bluuebunny/crossref_metadata_2025 huggingface dataset:
Localization of cortical activity associated with visual recognition in humans.
Authors: Srebro R
Published: December 2014

The Laplacian analysis described previously is used to localize cortical activity subserving visual object recognition in humans. In the first of two experiments, subjects are shown pictures of a human face corrupted by varying amounts of noise. After each picture has been presented for 34 ms against a large uniformly illuminated background, the subject is required to report whether or not he saw the face, by pressing a button. The Laplacian response associated with the report that the face is seen differs from that associated with the report that the face is not seen. The difference between these two Laplacian responses has a simple wave form with peak activity at approximately 206 ms after stimulus onset and approximately 196 ms before median reaction time for the button‐press report. Its amplitude and polarity, which vary with centre‐electrode location over the posterior scalp, are used to construct a map showing the location of cortical activity subserving recognition of the face. This cortical activity localizes to both temporal lobes with some degree of right hemispheric lateralization in right‐handed subjects. In the second of the two experiments, subjects are shown the silhouette of a simple shape, such as a triangle, embedded in a large random dot field. Each silhouette is presented for 17 ms. The visibility of the shape is made to vary from trial to trial and the subject is required to report for each trial whether or not the shape is seen. The Laplacian response associated with the report that no shape is seen is very much smaller than that correctly identifying the shape. The difference between these two Laplacian responses has a simple wave form with peak activity at approximately 207 ms after stimulus onset. Its wave form is essentially the same as that associated with face recognition. Its amplitude and polarity, which vary with centre‐electrode location over the posterior scalp, are used to construct a map showing the location of cortical activity subserving recognition of the simple shape. This cortical activity localizes to both temporal lobes with strong right hemispheric lateralization in right‐handed subjects. The general topography of this activity is similar to that subserving face recognition. Although generally similar, there are measurable differences between the topographies of right temporal lobe activity associated with face recognition and that associated with simple shape recognition.(ABSTRACT TRUNCATED AT 400 WORDS)
Post‐synaptic activity evoked in the nucleus tractus solitarius by carotid sinus and aortic nerve afferents in the cat.
Authors: Donoghue S , Felder R B , Gilbey M P , Jordan D , Spyer K M
Published: December 2014

Post‐synaptic responses evoked in neurones of the nucleus tractus solitarius by electrical stimulation of the carotid sinus, aortic and vagal nerves, alone or in combination, have been studied in anaesthetized cats using both extracellular and intracellular recording techniques. A total of 292 neurones received an input from at least one of the three nerves tested. The activity of the large majority of these cells (249) could only be shown to be altered by stimulation of one of these nerves and in 222 of these cases this was an excitatory response. These responses showed the expected post‐synaptic characteristics including temporal summation and, in intracellular records, a summation of evoked excitatory post‐synaptic potentials (e.p.s.p.s). The minimum latency to onset of these responses was variable, both for individual cells and for the population as a whole and varied within the range 2‐124 ms. In a small number of cells (twenty‐seven), the input was purely inhibitory in nature. In neurones showing a tonic discharge this produced a decrease in the rate of firing. This influence was most marked in intracellular records where membrane hyperpolarizations were noted. Again, the latency to onset was variable, in the range 4‐27 ms. Convergent inputs from two or more of the nerves were identified in forty‐three neurones. The effects of these were always excitatory. They could be observed both as a facilitation of spike activity recorded extracellularly and as summation of subliminally evoked e.p.s.p.s recorded intracellularly. On the basis of threshold voltages and latency to onset, the afferents to these neurones are indistinguishable from those providing an exclusive input. It can be concluded that at least some of the neurones in the nucleus tractus solitarius and its vicinity receive inputs from more than one source. The implications of these observations on the role of this brain‐stem area in cardiorespiratory reflexes is discussed.
Dual effects of internal n‐alkyltrimethylammonium ions on the sodium current of the squid giant axon.
Authors: Elliott J R , Haydon D A , Hendry B M
Published: December 2014

The actions of members of the homologous series of alkyl cations CH3 (CH2)n‐1 N+ (CH3)3 (Cn TMA) on the sodium current in giant axons of Loligo forbesi have been investigated. The substances tested correspond to n = 6, 8, 10, 12, 14 and 16. These cations only produced significant sodium current suppression when applied inside the axon. Actions on first‐pulse sodium currents and use‐dependent effects were separately studied. The shorter members of the series (C6TMA and C8TMA) produced suppression of first‐pulse sodium currents without causing significant use dependence. The first‐pulse suppression arose partly from a positive shift along the voltage axis of the steady‐state activation parameter (m infinity) and partly from a reduction in the maximum sodium conductance (gNa). C12TMA and C14TMA produced little first‐pulse suppression but caused clear use dependence. C10TMA showed intermediate properties while C16TMA was inactive. The use‐dependent actions have been quantitatively investigated using a double‐pulse protocol. The results are consistent with a model in which the cations enter a blocking site on the ion‐channel via the intra‐axonal aqueous phase. The cations appear able to bind to inactivated sodium channels at significant rates. The possible molecular locations of the sites responsible for m infinity shifts and use dependence are discussed. It is argued that the existence of two separate sites may help to explain certain distinctions between the actions of neutral general anaesthetics and clinical local anaesthetics on the sodium channel.
Calcium channels and intracellular calcium release are pharmacologically different in frog skeletal muscle.
Authors: McCleskey E W
Published: December 2014

