering the temperature to 7‐10 degrees C, we have been able to resolve the Ca tail currents. The block of Ca current by Cd2+ is voltage dependent, being more effective at more positive potentials. As determined from the magnitude of the tail currents, the Ca permeability is not maximally activated until the membrane potential is greater than +70 mV. The Ca permeability is half activated in the range 30‐35 mV. The open‐channel current‐voltage relation for the Ca current is in rough agreement with the prediction of the constant‐field equation. There is no indication of current saturation at negative potentials for potentials down to ‐60 mV. The Ca tail current decays with at least two time constants, one 200‐400 microseconds and the other 2‐4 ms. Although these time constants are not strongly voltage dependent, the ratio of the amplitude of the fast component of the tail current to that of the slow component is much larger at ‐60 mV than at 0 mV. The time course of the Ba tail current is very similar to that of the Ca tail current. The time course of the activation of the Ca current follows m2 kinetics and does not show evidence for a Cole‐Moore‐type shift for holding potentials between ‐50 and ‐110 mV. During a second positive pulse applied 1 ms after the first, the Ca current activates more rapidly, without the delay characteristic of the Ca current of a single positive pulse. The activation of the Ca current can be represented by a linear sequential model. The simplest model that describes both the turn‐on and the turn‐off of the Ca current must have at least three closed states, followed by a single open state.
Responses of solitary retinal horizontal cells from Carassius auratus to L‐glutamate and related amino acids.
Authors: Ishida A T , Kaneko A , Tachibana M
Published: December 2014

Effects of L‐glutamate and its analogues on membrane potentials of solitary horizontal cells were studied by intracellular recording. L‐glutamate depolarized these cells at micromolar concentrations (greater than or equal to 10 microM), while D‐glutamate and L‐alpha‐amino adipic acid produced slight depolarizations only at millimolar concentrations. Neither L‐ nor D‐aspartate, even at millimolar doses, produced any change in solitary horizontal‐cell resting potential. Solitary horizontal‐cell responses to L‐glutamate did not desensitize detectably. Responses to pairs of brief, ionophoretic pulses of L‐glutamate were nearly equal in amplitude at inter‐pulse intervals as short as 50 ms. Responses to maintained applications of low doses of L‐glutamate did not decline for as long as 2 min. Depolarizing responses were produced by ionophoretic applications of L‐glutamate near cell somata as well as dendrites. The mean sensitivity was 1.4 +/‐ 1.5 mV/nC with a maximum of 5.1 mV/nC. Depolarizing responses to L‐glutamate reversed in polarity at membrane potentials between 0 and ‐20 mV, were accompanied by a decrease in membrane slope resistance, and were suppressed by replacement of extracellular sodium ions with choline. These results demonstrate that chemosensitivity of retinal horizontal cells to acidic amino acids persists after dissociation protocols, and in several respects resembles that found in horizontal cells in situ. These findings are consistent with the notion that retinal horizontal cells receive a synaptic input involving L‐glutamate or a similar substance.
Relationship between the three‐hour‐period sleep‐wakefulness cycle and growth hormone secretion in the immature rat.
Authors: Kawakami M , Kimura F , Tsai C W
Published: December 2014

The temporal pattern of growth hormone (GH) secretion throughout a day and its correlation with the sleep‐wakefulness cycle in the 29‐31‐day‐old female rat were studied by serial blood sampling through an intracardiac cannula at 10‐min intervals. Electroencephalograms (e.e.g.s) recorded continuously during blood sampling periods were scored into wakefulness and sleep, and the amount of sleep for every 10 min was plotted against the GH value as assessed by radio‐immunoassay. B analysis of the power spectrum using the least‐squares method, the time series of GH concentration was found to have a periodicity of approximately 3.0 h in any of the 6‐h periods sampled, beginning at 12.00, 18.00, 00.00 and 06.00 h, and in either sex. The peak time which was estimated for the time series of GH concentrations was found to occur consistently around 02.00‐03.00, 05.00‐06.00, 08.00‐09.00, 11.00‐12.00, 14.00‐15.00, 17.00‐18.00, 20.00‐21.00 and 23.00‐24.00 h in either the male or the female rat. The cross‐correlation analysis performed between the time series of the amount of sleep and the GH concentration, which were obtained for the 6‐h period from 12.00 to 18.00 h, revealed a significant positive correlation between the GH level and the amount of sleep during the preceding 10 min. The time series of the amount of sleep over a 24‐h period from the data obtained in the continuous recording of e.e.g.s from 27 to 31 days of age revealed an ultradian rhythm with a periodicity of approximately 3.0 h. These findings indicate that the rat GH secretory rhythm with a 3.0‐h periodicity develops by 30 days of age in both sexes, relating to the 3.0‐h‐period ultradian rhythm of the sleep‐wakefulness cycle entrained by the light cycle.
Oxygen and coronary vascular resistance during autoregulation and metabolic vasodilation in the dog.
Authors: Drake-Holland A J , Laird J D , Noble M I , Spaan J A , Vergroesen I
Published: December 2014

