bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evidence for non‐cholinergic, non‐adrenergic transmission in the guinea‐pig ileum
Authors: Bauer V. , Kuriyama H. 
Published: December 2014

To elucidate further the innervation of the longitudinal and circular muscle cells of the guinea‐pig ileum, junction potentials elicited by field stimulation were recorded from both muscle layers in the presence and absence of atropine (1‐2 μM) with guanethidine (10 μM) at 36 °C.1. In longitudinal muscle cells, a single stimulus elicited an atropine‐sensitive transient depolarization (cholinergic e.j.p.), whereas in circular muscle cells, a transient hyperpolarization (non‐cholinergic non‐adrenergic i.j.p.) was elicited. With stimulation of nerves in the presence of atropine and guanethidine, responses of circular muscle cells to nerve stimulation were preserved while the longitudinal muscle cells generated depolarization (non‐ch., non‐adr. e.j.p.), hyperpolarization (non‐ch., non‐adr. i.j.p.) or both depolarization and subsequent hyperpolarization. These potential changes ceased with application of TTX or excess Mg2+.2. The latency for junction potentials recorded from longitudinal muscles after field stimulation was in the following order; non‐ch., non‐adr. e.j.p. < cholinergic e.j.p. < non‐ch., non‐adr. i.j.p. The cholinergic e.j.p.s had a lower, and non‐ch., non‐adr. i.j.p.s a higher threshold.3. At low frequencies of stimulation (below 1 Hz) amplitudes of successively generated cholinergic e.j.p.s and non‐ch., non‐adr. i.j.p.s were gradually reduced, but at higher frequencies (2‐20 Hz) of stimulation they were summated. The amplitudes of non‐ch., non‐adr. e.j.p.s were, however, not affected at low frequencies of stimulation (up to 0·5 Hz) and were summated at higher frequencies (over 1 Hz) of stimulation.4. Reversal potentials for non‐ch., non‐adr. e.j.p.s and i.j.p.s estimated from the amplitude of junction potentials and membrane potential were ‐27 and ‐80 mV, respectively. The reversal potential for non‐ch., non‐adr. e.j.p.s was higher (more negative) than that for cholinergic e.j.p.s5. Generation of i.j.p.s in longitudinal muscle cells elicited by repetitive stimulation was followed by a rebound depolarization on which was superimposed a burst of spikes. During repetitive stimulation, the amplitude of hyperpolarization was gradually reduced but the rebound depolarization and spike discharge were enhanced. Thus, while the rebound depolarization was related to the amplitude of the preceding hyperpolarization it was more related to the duration of the stimulation.6. Therefore longitudinal muscles of the guinea‐pig ileum show evidence of having in addition to cholinergic and adrenergic innervation, both excitatory and inhibitory non‐ch., non‐adr. innervation. In the longitudinal muscle layer of the ileum, the non‐ch., non‐adr. excitatory fibres are more densely distributed in the terminal rather than in the proximal region, while in the case of non‐ch., non‐adr. inhibitory fibres, the distribution is reversed. Circular muscle cells are, however, homogenously innervated by non‐ch., non‐adr. inhibitory nerves.
The effects of sodium replacement on the responses of toad rods
Authors: Bastian Bruce L. , Fain Gordon L. 
Published: December 2014

1. We have investigated the effects of Na+ substitution on the membrane potential and light responses of rods in the superfused retina of the toad, Bufo marinus.2. When all of the Na+ in the Ringer was replaced with Li+, the effects on the rods depended upon the external free Ca2+ concentration ([Ca2+]o). At [Ca2+]o ≥ 10−6 M, the membrane potential (Em) hyperpolarized and light responses were greatly diminished or abolished. At [Ca2+]o ≤ 10−7 M, Li+ replacement had little effect on Em or response amplitude.3. We interpret these results as revealing a Na+—Ca+ counter‐transport in rods. At high [Ca2+]o, replacing Na+ with Li+ would have produced an increase in the rod cytosol free Ca2+ concentration ([Ca2+]i) and the blockage of the light‐dependent conductance, leading directly to the suppression of light responses. At [Ca2+]o ≤ 10−7 M, this presumably would not have occurred.4. Since at these low Ca2+ concentrations we observed light responses of nearly normal amplitude in Li+, our results suggest that the light‐dependent conductance is permeable to Li+.5. Substitution of Na+ with K+ in low Ca2+ produced a complete suppression of the responses. However, it was still possible to measure large light‐induced changes in rod input resistance.6. Substitution of Na+ with tetramethylammonium, tetraethylammonium, Tris, or choline in low Ca2+ produced a large hyperpolarization of the membrane potential and a diminution of response amplitude. However, we were unable to observe a complete suppression of the responses for these cations.7. Substitution of Na+ with tetrapropylammonium or with an uncharged substance (glucose or urea) in low Ca2+ produced a large hyperpolarization of membrane potential and a considerable decrease in the light responses. In about half our attempts, the responses were observed to decline reversibly to less than 20% of their peak amplitude in Na+.8. Results with tetrapropylammonium were indistinguishable from those of glucose or urea, indicating that the light‐dependent conductance probably is not permeable to TPA. The resistance changes measured with K+ substitution and the responses observed in the presence of the organic ions TMA, TEA, Tris and choline suggest that these species may be permeable, but we are unable to discount alternative explanations.
Association of 45calcium with rat mast cells stimulated by 48/80: effects of inactivation, calcium and metabolic inhibition
Authors: Cochrane David E. , Distel Daniel L. 
Published: December 2014