The pharmacology of Ca2+ channels and intracellular Ca2+ release from the sarcoplasmic reticulum (s.r.) were compared by injecting Ca2+ channel blockers into the cytoplasm and observing contraction under voltage clamp of frog skeletal muscle fibres, a preparation that contracts only in response to Ca2+ release from the s.r. A method for quantifying intracellular injections by co‐injecting a fluorescent dye is described. Nifedipine injected into cells blocks Ca2+ current through the cell membrane showing that nifedipine is active when applied to the cytoplasmic side of the membrane in which Ca2+ channels are located. Neither the presence of Ca2+ channel blockers in the extracellular medium nor 24 h incubation in nifedipine and D‐600 affect contraction. Nifedipine and D‐600 injected to intracellular concentrations much greater than necessary to block Ca2+ channels do not affect contraction. The presence of 30 microM‐D‐600 during K+ contractures caused paralysis but 20 microM‐nifedipine did not. Thus, contracture‐dependent D‐600 paralysis is not due to blockade of the transverse tubule Ca2+ channel. It is concluded that: (a) a functioning Ca2+ channel on the cell membrane is not necessary to trigger Ca2+ release from the s.r.; (b) s.r. Ca2+ release and Ca2+ channels are pharmacologically different.
The calcium current in a myenteric neurone of the guinea‐pig ileum.
Authors: Hirst G D , Johnson S M , van Helden D F
Published: December 2014

The active and passive electrical properties of the after‐hyperpolarizing (AH) cell of the guinea‐pig myenteric plexus were analysed using a single‐electrode voltage or current clamp. Action potentials were compared under normal conditions, in the presence of tetrodotoxin (TTX) and in the presence of both TTX and tetraethylammonium chloride (TEA). Calcium action potentials were studied by examining their calcium dependence, the actions of manganese and the effect of substituting barium for calcium. The maximum rate of rise of the action potential did not increase in calcium concentrations above 10 mM. The half‐saturation concentration was 2 mM‐calcium. AH cells exhibited five predominant currents consisting of an inward sodium current, an inward calcium current and three outward currents. There was a transient outward current which was inactivated at holding potentials more positive than ‐65 mV and was suppressed by 4‐aminopyridine and barium but not by external TEA. A second outward current observed in the presence of 10 mM‐external TEA had properties consistent with that of the delayed rectifier (Hodgkin & Huxley, 1952). A third outward current was the calcium‐dependent slow after‐hyperpolarizing current (Hirst, Johnson & van Helden, 1985). The voltage dependence, the action of calcium antagonists, the effect of barium substitution and the temporal characteristics of calcium currents were studied. The peak calcium current density was in excess of 100 microA/cm2 in 2.5 mM‐calcium solution at 35 degrees C for depolarizations to ‐10 mV. Calcium currents showed at least two phases of inactivation. Both calcium and barium currents showed early inactivation with decay occurring over the first 10‐40 ms. The calcium‐activated current precluded direct measurement of slow inactivation of the calcium current. Barium currents studied over the first 100‐150 ms had a very slow inactivating component.
The slow calcium‐dependent potassium current in a myenteric neurone of the guinea‐pig ileum.
Authors: Hirst G D , Johnson S M , van Helden D F
Published: December 2014

Experiments were performed in current‐clamped and voltage‐clamped after‐hyperpolarizing (AH) neurones of the guinea‐pig myenteric plexus to examine the properties of the potassium conductance (gK, Ca) underlying the slow calcium‐activated after‐hyperpolarization (VK, Ca). The action potential plateau lengthened by the addition of tetraethylammonium chloride (TEA) to the bathing medium was compared to VK, Ca. Results were consistent with enhanced calcium entry causing an increase of VK, Ca. 4‐Aminopyridine (4‐AP) directly reduced VK, Ca. Voltage‐clamp data of gK, Ca were well fitted by a process with a delay (approximately equal to 60 ms) followed by exponential activation (time constant approximately equal to 300 ms) and inactivation (time constant approximately equal to 2 s). The presence of a small, much slower inactivating process was noted. Values for time constants were similar to those reported by Morita, North & Tokimasa (1982) and North & Tokimasa (1983) where gK, Ca was measured during VK, Ca subsequent to action potential stimulation. The relation between gK, Ca (or the calcium‐activated potassium current IK, Ca) and estimated calcium influx resulting from short‐duration calcium currents elicited at various voltages was compared. Both the integral of the calcium current and gK, Ca showed a similar dependence on the depolarizations used to elicit IK, Ca except there was a positive shift of about 4 mV for the gK, Ca curve. This shift was attributed to a requirement for calcium ions to prime the gK, Ca mechanism. An inward ion charge movement of about 8 pC was required before significant activation of gK, Ca occurred. After the 'priming' condition had been established, the sensitivity of gK, Ca to inward calcium current measured at the resting potential was about 500 pS/pC of inward charge. Large calcium entry obtained by prolonged calcium currents caused saturation of the peak amplitude of IK, Ca and initiated currents with slower time to peak amplitude and longer duration. Increasing the calcium concentration of the external solution provided proportionally larger IK, Ca currents before saturation. The saturation amplitude of IK, Ca (namely gK, Ca) was relatively unaffected.
Potassium channels in isolated presynaptic nerve terminals from rat brain.
Authors: Bartschat D K , Blaustein M P
Published: December 2014