The hypothesis that tissue oxygen tension controls coronary vascular resistance during changes in perfusion pressure and oxygen consumption was expressed in a simplified mathematical form capable of making quantitative predictions. The predictive value of this formulation of the hypothesis was tested in experiments on anaesthetized mongrel dogs subjected to constant‐pressure perfusion of the left main coronary artery, with measurements of coronary blood flow and arterio‐venous oxygen content differences. Coronary venous oxygen content was used as an index of tissue oxygenation. The responses of coronary blood flow and arterio‐venous oxygen content difference, made over a range of perfusion pressures (which caused autoregulation) and heart rates (which caused metabolic regulation) were predicted qualitatively by the model. Coronary vascular conductance was positively related to metabolic rate only during metabolic regulation (heart rate changes); during autoregulation the relationship between these two variables was inverse. Coronary vascular conductance and resistance values taken from both interventions (both perfusion pressure and heart rate variations) were closely related to coronary venous oxygen content and calculated PO2. These findings suggest that further examination of oxygen tension, as the controller of the coronary vascular bed under physiological conditions should be considered.
The role of cyclic nucleotides and calcium in the mediation of the modulatory effects of octopamine on locust skeletal muscle.
Authors: Evans P D
Published: December 2014

The role of cyclic AMP and calcium in the mediation of the effects of octopamine has been investigated in the extensor tibiae muscle of the hind leg of the locust. Elevation of cyclic AMP levels in the preparation by means of the phosphodiesterase inhibitor, 3‐isobutyl‐1‐methylxanthine (IBMX), by means of the diterpene adenylate cyclase activator, forskolin, and by means of cyclic nucleotide analogues mimics the post‐synaptic effects of octopamine application at different frequencies of neuronal stimulation. These conditions also mimic the presynaptic effects of octopamine on spontaneous release of transmitter from the slow motoneurone. The effects of octopamine on the preparation are calcium sensitive, with the maximal sensitivity occurring between 0.5 and 4.0 mM‐external calcium. The results are discussed in terms of the role of cyclic AMP and calcium in the mediation of the effects of octopamine.
Characterization of the pace‐maker current kinetics in calf Purkinje fibres.
Authors: DiFrancesco D
Published: December 2014

Kinetics of the cardiac pace‐maker current (if) were studied using high K+, low Na+ solutions under conditions where the current time course could be dissected from other components. Activation of if during relatively large negative pulses is S‐shaped, and is approximated by an exponential function of time to the third power. Less‐pronounced S‐shaped activation occurs at potentials close to the middle of the activation curve (near ‐70/‐80 mV). Here, allowing for the presence of a very slow component, the power required to fit the current activation approaches 1. The comparison between current activation and deactivation at the same potentials shows that although deactivation can be approximated by a single exponential, the two processes have a quite different time dependence, and this difference depends on the membrane potential. This behaviour is not compatible with Hodgkin‐Huxley kinetics. While near the half‐activation range the current decays with an apparently single exponential time course, at more positive potentials the current deactivation becomes sigmoidal. At least the third power of an exponential is required to fit its time course at potentials positive to about ‐40 mV. These data imply that both open and closed states correspond to several distinct channel configurations. The 'delay' in the current onset during a hyperpolarization is decreased by applying large, short hyperpolarizations before activation. Suitable pre‐pulse durations and/or amplitudes can reduce the subsequent current activation to a single exponential. Records with and without a pre‐pulse do not always superimpose. After the activation 'delay' has been removed by a suitable hyperpolarization preceding an activating pulse, the time course of its recovery can be studied by applying depolarizations of given amplitude and variable duration. The time course of the delay recovery does not seem to be linked to the time course of current deactivation recorded at the same voltage. Reduction of the activation 'delay' by conditioning pre‐hyperpolarizations does not affect current decay during a subsequent depolarizing pulse. The current decay appears to depend only on the current amplitude reached before a deactivating pulse is applied. This, and the evidence in the preceding paragraph, suggest that the delay recovery and the current deactivation are independent processes. A reaction scheme is proposed, which has been developed on the basis of the experimentally determined kinetic properties of if. The channel model is composed of five gating subunits of three different types, not all independent in their movements.(ABSTRACT TRUNCATED AT 400 WORDS)
Active sodium transport and fluid secretion in the gall‐bladder epithelium of Necturus.
Authors: Giraldez F
Published: December 2014