1. Stimulation by compound 48/80 of mast cells deprived of Ca released histamine when Ca was subsequently added. This secretory response was accompanied by a pronounced increase in the amount of cell‐associated 45Ca.2. The level of cell‐associated 45Ca declined as the interval between stimulation by compound 48/80 and the introduction of 45Ca increased.3. This decline in the amount of 45Ca paralleled the decline in histamine secretion that is called inactivation and each curve could be fitted by linear regression to a first‐order equation with a half‐life of between 1 and 2 min.4. When histamine secretion was held constant, the amount of cell‐associated 45Ca steadily and significantly declined as the interval between stimulation and the addition of 45Ca increased. This decline in the level of 45Ca was significantly reduced when fully inactivated cells were used.5. The amount of cell‐associated 45Ca could not be significantly reduced by repeated or prolonged washing with EGTA or LaCl3.6. The addition of the ionphore, A23187, or compound 48/80, to mast cells loaded with 45Ca by prior stimulation with 48/80 and bathed in Ca‐free media, significantly reduced the level of cell‐associated 45Ca. This effect of 48/80 but not of A23187 was prevented by including either dinitrophenol or 45Ca in the extracellular solution.7. When [3H]N‐methyl‐methoxy‐inulin was included with the 45Ca or added alone, no significant change in the level of cell‐associated [3H]inulin was found during the course of inactivation.8. Increasing the Ca concentration increased the amount of cell‐associated 45Ca when Ca was added 10 sec after stimulation by 48/80 but not when Ca was added 10 min after stimulation.9. Incubation of mast cells in media containing deoxyglucose and either antimycin A or dinitrophenol prevented both histamine release and any increase in the level of cell‐associated 45Ca in response to stimulation by 48/80. A similar result was obtained using sensitized mast cells stimulated by antigen. The addition of the ionophore, A23187, to the mast cells prompted a significant increase in the level of cell‐associated 45Ca.10. These results are considered to be support for the hypothesis that the process of inactivation to compound 48/80 results from a time‐dependent decay in membrane permeability. It is suggested that those events associated with initiating changes in membrane permeability are effected by metabolic inhibition and calcium.
The appearance and development of chemosensitivity in Rohon—Beard neurones of the Xenopus spinal cord
Authors: Bixby John L. , Spitzer Nicholas C. 
Published: December 2014

1. We have examined the onset and subsequent development of chemosensitivity in Rohon—Beard neurones from the Xenopus spinal cord. These cells become sensitive to bath‐applied γ‐aminobutyric acid (GABA) around stage 25 (early tailbud, about 1 d old), and remain so at least until stage 49 (9 d old). In contrast, a number of other neurotransmitter candidates tested caused no potential or conductance change during the same period.2. We examined ionophoretic dose—response relations of the cells at stage 26, a couple of hours after the first acquisition of GABA sensitivity. Sensitivities as high as 450 mV/nC were recorded. Comparable sensitivities were recorded between stages 46‐49 (5‐9 d old).3. Measurements of ionophoretic sensitivities and input resistances during several periods from stage 26 to maturity show that the underlying conductance change for a given GABA dose is likely to increase steadily during this time. A ‘sensitivity index’ (ionophoretic sensitivity/input resistance) was calculated, which is low at stage 26, higher at intermediate stages (stages 31‐42), and highest for mature cells (stages 46‐49; 5‐9 d of development).4. The reversal potential of the ionophoretic GABA response is the same at stage 26 (‐30 mV) as it is in mature cells. Ion substitution experiments show that Na+ and K+, but not Cl− or Ca2+, are involved in the response.5. GABA responses at stage 26 are pharmacologically similar to those of mature cells. The responses are blocked by 10 μM‐picrotoxin or curare, and muscimol is an agonist in concentrations as low as 1 μM.6. GABA responses at stage 26 desensitize in a manner similar to that seen for mature cells, either with prolonged bath application of GABA or with repetitive ionophoretic application.7. Nearly half of the cells tested at stage 26 respond to glycine, in concentrations as low as 5 μM. This sensitivity is absent by 3½ d of development.8. The responses of Rohon—Beard neurones to GABA are similar to those of other cells in that they involve a conductance increase, are mimicked by muscimol, and are blocked by picrotoxin. These responses are different in that they do not involve Cl− and are blocked by low concentrations of curare.9. Many of the characteristics of GABA receptors, i.e. the reversal potential, desensitization, and pharmacology, are constant during development. However, the sensitivity of the cells to GABA and the spectrum of transmitters to which they are sensitive appear to change.
The effects of intracochlear and systemic furosemide on the properties of single cochlear nerve fibres in the cat
Authors: Evans E. F. , Klinke R. 
Published: December 2014