86Rb efflux from pinched‐off rat brain presynaptic nerve terminals (synaptosomes) was used to measure the K permeability of the terminals. Synaptosomes were pre‐loaded with 86Rb and the suspensions were then filtered on glass fibre filters. The terminals trapped on the filters were superfused with 'efflux solutions', and the effluent and filters were then counted. 86Rb efflux into physiological saline (PSS) containing 5 mM‐K and 145 mM‐Na was about 0.4% of the 86Rb load per second (component 'R'). Increasing extracellular K concentration [( K]o), or adding veratridine and sea anemone toxin, stimulated efflux; presumably by depolarizing the nerve terminals. The K‐stimulated 86Rb efflux was a graded function of [K]o. High [K]o evoked at least three components of efflux: a 'fast phase' (T) that apparently inactivated in less than 1 s, a 'slower phase' (S) that was linear for 3‐5 s, and a Ca‐dependent phase (C). Some, but not all, of the slow phase 86Rb efflux (component S) may be attributable to increased efflux mediated by the 'resting' K permeability mechanism when the driving force is increased by depolarization. K efflux was also studied and was found to be qualitatively similar to 86Rb efflux. 86Rb: 42K permeability ratios were 0.6‐0.8 for most components of the efflux. Raising the Mg concentration in the efflux solution shifted the 86Rb efflux versus [K]o curve in the direction of increased [K]o. This shift may be the result of screening of surface charges by Mg. Several agents that block various K channels in other preparations inhibited K‐stimulated 86Rb efflux in synaptosomes: tetraethylammonium (TEA), tetrabutylammonium (TBA), and 4‐aminopyridine (4‐AP). The fast component (T) of high [K]o‐stimulated 86Rb efflux was selectively blocked by low concentrations of 4‐AP (apparent half‐maximal inhibition, KI = 0.1‐0.2 mM); it was also blocked by TEA (KI = 0.6 mM) and TBA (KI = 0.8‐1.0 mM). Dose‐response curves for inhibition of component T by all three agents were monophasic. the slow component (S) of the K‐stimulated 86Rb efflux was much less sensitive to all three agents, than was component T; the broad dose‐response curves were consistent with the view that two (or more) different K conductances may contribute to component S.(ABSTRACT TRUNCATED AT 400 WORDS)
Calcium‐dependent inward current in Aplysia bursting pace‐maker neurones.
Authors: Kramer R H , Zucker R S
Published: December 2014

Depolarizing voltage‐clamp pulses elicit a triphasic series of tail currents (phase I, II and III) in Aplysia burst‐firing neurones L2‐L6. The sequence and time course of the tail currents resemble slow changes in membrane potential which follow bursts in the unclamped cell. The phase II tail current is an inward current with a time course similar to that of the depolarizing after‐potential (d.a.p.) which follows bursts in the unclamped cell. The phase II tail current is suppressed by depolarizing pulses which approach ECa, is blocked by Ca2+ current antagonists (Co2+ and Mn2+), and is blocked by intracellular injection of EGTA. The phase II tail current is not blocked by agents which block Na+‐dependent action potentials, the Na+‐Ca2+ exchange pump, or the Na+‐K+ exchange pump. The phase II tail current is not blocked by the elimination of large outward K+ currents which can lead to extracellular K+ accumulation. Thus, the phase II tail current is not generated by any of these processes. The phase II tail current is reduced by about 60% following substitution of tetramethylammonium (TMA+) for external Na+, but is unaffected by reducing external Cl‐. The phase II tail current is distinct from a persistent inward Ca2+ current which underlies the negative resistance region of the steady‐state current‐‐voltage relation of bursting cells. The persistent inward current is only slightly reduced by TMA+ substitution for Na+, and is enhanced by EGTA injection. Injection of Ca2+ into Aplysia bursting cells elicits a biphasic (inward‐outward) current. The inward current can be observed in isolation after blocking the outward component (Ca2+‐activated K+ current) with 50 mM‐external tetraethylammonium. The Ca2+‐elicited inward current has a reversal potential near ‐22 mV, and is non‐selective for Na+, K+ and Ca2+. The reversal potential is unaffected by changes in Cl‐ and pH. The Ca2+‐ activated conductance is apparently voltage independent. We propose that the phase II tail current, and hence the d.a.p., is due to the Ca2+‐dependent activation of a voltage‐independent non‐specific cationic conductance. This conductance participates in generating the depolarizing phase of bursting pace‐maker activity.
Calcium‐induced inactivation of calcium current causes the inter‐burst hyperpolarization of Aplysia bursting neurones.
Authors: Kramer R H , Zucker R S
Published: December 2014