Intracellular Na, K and Cl activities (acNa, acK and acCl) and membrane potentials were measured in Necturus gall‐bladder epithelium using double‐barrelled ion‐sensitive micro‐electrodes. Mucosal membrane potential was about ‐55 mV and the mean control activities were acNa = 14.7 mM, acK = 91.6 mM and acCl = 20.3 mM. Replacing mucosal Na by K caused a fall in acNa that followed an exponential time course. The rate of change in acNa was linearly related to acNa above a certain value (congruent to 3 mM). acK and acCl both increased in K Ringer solution. From the change in all three ions the cell was estimated to swell at an initial rate of 0.13% s‐1. From the initial rate of change in acNa, a net cell efflux of Na of 405 pmol cm‐2 s‐1 was calculated. Replacement of Na by Tris or choline led to a similar result. The transepithelial Na transport rate was for this group of animals 346 pmol cm‐2 s‐1. Ouabain (10(‐3) M) produced an increase in acNa and acCl, whereas acK decreased. The cells were estimated to swell at an initial rate of 0.06% s‐1. The initial Na influx after Na‐pump inhibition was calculated to be 162 pmol cm‐2 s‐1. The parallel measure of the transepithelial rate of transport of Na gave a value of 189 pmol cm‐2 s‐1. Ouabain inhibited the decrease in acNa after replacement of Na by K by about 80%. A fast depolarization, ranging from 2 to 7 mV, occurred after the perfusion with ouabain. Em then slowly decreased from about 53 to 32 mV in 1 h. It is concluded that (a) the major fraction of the transepithelial transport of Na is transcellular and mediated by the Na pump, (b) the pumping rate is linearly dependent on internal Na within a certain range and (c) the Na pump is electrogenic under normal circumstances.
Increased or decreased thirst caused by inhibition of angiotensin‐converting enzyme in the rat.
Authors: Evered M D , Robinson M M
Published: December 2014