1. Tuning properties and spontaneous discharge rate of single cochlear fibres in the anaesthetized cat were determined during short‐ and long‐term poisoning of the cochlea by locally and systemically applied furosemide.2. With intra‐arterial administration of furosemide, short‐term reversible elevation occurred of the low threshold sharply tuned ‘tip’ segment of the frequency threshold (‘tuning’) curve (f.t.c.) by up to 40 db, without substantial changes in the threshold of the low frequency ‘tail’ segment of the f.t.c. These changes could occur in part without changes in the spontaneous activity and entirely without changes in the maximal evoked activity. These effects were observed in all fibres examined, the characteristic frequencies of which ranged from 3·5 to 31 kHz.3. Intracochlear administration of furosemide in 0·9 mM concentrations produced similar changes, but these were not reversible.4. The changes correlated with the depression of the amplitude of the gross cochlear action potential. The cochlear microphonic potential, however, was either unchanged, or only slightly reduced.5. In long‐term furosemide poisoning of the cochlea, fibres with anomalous response properties were found alongside fibres having normal tuning. The former exhibited either reduced excitability of the low threshold tip segment, or a tip segment attenuated in both excitability and threshold.6. It is concluded that the selective effects of furosemide on the tip segment of cochlear fibre f.t.c.s offer further evidence for a physiologically vulnerable ‘second filter’ in the cochlea. The selective influence of the furosemide on the low threshold tip segment provides support for the hypothesis that the normal f.t.c. is generated by two largely independent processes: one vulnerable, low threshold and sharply tuned, and the other less vulnerable, but high threshold and more broadly tuned.7. The findings, obtained with an agent known to produce reversible impairment of hearing in man, provide direct physiological evidence in support of the hypothesis that in sensorineural hearing loss of cochlear origin the frequency selectivity of cochlear nerve fibres is impaired.
A range of different stretch reflex responses in the human thumb
Authors: Brown T. I. H. , Rack P. M. H. , Ross H. F. 
Published: December 2014

1. Imposed sinusoids were used to assess the resistance to movement at the thumb interphalangeal joint.2. The resistance to high‐frequency movements (> 12 Hz) increased when the subject exerted a large voluntary flexing force; this increase was attributable to a greater non‐reflex resistance of the contracting flexor muscles. This resistance was essentially ‘visco‐elastic’, and the force was phase‐advanced on joint position. At moderately large forces (up to half maximal), however, the resistance changed with changing frequency, and over a range 4‐12 Hz the vectors which represented joint stiffness described the wide path that is characteristic of an active stretch reflex (Brown, Rack & Ross, 1982a). At frequencies between about 4 and 6 Hz the force was sometimes phase‐delayed on position, and the joint exhibited a negative viscous stiffness. When the voluntary flexing force was very large the reflex contributed less to the resisting force, which was then phase‐advanced on position at all frequencies of movement.3. Large amplitude movements did not generate correspondingly large reflex responses; as the amplitude of movement was increased, the reflex component of the resisting force became relatively smaller and the total resisting force was then phase‐advanced on joint position at all frequencies.4. The reflex component of the resisting force (as indicated by the excursion of the joint stiffness vectors) varied from subject to subject and from time to time; the reflex usually became more active late in an experiment when the subject had exerted flexing forces against the imposed movement for some minutes. Extreme fatigue, however, diminished the amount of reflex force.5. In some subjects the joint‐stiffness records indicated a particularly vigorous reflex response at 8‐11 Hz, in contrast to a rather feeble response at 6 or 7 Hz. It is suggested that the reflex pathways then had a relatively low impedance to afferent signals that were modulated at 8‐11 Hz, related perhaps to the firing patterns of the most recently recruited motoneurones.6. Under the conditions of these experiments, it appears that the stretch reflex has too small a gain to function as a very effective error‐controlled position servo‐mechanism.
Central innervation of neurones in the inferior mesenteric ganglion and of the large intestine of the cat
Authors: Krier J. , Schmalz P. F. , Szurszewski J. H. 
Published: December 2014