A triphasic series of tail currents which follow depolarizing voltage‐clamp pulses in Aplysia neurones L2‐L6 was described in the preceding paper (Kramer & Zucker, 1985). In this paper, we examine the nature of the late outward component of the tail current (phase III) which generates the inter‐burst hyperpolarization in unclamped cells. The phase III tail current does not reverse between ‐30 and ‐90 mV, and is relatively insensitive to the external K+ concentration. In contrast, Ca2+‐dependent K+ current (IK(Ca)), elicited by intracellular Ca2+ injection, reverses near ‐65 mV, and the reversal potential is sensitive to the external K+ concentration. Addition of 50 mM‐tetraethylammonium (TEA) to the bathing medium causes a small increase in the phase III tail current. In contrast, IK(Ca) is completely blocked by addition of 50 mM‐TEA. The phase III tail current is suppressed by depolarizing pulses which approach ECa, is blocked by Ca2+ current antagonists (Co2+ and Mn2+), and is blocked by intracellular injection of EGTA. The phase III tail current is reduced by less than 10% after complete removal of extracellular Na+. These bursting neurones have a voltage‐dependent Ca2+ conductance which exhibits steady‐state activation at a membrane potential similar to the average resting potential of the unclamped cell (i.e. ‐40 mV). The steady‐state Ca2+ conductance can be inactivated by Ca2+ injection, or by depolarizing pre‐pulses which generate a large influx of Ca2+. The steady‐state Ca2+ conductance has a voltage dependence similar to that of the phase III tail current. The Ca2+‐dependent inactivation of the steady‐state Ca2+ conductance occurs in parallel with the phase III tail current; both have a similar sensitivity to Ca2+ influx, and both processes decay with similar rates after a depolarizing pulse. Hence, we propose that the phase III tail current is due to the Ca2+‐ dependent inactivation of a steady‐state Ca2+ conductance. The decay of IK(Ca) following simulated spikes or bursts of spikes is rapid (less than 1 s) compared to the time course of the phase III tail current and the inter‐burst hyperpolarization (tens of seconds). Thus, we conclude that IK(Ca) does not have a major role in terminating bursts or generating the inter‐burst hyperpolarization in these cells. We present a qualitative model of the ionic basis of the bursting pace‐maker cycle. The central features of the model are the voltage‐dependent activation and the Ca2+‐dependent inactivation of a Ca2+ current.
Effect of ouabain on tone, membrane potential and sodium efflux compared with [3H]ouabain binding in rat resistance vessels.
Authors: Aalkjaer C , Mulvany M J
Published: December 2014

To investigate the mechanism by which ouabain causes acute increase in peripheral resistance, the effect of ouabain on vessel tone, 22Na efflux and membrane potential has been compared with the binding of [3H]ouabain in rat isolated mesenteric resistance vessels (lumen diameter approximately 200 microns). Ouabain at concentrations between 1 X 10(‐8) and 1 X 10(‐3) M had no effect on the tone of resting vessels but caused potentiation of the tone of vessels which were submaximally contracted with noradrenaline. In the entire concentration range, these acute potentiating effects of ouabain on vessel tone correlated well with an acute inhibitory effect on 22Na efflux and with acute [3H]ouabain binding, consistent with the vasoconstrictor effect of ouabain being associated with inhibition of the Na‐K pump. At all concentrations, in both resting and activated vessels, ouabain exposure caused an acute concentration‐dependent depolarization of the membrane. At low ouabain concentrations (1 X 10(‐6) and 1 X 10(‐5) M) the potentiating effect on vessel tone and the inhibitory effect on 22Na efflux were transient, so that after 10 min no effect of ouabain was seen. This was consistent with these ouabain concentrations failing to cause a measurable increase in the intracellular Na concentration ([Na]i) after longer term (up to 2 h) exposure. The recovery of 22Na efflux was due to a recovery of the ouabain‐sensitive part of the 22Na efflux, suggesting that the transitory nature of these effects is due to stimulation of uninhibited Na‐K pumps. The transient effects of low ouabain concentrations contrasted with binding experiments where, with 1 X 10(‐6) M‐ouabain, the binding first peaked after 30 min with only a small decline thereafter. With higher concentrations of ouabain (1 X 10(‐4) and 1 X 10(‐3) M), the potentiating effect was also transitory, but 22Na efflux was permanently inhibited and the [Na]i rose. The possibility of there being two populations of ouabain binding sites having different affinities, was supported by the observation of shoulders in the ouabain concentration‐effect characteristics obtained with respect to the mechanical potentiation of noradrenaline responses, the 22Na efflux and the acute ouabain binding. In all cases a shoulder was seen between 1 X 10(‐6) and 1 X 10(‐5) M‐ouabain. The results are consistent with the vasoconstrictor effect of ouabain being due to depolarization of the membrane as a consequence of inhibition of the Na‐K pump.
Acetylcholine receptors of skeletal muscle cells in cultures of rat thymus glands.
Authors: Dhillon D S , Harvey A L
Published: December 2014

Skeletal muscle fibres develop in cultures established from dissociated rat thymus glands. The properties of their acetylcholine receptors were compared with those on fibres in skeletal muscle cultures. Acetylcholine depolarized the thymus‐derived muscle cells in a concentration‐dependent manner. Under voltage clamp the reversal potential was determined to be ‐0.4 mV, which was not significantly different from the reversal potential of cells in the muscle cultures. In both types of cultures, sensitivity to ionophoretically applied acetylcholine decreased during the period when fibres were growing rapidly and then increased. The mean channel lifetime of acetylcholine‐activated channels was similar in both types of muscle fibre (3‐4 ms at ‐40 mV), but the single channel conductance was significantly higher in the thymus‐derived cells (70‐75 pS compared to 55‐60 pS). The cholinoceptors on both types of muscle fibre had nicotinic properties as judged by their preferential activation by acetylcholine rather than by acetyl‐beta‐methylcholine and oxotremorine and by the selective blockade by tubocurarine and erabutoxin b rather than by atropine.
A dopaminergic receptor modulates catecholamine release from the cat adrenal gland.
Authors: Artalejo A R , García A G , Montiel C , Sánchez-García P
Published: December 2014