We have investigated the effects on water intake of subcutaneous (S.C.) injections of low (0.5 mg/kg) and high (100 mg/kg) doses of captopril, an inhibitor of angiotensin‐converting enzyme (CE). Low doses block the synthesis of angiotensin II only in the circulation whereas high doses block CE in both the blood and the brain. The low dose of captopril enhanced drinking in response to three hypotensive drugs, isoprenaline (0.1 mg/kg, S.C.), phentolamine (5 mg/kg, S.C.) and serotonin (2 mg/kg, S.C.), whereas the high dose of captopril abolished drinking in response to these stimuli. The low dose of captopril also enhanced drinking in response to histamine (0.25‐5.0 mg/kg, intraperitoneal, I.P.), but in this case the high dose of captopril only partially reduced the drinking response. The low dose of captopril enhanced drinking after 24 h water deprivation but high doses had no significant effect on deprivation‐induced thirst. Hypovolaemia was produced either by injecting polyethylene glycol (30% w/v, 10 ml/kg) S.C. or by replenishing the cellular deficit in water‐deprived rats with 10 ml water (by gavage). The low dose of captopril enhanced the drinking response to hypovolaemia but the high dose had no significant effect. Neither the high nor the low dose of captopril significantly affected drinking in response to cellular dehydration caused by injecting 2 M‐NaCl (2 ml) I.P. or by replenishing the extracellular deficit in water‐deprived rats (10 ml balanced salt solution by gavage). Nephrectomy (but not ligation of the ureters) or injections of propranolol (5 mg/kg, S.C.) to prevent renin secretion prevented the enhancement of deprivation‐or serotonin‐induced thirst by the low dose of captopril. The low dose of captopril did not enhance drinking in response to I.V. injections of renin (1 Goldblatt unit), or intracerebroventricular (I.C.V.) injections of angiotensin I or II. The high dose of captopril blocked drinking in response to I.V. injections of renin or I.C.V. injections of angiotensin I but did not reduce drinking in response to angiotensin II, I.C.V. These results are consistent with the hypothesis that blocking CE only in the circulation enhances drinking in response to hypotension or hypovolaemia because angiotensin I, accumulating in high concentration in the blood, enters the brain and is converted intracerebrally to angiotensin II. These findings suggest that the enhancement of drinking caused by low doses of captopril s.c. is a sensitive indicator of whether the renin‐ angiotensin system participates at all in the regulatory response to a particular stimulus to drink.(ABSTRACT TRUNCATED AT 400 WORDS)
Differential effects of temperature on three components of passive permeability to potassium in rodent red cells.
Authors: Hall A C , Willis J S
Published: December 2014

The effect of temperature on ouabain‐insensitive fluxes of K+ was characterized in red cells from a non‐hibernator (guinea‐pig) and a hibernator (thirteen‐lined ground squirrel). The residual K+ influx which remains in the presence of ouabain and bumetanide, and which is linearly dependent on [K+]o was the same in the erythrocytes of the two species at low temperature (5 degrees C). At 5 degrees C co‐transport of K+ was abolished in guinea‐pig red cells but was still present in ground squirrel red cells. In guinea‐pig cells, ouabain‐and‐bumetanide‐insensitive K+ flux was increased by Ca2+ at low temperatures. This flux was inhibited by quinine and selective for K+ over Na+, indicating activation of the Ca2+‐sensitive K+ pathway (Gárdos channel). Ouabain‐and‐bumetanide‐insensitive K+ permeability in red cells from the ground squirrel was insensitive to Ca2+ added to the medium at low temperature. When ground squirrel red cells were depleted of ATP or treated with A23187, Ca2+ induced a flux which was inhibitable by quinine. Hence, ground squirrel red cells possess Gárdos channels. The temperature sensitivity of the K+ channels was assessed using A23187‐mediated K+ influx as a measure of Gárdos channel activation. The influence of temperature on the Ca2+‐stimulated K+ fluxes under these conditions was indistinguishable between the two species. It is concluded that K+ loss through the Ca2+‐sensitive K+ channel is minimal in hibernators' erythrocytes because of more efficient regulation of cytoplasmic Ca2+ during cold storage.
Post‐natal development of ganglia in the lower lumbar sympathetic chain of the rat.
Authors: Hirst G D , McLachlan E M
Published: December 2014

The initial stages in the development of functional synapses have been examined in ganglia of the lower lumbar sympathetic chain of the rat using intracellular recording techniques. In animals of age up to 7 days post‐natal, many impaled cells were inexcitable and possessed no synaptic input. The proportion of excitable cells impaled increased with the age of the animal. Two types of action potential could be identified. Initially the synaptic input consisted of one or a few subthreshold synaptic potentials. The number of preganglionic inputs to each cell increased over the first 1‐2 weeks after birth. The quantal content of each input was initially very low. At least some inputs showed an increase in quantal content during development; eventually one or occasionally two inputs became suprathreshold. Voltage‐clamp studies indicated that the time course of excitatory synaptic currents did not change during development. The amplitudes of miniature excitatory synaptic currents in animals aged less than 10 days were some three to five times the size of those recorded from mature animals.
Corticomotoneuronal cells contribute to long‐latency stretch reflexes in the rhesus monkey.
Authors: Cheney P D , Fetz E E
Published: December 2014

To test the hypothesis that a transcortical reflex contributes to the stretch‐evoked long‐latency electromyographic (e.m.g.) response we documented the responses of identified corticomotoneuronal (c.m.) cells and their target muscles to perturbations of active wrist movements. Macaque monkeys performed ramp‐and‐hold wrist movements against elastic loads, alternating between flexion and extension zones; brief (25 ms) torque pulses were intermittently applied during the hold period. C.m. cells were identified by a clear post‐spike facilitation in spike‐triggered averages of forelimb muscle e.m.g. activity. Activity of c.m. cells and twelve wrist and digit flexor and extensor muscles was recorded during: (a) active ramp‐and‐hold wrist movements, (b) passive ramp‐and‐hold wrist movements, and (c) torque perturbations applied during the hold phase of active flexion and extension which either lengthened or shortened the c.m. cell's target muscles. Muscle‐lengthening perturbations evoked a reproducible pattern of average e.m.g. activity in the stretched muscles, consisting of two peaks: the first response (M1) had an onset latency of 11.2 +/‐ 2.1 ms (mean +/‐ S.D.), and the second (M2) began at 27.9 +/‐ 5.1 ms. Torque perturbations which shortened the active muscles also evoked a characteristic e.m.g. response consisting of an initial cessation of activity at 13.5 +/‐ 3.4 ms followed by a peak beginning at 33.9 +/‐ 3.0 ms. The responses of twenty‐one c.m. cells which facilitated wrist muscles were documented with torque pulse perturbations applied during active muscle contraction. Twenty of twenty‐one c.m. cells responded at short latency (23.4 +/‐ 8.8 ms) to torque perturbations which stretched their target muscles. For each c.m. cell‐target muscle pair, transcortical loop time was calculated as the sum of the onset latency of the c.m. cell's response to lengthening perturbations (afferent time) and the onset latency of post‐spike facilitation (efferent time). The mean transcortical loop time was 30.4 +/‐ 10.2 ms, comparable to the mean onset latency of the M2 peak (27.9 +/‐ 5.1). The duration of a c.m. cell's response to torque perturbations provides a further measure of the extent of its potential contribution to the M2 muscle response. In all cases but two, the c.m. cell response, delayed by the latency of the post‐spike facilitation, overlapped the M2 e.m.g. peak.
Relation between structural and release parameters at the frog sensory‐motor synapse.
Authors: Grantyn R , Shapovalov A I , Shiriaev B I
Published: December 2014

The sensory‐motor synaptic connexions in the frog lumbar cord have been used to examine the relationship between the statistical characteristics of the unitary excitatory post‐synaptic potential (e.p.s.p.) and the number and organization of synaptic contacts determined when the primary afferent fibre used in evoking the e.p.s.p., and a motoneurone in which it was recorded, were both labelled with horseradish peroxidase (HRP). A significant correlation is found between the number of contacting boutons and the amplitude of the chemical component of the unitary e.p.s.p.s generated at the same connexions. The amplitude fluctuation patterns of the single‐fibre e.p.s.p.s could be fitted by both Poisson and binomial distribution. The number of presumed Poisson release sites as estimated from the ratio Vmax/v (where Vmax is the maximal amplitude of the chemical component of e.p.s.p. and v is quantal size) is always less than or equal to the total number of boutons observed histologically. In three connexions there was a close correspondence between the number of binomial release units, n, and the number of contact regions formed by the tight clusters of contacting boutons. The unit potential amplitude estimated from the Poisson distribution is found to be two to three times smaller than the quantal size calculated from binomial distribution. A similar numerical relationship was found between the number of contacting boutons and the number of contact regions. It is suggested that at a single bouton, transmission results in release of a single quantum of transmitter, whereas the binomial quantum probably reflects the multi‐quantal release occurring simultaneously at boutons comprising a contact region. A significant correlation is found between the mean quantum content estimated either from Poisson or binomial distribution and the number of contacting boutons and contact regions respectively, indicating the dependence of quantal release on the magnitude of synaptic surface. No correlation is found between the motoneuronal soma diameter and the quantal size, although the former is significantly correlated with the number of contacting boutons.
On re‐excitation of feline motoneurones: its mechanism and consequences.
Authors: Gogan P , Gustafsson B , Jankowska E , Tyc-Dumont S
Published: December 2014