Nicotine evokes the release of catecholamines from perfused cat adrenal glands in a concentration‐dependent manner, the median effective concentration for nicotine being 5 microM. Two 2 min pulses of 5 microM‐nicotine, 40 min apart (S1 and S2) gave net catecholamine outputs of 7.64 and 3.55 micrograms/8 min, respectively. The ratio S2/S1 in control glands was 0.5. Increasing concentrations of apomorphine (1‐10 microM) markedly inhibited catecholamine release during the second nicotine pulse (S2). At 1 microM‐apomorphine, the release during S2 was significantly reduced to 16% of S1; with 10 microM‐apomorphine, the secretory response was reduced further to only 3% of S1, the ratio S2/S1 being 0.03. The presence of haloperidol, sulpiride or picobenzide (each 0.5 microM) during S2, completely reversed the inhibition of catecholamine release produced by apomorphine. Haloperidol itself increased the nicotinic secretory response during S2; so, while the ratio S2/S1 was 0.5 in control conditions, this ratio increased significantly to 0.95 if haloperidol (0.5 microM) was present during S2, suggesting that the presence of this dopaminergic antagonist removed a negative feed‐back mechanism that inhibits nicotine‐evoked catecholamine release. If present during S2, dopamine (1 microM) also markedly inhibited catecholamine release evoked by nicotine; this inhibition was again reversed by 0.5 microM‐haloperidol. Neither the opiate antagonist naloxone nor the alpha‐adrenoceptor blocking agent phentolamine (at concentrations of 0.5‐5 microM) affected the inhibition by apomorphine of the secretory response to nicotine. These data strongly suggest that the cat adrenal medulla chromaffin cell membrane contains a dopaminergic receptor which modulates the catecholamine secretory process triggered by stimulation of the nicotinic cholinoceptor. The fact that dopamine is released in measurable amounts, together with adrenaline and noradrenaline, from perfused cat adrenal glands in response to nicotinic stimulation (V. Ceña, unpublished results), favours a role for this dopaminergic receptor in modulating catecholamine release from the chromaffin cell.
Action and localization of glycine and taurine in the cat retina.
Authors: Bolz J , Thier P , Voigt T , Wässle H
Published: December 2014

The effects on retinal ganglion cells of iontophoretically applied glycine, taurine and strychnine were studied in the optically intact eye of the cat. Glycine and taurine suppressed the light‐evoked discharge of all on‐centre and off‐centre brisk ganglion cells, regardless of the visual stimulus used. Strychnine blocked the action of externally applied glycine and taurine. The light‐evoked response of all ganglion cells was raised by strychnine. The tonic discharge of the light response was suppressed or raised by the drugs more than the phasic response. A population of amacrine cells, which was heavily labelled by [3H]glycine, did not take up [3H]taurine. [3H]taurine was only weakly accumulated by inner nuclear layer neurones and was predominantly located in the outer retina.
Reciprocal inhibitory interneurones in the Xenopus embryo spinal cord.
Authors: Dale N
Published: December 2014

The mechanism of reciprocal inhibition between antagonistic motor centres during swimming in the paralysed Xenopus embryo has been investigated further. Paired intracellular recordings have been made from interneurones and motoneurones in an attempt to identify neurones which make direct inhibitory synapses onto motoneurones on the opposite side of the spinal cord. A physiological class of inhibitory interneurones is described which, when stimulated by intracellular current passage, evoke short‐latency, probably monosynaptic, strychnine‐sensitive inhibitory potentials in contralateral motoneurones. These inhibitory interneurones fire once per swimming cycle in phase with the ipsilateral motor root discharge. They therefore have a pattern of activity which would cause them to inhibit motoneurones of the antagonistic motor centre at an appropriate part of the swimming cycle. The intracellular injection of horseradish peroxidase (HRP) has allowed the morphology of these inhibitory interneurones to be characterized. They have unipolar cell bodies with a thick proximal process with short dendrites which crosses the spinal cord ventrally and then bifurcates with one axonal branch ascending into the hind brain and the other descending the spinal cord. These anatomical features are typical of the 'commissural interneurones' first described by Roberts & Clarke (1982). There are also some inhibitory interneurones which can inhibit motoneurones on the same side of the spinal cord. At least some of these interneurones may be commissural interneurones with ipsilateral axons and they may play a role in the generation of the swimming rhythm.
Naloxone increases blood flow in the human hand.
Authors: Archer A G , Benroubi M , Pyke D A , Wiles P G
Published: December 2014

Intravenous injection of 2 mg naloxone produced a rapid and pronounced rise of blood flow (6.3 +/‐ 5.0 to 67.0 +/‐ 15.1 ml min‐1 100 ml‐1) and skin temperature (28.3 +/‐ 3.0 to 32.4 +/‐ 1.2 degrees C) in the finger and hand of seven of ten normal volunteers. In the other three there was only a small response. Skin temperature did not change in either the face or the foot. Three responding subjects who were retested with 0.4 mg naloxone showed a smaller and briefer response. To exclude a local effect of naloxone on skin blood flow due to release of histamine, responders and non‐responders were tested with naloxone and morphine pricked into the skin of the hand and forearm. All showed a weal and flare reaction to morphine which was not abolished by mixture with naloxone; none showed any reaction to naloxone alone. These results suggest that, in some subjects at least, skin blood flow in the hand may be under endogenous opioid control and they raise the possibility that opioid antagonists might have value in the treatment of disorders of skin blood flow such as Raynaud's disease.
The effect of vitamin D deficiency on secretion of saliva by rat parotid gland in vivo.
Authors: Glijer B , Peterfy C , Tenenhouse A
Published: December 2014

The role of vitamin D in parotid gland function was investigated by measuring the composition and rate of production of parotid saliva in response to pilocarpine injection in vitamin‐D‐deficient and replete rats in vivo. Rats fed a vitamin‐D‐free diet from weaning (G1) were studied after 8 weeks of diet at which time they had a decreased rate of growth, were hyperparathyroid and hypocalcaemic but still had detectable serum 1,25‐dihydroxycholecalciferol (1,25(OH)2D3). Rats which were the offspring of vitamin‐D‐deficient mothers and which were maintained on a vitamin‐D‐free diet from weaning (G2) had a decreased rate of growth from birth, were hypocalcaemic and hyperparathyroid and at no time had any detectable serum 1,25(OH)2D3. In response to pilocarpine, the volume of parotid saliva produced by G1 animals was no different from the controls (G1 animals receiving supplemental vitamin D) whereas that produced by G2 animals was reduced more than 65%. The total amount of amylase secreted was unchanged in either group of experimental animals so that the concentration of amylase in the parotid saliva from G2 animals was increased. The concentration of calcium in parotid saliva changed in parallel with the changes in serum calcium in G1 and G2 animals. It is concluded that the primary source of parotid saliva calcium is the extracellular fluid and not zymogen granules and the transepithelial transport of this calcium is independent of vitamin D; the secretion of electrolytes and water, which in the parotid gland require extracellular calcium, is dependent on vitamin D. It is proposed that the vitamin is necessary for the synthesis of a protein(s) which is essential for the utilization of extracellular calcium in this secretion process.
Dopaminergic modulation of neuromuscular transmission in the prawn.
Authors: Miller M W , Parnas H , Parnas I
Published: December 2014

The action of the putative crustacean neurohormone dopamine was examined in the fast extensor musculature of the prawn with intracellular and extracellular recording techniques. Dopamine produced a concentration‐dependent (10(‐7)‐10(‐5) M) decrease in the size of the excitatory junctional potential (e.j.p.). It had no effect on the muscle fibre resting membrane potential or input resistance. High concentrations (10(‐5)M) of dopamine had no effect on the amplitude distribution or decay time of quantal unit currents, indicating that the agent does not act by blocking post‐synaptic receptors or channels. Bath application of dopamine reduced the quantal content at single release sites with a similar time course and concentration dependence as that observed for the e.j.p. Dopamine had no effect on histograms of synaptic delays determined over a 10 degree C range, indicating that it does not modify the time course of phasic neurosecretion. Twin‐impulse facilitation experiments showed a marked decrease in the duration of facilitation in the presence of dopamine. These results are interpreted according to recent theoretical and experimental findings as indicating that the dopamine‐induced reduction in transmitter release is produced by a decrease in the entry of Ca during the nerve terminal action potential.
The post‐natal development of cutaneous afferent fibre input and receptive field organization in the rat dorsal horn.
Authors: Fitzgerald M
Published: December 2014

The responses evoked in lumbar dorsal horn cells by both natural and electrical hind‐limb skin stimulation were recorded in the spinal cord of rat pups aged 0‐15 days under urethane anaesthesia. The input volley was recorded on the L4 dorsal root and consisted of two separate waves from birth. Latency and threshold measurements were consistent with these two waves being immature A (myelinated fibre) waves and C (non‐myelinated fibre) waves. On the first 3 days of life background activity of cells in the dorsal horn was low and evoked discharges were sluggish. On electrical stimulation of the skin, neonatal dorsal horn cells frequently responded with only 1 or 2 impulses per input volley with long central delays of up to 20 ms. Synaptic linkage appeared weak and many cells failed to follow stimulation rates of 5 Hz. Natural skin stimulation showed that the majority of cells at days 0‐3 responded to pinching the skin only. The development of responses evoked by C fibres in the dorsal horn was delayed compared to that of responses evoked by A fibres. Short and long latency responses corresponding to the early A and late C afferent input volleys could be recorded in the superficial laminae (I, II and III) of the dorsal horn from day 0, but in the deeper laminae only early short latency A responses were evoked until the age of day 7‐8. After this time, a long latency C response also appeared and increased in strength with age. Convergence of low and high threshold inputs onto dorsal horn cells was rare at birth but increased gradually over the following two weeks. Receptive field areas, mapped by natural mechanical stimulation of skin, were large at birth and decreased in size with age. At birth the mean receptive field area was 14.2% of the total hind‐limb area whereas at day 15 it was 3.6%. This fall in size was particularly marked in cells of the deep dorsal horn. Pinching or brushing the receptive field of many neonatal dorsal horn cells resulted in long‐lasting after‐discharges (30‐90 s) which on days 0‐3 could be more pronounced than the initial evoked response. The duration and amplitude of these responses decreased with age. Repetitive electrical skin stimulation of the receptive fields of these cells produced 'wind‐up' and prolonged after‐discharge. Ipsilateral, contralateral and distant inhibitory components to receptive fields were observed from day 0.(ABSTRACT TRUNCATED AT 400 WORDS)
Properties of a sympatho‐inhibitory and vasodilator reflex evoked by superior laryngeal nerve afferents in the cat.
Authors: Bachoo M , Polosa C
Published: December 2014