Conditions required for re‐excitation of lumbosacral motoneurones, i.e. for double impulses in the motor axons associated with a single soma‐dendritic action potential, were examined in cats anaesthetized with pentobarbitone and paralysed with gallamine triethiodide. Simultaneous recording from a motoneurone (intracellular, and in some experiments also extracellular), and from its axon in a ventral root, was used to assess the relations between the soma and the double axonal action potentials. Action potentials (greater than 70 mV) evoked by brief depolarizing current pulses applied intracellularly were never observed to cause re‐excitation. Re‐excitation could, however, be regularly induced by procedures which increased the delay between the initial segment and soma‐dendritic components of these potentials. Re‐excitation could be evoked (i) when brief hyperpolarizing pulses were applied before the onset of the soma‐dendritic spikes, (ii) when the depolarizing pulses were applied on a background of long hyperpolarizing pulses or (iii) when two action potentials were evoked in a quick succession (by two brief depolarizing pulses). No relationship was found between the presence of re‐excitation of motor axons and the presence of the delayed depolarization which follows the soma‐dendritic spikes. Neither re‐excitation nor delayed depolarization were found to be dependent upon re‐excitation of the initial segment. These observations are thus at variance with previous suggestions that the initial segment spikes induce the re‐excitation of motor axons and that the initial segment spikes cause the delayed depolarization following soma‐dendritic spikes. Since re‐excitation of a motor axon occurred without any signs of a second initial segment spike, it is concluded that it is initiated at the level of the axon, most likely at the first node of Ranvier. Re‐excitation of motor axons was also observed during repetitive firing induced by intracellular current injection. However, it occurred then only occasionally, and only under strong depolarizing drive. It is thus not expected to be a common phenomenon under natural conditions of repetitive firing.
Water flow across the walls of single muscle capillaries in the frog, Rana pipiens.
Authors: Curry F E , Frøkjaer-Jensen J
Published: December 2014

Individual capillaries of the transilluminated frog muscle cutaneous pectoris were perfused with suspensions of human red cells in frog Ringer solution containing 1 g/dl bovine serum albumin. The modified Landis technique (Michel, Mason, Curry & Tooke, 1974) was used to measure hydraulic conductivities of the capillary wall. Sucrose osmotic reflexion coefficients of the capillary wall were measured in four capillaries when the superfusate contained 100 mM‐sucrose. All experiments were made at 22‐24 degrees C. The hydraulic conductivity of arterial capillaries varied from 0.3 to 1.26 X 10(‐7) cm/(s cmH2O) with a mean of 0.79 X 10(‐7) cm/(s cmH2O) (six capillaries). The hydraulic conductivities of mid‐capillaries varied from 0.43 to 1.86 X 10(‐7) cm/(s cmH2O) with a mean value of 0.72 X 10(‐7) cm/(s cmH2O) (six capillaries). The mean reflexion coefficient to sucrose was 0.12 +/‐ 0.05 (S.D.). The measured reflexion coefficients to sucrose conform to the hypothesis that 90% of the transcapillary water flow crosses the capillary wall via the principal hydrophilic pathway. The remaining 10% crosses via an exclusive water pathway. The distribution of water flow is similar to that previously described in frog mesenteric capillaries. The mean value of the hydraulic conductivity of frog muscle capillaries is about one‐seventh the mean value of the hydraulic conductivity of frog mesenteric capillaries measured at the same temperature. The result conforms to the hypothesis that only a small fraction (mean 10%) of the area of junctional contact between adjacent endothelial cells is available for water and solute exchange in frog muscle capillaries. The hydraulic and diffusional conductances per unit length of open junction appear to be very similar when muscle capillaries are compared to mesenteric capillaries in the frog. Our results lead us to speculate that structures within the intercellular junctions determine the extent of open junction and may modulate the hydraulic conductivity of both the principal water pathway and the exclusive water pathway.
Regulation of bicarbonate transport across the brush border membrane of the bull‐frog choroid plexus.
Authors: Saito Y , Wright E M
Published: December 2014