The background discharge of sympathetic preganglionic neurones shows a marked inspiration‐synchronous component which is known to originate from within the central nervous system. The contribution of this component to total neurogenic vasoconstrictor tone is unknown. In order to estimate its extent we have exploited the inspiration‐suppressing effect of a group of low threshold afferent fibres in the superior laryngeal nerve. The electrical activities of the cervical sympathetic trunk and of the phrenic nerve were recorded in pentobarbitone‐anaesthetized, paralysed, artificially ventilated, sino‐aortic denervated and vagotomized cats, together with the perfusion pressure of an innervated hind limb perfused at a constant flow rate. Repetitive stimulation of the superior laryngeal nerve at an intensity just sufficient to suppress phrenic nerve activity inhibited the inspiration‐synchronous sympathetic discharge and caused hind limb vasodilatation. This vasodilatation was abolished by hexamethonium or phentolamine, but was not affected by atropine or propranolol. Following the elimination of phrenic nerve activity and inspiration‐synchronous sympathetic discharge by systemic hypocapnia, repetitive stimulation of the superior laryngeal nerve either failed to affect the residual sympathetic activity and hind limb perfusion pressure, or caused an increase of both. Stimulation of the superior laryngeal nerve with short (0.2 s) trains of stimuli, delivered at selected times of the respiratory cycle for several consecutive cycles, had similar effects on phrenic nerve bursts, inspiration‐synchronous sympathetic discharge and hind limb perfusion pressure. Stimulation at progressively earlier times during inspiration produced a graded reduction in all three variables, while stimulation during late inspiration or early expiration had no effect on any of them. The results suggest that the vasodilator reflex, elicited by inspiration‐suppressing afferents in the superior laryngeal nerve, results from selective abolition of the excitatory input which causes the inspiration‐synchronous discharge of sympathetic neurones. The magnitude of the hind limb vasodilatation can therefore be taken as an indication of the extent of control of hind limb vasoconstrictor tone exerted by this particular input. By comparing the magnitude of the reflexly evoked vasodilatation with that of the vasodilatation resulting from ganglionic blockade, it was estimated that 24.2% of the neurogenic vasoconstrictor tone of the hind limb was attributable to the inspiration‐synchronous component of sympathetic discharge.
Interactions between motor units and Golgi tendon organs in the tibialis posterior muscle of the cat.
Authors: Binder M D , Osborn C E
Published: December 2014

The responses of Golgi tendon organs to single motor unit contractions were studied to determine whether receptors located in the same muscle region respond to a common set of motor units. In each of five experiments we isolated a large fraction (25‐65%) of the motor units of the cat tibialis posterior muscle and determined to which of the units each of several tendon organs was responsive. Each tendon organ was excited by from two to fifteen of the isolated motor units, including units which produced very small forces. However, there was a much greater probability for large force units to excite a given receptor than for small force units to do so. The number of motor units which produced either an 'unloading' or an 'off response' exceeded, on average, the number of motor units which excited the same tendon organ. The extent to which single motor units excited both of a pair of tendon organs was examined statistically in relation to the mutual proximity of the receptors within the muscle. It was found, on average, that the closer were two receptors, the greater was the number of motor units that excited both of them. These results suggest that despite the extensive territories of individual motor units, the spike trains of tendon organs may still encode information about localized muscle activity.
Cutaneous receptive field and morphological properties of hamstring flexor alpha‐motoneurones in the rat.
Authors: Cook A J , Woolf C J
Published: December 2014

Intracellular recordings have been made from twenty antidromically identified posterior biceps femoris/semitendinosus (p.b.s.t.) hamstring flexor alpha‐motoneurones in the decerebrate‐spinal rat. The hamstring motoneurones had either low or no spontaneous background activity. In nineteen of the twenty cells high‐frequency phasic responses could be elicited by stimulation of the ipsilateral hind paw with firm pressure or pinch. There was no response to light touch or brush. Contralateral cutaneous mechanoreceptive fields with higher thresholds and weaker responses were present in 70% of the motoneurones. Noxious heating of the ipsilateral hind paw produced excitatory responses in six of eight cells tested and two of these cells also responded to heating of the contralateral hind paw. Stimulation of the ipsilateral sural nerve at graded strengths that successively activated A beta, A delta and C afferents produced excitatory post‐synaptic potentials (e.p.s.p.s) at progressively longer latencies in the motoneurones. The C‐fibre induced e.p.s.p. lasted up to 200 ms. Horseradish peroxidase was injected into ten motoneurones and in seven cases full reconstructions of dendritic field, cell body and axon could be made. In agreement with previous reports from studies in the cat, the dendritic fields of rat motoneurones are very extensive in the rostrocaudal, mediolateral and dorsoventral planes. The general pattern of dendritic branching for each motoneurone in this functionally homogeneous population was uniformly organized. Three major spatial orientations were always present: a rostrocaudally restricted series of dendrites emerging from the cell body and directed dorsolaterally towards the dorsolateral funiculus with branches in the lateral dorsal horn, a laterally, and a ventromedially directed series of branches arranged obliquely in the ventral horn, both of which were distributed rostrocaudally for equal distances from the cell body. Many of these dendritic branches terminated within the lateral and ventral white columns. Although the sizes of the rat flexor motoneurones' somas (51 +/‐ 4.9 micron, S.E., n = 10) were similar to those of cat lumbosacral alpha‐motoneurones, the tip‐to‐tip rostrocaudal extent of their dendritic fields (1130 +/‐ 34 micron, S.E., n = 7) was half that reported in the cat. These results are discussed in terms of the organization of the cutaneous flexor withdrawal reflex in the rat.
Electromyographic activity in the cross‐reinnervated soleus muscle of unrestrained cats.
Authors: Luff A R , Webb S N
Published: December 2014

Electromyographic (e.m.g.) activity was recorded from cross‐ and self‐reinnervated soleus and extensor digitorum longus (e.d.l.) muscles of the cat during normal activity, including standing, walking and jumping. Activity patterns of normal soleus, e.d.l., and lateral gastrocnemius (l.g.) were essentially similar to those shown by other investigators. The self‐reinnervated soleus fired phasically and synchronously with l.g. during walking but the activity was not trimmed to the extent that is seen in normal soleus. This is attributed to the relatively limited amount of proprioceptive information arising from such muscles. The activity pattern of the cross‐reinnervated soleus muscles was variable. During walking, the phase of activity was sometimes coincident with that of a normal e.d.l., at other times (even in the same animal) it would be approximately coincident with l.g. The phase of activity usually consisted of an initial burst which was not sustained. Reflex activity elicited from the cross‐reinnervated soleus was very similar to that of normal e.d.l., indicating the rigidity of connexions for reflex responses. reinnervated e.d.l. muscles; the activity attributable to the cross‐reinnervated portion was similar to that seen in a self‐reinnervated soleus. The activity pattern of soleus, reinnervated by the nerve to e.d.l. (an effective antagonist) is unlike that of either a normal soleus or e.d.l. muscle. This is attributed to a combination of lack of proprioceptive information and/or some degree of central remodelling.
Slow inactivation of the calcium current of Paramecium is dependent on voltage and not internal calcium.
Authors: Hennessey T M , Kung C
Published: December 2014

The isolated Ca2+ current from Paramecium caudatum was examined under voltage clamp with long conditioning depolarizations lasting for up to 5 min. The isolated transient Ca2+ current inactivates with tens of milliseconds due to Ca2+ ‐dependent Ca2+ ‐channel inactivation (Brehm & Eckert, 1978). When this fast inactivation was blocked by internally delivered EGTA, a much slower inactivation of the Ca2+ current was discovered. This slow inactivation had time constants of tens of seconds, depending on voltage. The development of this slow inactivation was further examined by following the Ca2+ transient after 1 s interruptions of the long depolarization. This development is voltage dependent; the rate of inactivation is higher with a larger depolarization. After a long depolarization, the Ca2+ current returns in two clearly separable steps. A portion of the current returns rapidly along an exponential time course with time constants of tens to hundreds of milliseconds. The remainder of the current returns slowly with time constants of tens of seconds. A longer conditioning depolarization generates a larger portion that recovers slowly. Internally delivered EGTA, sufficient to prevent most of the fast inactivation, did not change the time course or the extent of either the onset or the removal of the slow inactivation. The compound W‐7, which inhibits the Ca2+ current itself, does not block the onset of this slow inactivation during depolarization. We conclude that the slow inactivation of the Ca2+ channel is a mechanistically different phenomenon from the fast Ca2+ ‐dependent Ca2+ ‐channel inactivation. The possible physiological and behavioural roles of this slow inactivation are discussed.
Effects of prior instruction and anaesthesia on long‐latency responses to stretch in the long flexor of the human thumb.
Authors: Loo C K , McCloskey D I
Published: December 2014

Long‐latency (40‐80 ms) electromyographic (e.m.g.) responses of the contracting flexor pollicis longus to stretches applied at the thumb‐tip, were studied in normal human subjects. Stretches were applied during four classes of contraction: (i) isometric 'hold', in which the subject held a steady isometric contraction; (ii) isometric tracking, in which the subject tracked a steadily rising force target; (iii) isotonic tracking, in which the subject flexed against a constant torque to track a position target; (iv) weight‐lifting, in which the subject lifted a weight hung at one end of a lever by pressing the thumb‐tip on the other end of the lever. The effects on the responses of prior instructions to 'resist' or to 'let go', and of local anaesthesia of the thumb, were studied. The ability to modify the size of the long‐latency e.m.g. response in accordance with prior instruction was variable. All subjects tested could do so during isometric holding contractions, but many could not do so during the other forms of contraction. Local anaesthesia of the thumb significantly reduced the long‐latency e.m.g. response in only some subjects, and abolished it in none. The reduction was most reliably seen for isometric force tracking contractions. During thumb anaesthesia in different subjects, there was a significant correlation between the proportional increase in apparent heaviness of an object lifted by thumb flexion and the proportional reduction in the size of the long‐latency e.m.g. response to muscle stretch.