Our previous study of the choroid plexus showed that elevation of cellular cyclic AMP stimulated HCO3 secretion into the cerebrospinal fluid (c.s.f.). To explore the mechanism of this stimulation, we have used micro‐electrodes to observe the effect of phosphodiesterase inhibitors on membrane potentials, resistances and electromotive forces (e.m.f.) in the bull‐frog plexus. The potential profile under control conditions was ‐45 mV across the apical membrane (Vvc) and ‐9 mV across the epithelium (Vvs) with respect to the c.s.f. Two‐dimensional cable analysis indicated that 70% of adjacent epithelial cells were electrically uncoupled, and that the coupling coefficient for the remaining cells was only 0.12. The results of circuit analysis gave values for membrane resistance and e.m.f. across the apical membrane of 200 omega cm2 and ‐135 mV, across the basolateral membrane of 386 omega cm2 and ‐138 mV, and across the paracellular shunt of 20 omega cm2 (the shunt e.m.f. was assumed to be negligible). Addition of phosphodiesterase inhibitors (10 mM‐theophylline or 1 mM‐3‐isobutyl‐1‐methylxanthine (IBMX) ) depolarized Vvc by 18 mV and Vvs by 2 mV. Circuit analysis showed that the inhibitor reduced the apical membrane resistance by more than 60% and depolarized the apical e.m.f. by 70 mV without affecting the basolateral membrane or the shunt parameters. In Cl‐free solutions IBMX depolarized Vvc and decreased the apical membrane resistance similar to that observed in regular buffer solution. However, in HCO3‐free buffer solutions, the effects of IBMX on Vvc and membrane resistances were insignificant. In thirty‐five cells in sixteen tissues a linear relationship was observed between the magnitude of the spontaneous membrane potential (Vvc) and the magnitude of IBMX‐induced depolarization (delta VIBMXvc): delta VIBMXvc = ‐0.8 Vvc ‐15 (in mV). This suggests that HCO3 is accumulated within the epithelium above electrochemical equilibrium. We conclude that cyclic AMP increases HCO3 secretion across the choroid plexus by increasing the apical membrane HCO3 conductance.
Changes in the electrical activity of dog cardiac Purkinje fibres at high heart rates.
Authors: Boyett M R , Fedida D
Published: December 2014

Rate‐dependent changes in the electrical activity of dog Purkinje fibres have been studied. At high rates of stimulation the rate of repolarization is greater, the action potential is shorter, the maximum diastolic potential is increased, the pace‐maker potential is reduced in amplitude, and on cessation of rapid stimulation there can be a suppression of spontaneous activity. After an increase of the stimulus frequency there is an abrupt shortening of the action potential, which can be attributed to incomplete recovery of the plateau currents; this is followed by a progressive decline in action potential duration over the next several hundred seconds. The factor responsible for the slow changes in duration could also be responsible for the accompanying increase in maximum diastolic potential because this develops along a similar time course. These slow changes in electrical activity have been investigated with the phase‐plane technique. They are the result of an increase in the net outward current over a wide range of potentials (approximately ‐10 to approximately ‐90 mV) during the repolarization phase of the action potential. In voltage‐clamp experiments background current has been observed to be strongly rate dependent: the background current during a test voltage‐clamp pulse after a train of action potentials is more outward at higher stimulus frequencies. When the frequency is increased, background current slowly becomes more outward over several hundred seconds, and this change therefore occurs along the appropriate time course to explain the slow alteration in electrical activity under these conditions. The extra outward background current at high rates is relatively independent of membrane potential in the range from ‐110 to ‐40 mV (more circumstantial evidence indicates that this range may extend to at least +10 mV); this potential dependence is similar to that of the Na‐K‐pump current (Eisner & Lederer, 1980). Strophanthidin and ouabain, agents known to block the Na‐K pump, alter both the changes in background current and the slow rate‐dependent changes in electrical activity. Although after an increase in rate there is a gradual change in background current that can be explained by an increase in electrogenic Na‐K‐pump activity, the initial effect of switching rate is to produce a change in current that is consistent with an increase of the extracellular K concentration. A transient increase in the K concentration of restricted extracellular clefts has been recorded under these conditions in dog Purkinje strands by Kline & Kupersmith (1982) using K‐sensitive microelectrodes. The effect on electrical activity of these changes is discussed.(ABSTRACT TRUNCATED AT 400 WORDS)