1. Segmental, lumbar sympathetic outflow to neurones in the cat inferior mesenteric ganglion and to the large intestine were studied. Synaptic responses of neurones in the inferior mesenteric ganglion were recorded intracellularly, in vitro, during electrical stimulation of preganglionic fibres in the lumbar white rami. Synaptic responses consisted of excitatory post‐synaptic potentials and/or action potentials.2. None of the neurones tested received synaptic input from spinal cord segment L1. There was synaptic input from segments L2‐L5 of the spinal cord. The strongest synaptic input arose from spinal cord segments L3 and L4.3. 42% of the neurones tested received synaptic input from only one spinal cord segment. 54% of the neurones tested received convergent synaptic input from two, three or four adjacent lumbar segments.4. Electrophysiological measurements indicated that the number of preganglionic fibres in any lumbar white ramus communicans which provided synaptic input ranged from one to thirteen. Each lumbar white ramus contained, on average, five preganglionic fibres which provided synaptic input to neurones in the inferior mesenteric ganglion.5. Changes in intraluminal colonic pressure were measured in vivo during electrical stimulation of preganglionic fibres in the different lumbar white rami and lumbar ventral roots. Electrical stimulation of white rami L3 and L4 abolished phasic changes in intraluminal colonic pressure and reduced basal pressure to near zero. Electrical stimulation of preganglionic fibres in lumbar ventral roots L3 and L4 abolished phasic changes in intraluminal colonic pressure and reduced basal pressure to near zero. Stimulation of ventral roots L1, L2 and L5 had little to no effect on intraluminal pressure.6. Based on the data obtained in this study, two hypotheses are proposed. First, spinal cord segments L3, L4 and L5 are the primary sources of central synaptic input to neurones in the inferior mesenteric ganglion. Secondly, spinal cord segments L3 and L4 control colonic motility.
The influence of injected cyclic AMP protein kinase catalytic subunit on the sodium efflux in barnacle muscle fibres
Authors: Bittar E. Edward , Chambers Geoffrey , Fischer Edmond H. 
Published: December 2014

1. A study has been made of the response of the Na efflux in single barnacle muscle fibres to the injection of cyclic AMP protein kinase catalytic subunit (CSU).2. (i) Injected CSU stimulates the Na efflux in unpoisoned and ouabain‐poisoned fibres. (ii) Stimulation in both situations is always sustained, and (iii) stimulation of the ouabain‐insensitive Na efflux is observed with as low a concentration as 10−7 M‐CSU.3. (i) The response to injected CSU depends on [Ca]o but is unaffected by prior external application of verapamil. (ii) An effect fails to occur in fibres cooled to 0 °C.4. (i) Injection of 5′‐guanylylimidodiphosphate (Gpp(NH)p) following peak stimulation by CSU causes a further sustained stimulatory response. (ii) Injection of CSU following peak stimulation by Gpp(NH)p causes a further sustained stimulatory response. (iii) Injection of undialysed cholera toxin following CSU causes little or no effect, whereas injection of dialysed cholera toxin causes a stimulatory effect. Injection of CSU following undialysed cholera toxin causes little or no effect, whereas its injection after dialysed cholera toxin causes a fairly appreciable effect.5. (i) The response to CSU is reduced by prior injection of protein kinase type 2 regulatory subunit (RII) but not when RII is injected following peak response to CSU. (ii) Injection of protein kinase inhibitor partially reverses the response to CSU.6. (i) Injection of Mg2+ fully reverses the response to CSU. (ii) Fe and Zn cause only partial reversal.7. (i) External imipramine but not trifluoperazine reduces the response to CSU. (ii) Diphenylhydantoin is ineffective.8. These results support the view that CSU behaves as a modulator of the ouabain‐insensitive Na efflux and that Mg2+, Fe and Zn are inhibitors of the catalytic reaction.
The contribution of the electrogenic sodium—potassium pump to the electrical activity of toad rods
Authors: Torre Vincent 
Published: December 2014

1. The membrane potential of rods in the isolated toad retina was recorded while changing the ionic composition of the extracellular medium.2. Caesium (Cs+) at a concentration of 1 mM was sufficient to completely block the sag from the peak to the plateau in the bright‐flash voltage response.3. In the presence of 10 mM‐Cs+ the bright‐flash response increased in amplitude to about 90 mV, thus reaching an absolute membrane potential of between ‐110 and ‐135 mV. These responses consisted of an initial fast component of about 35 mV followed by a much slower component which could be as large as 50 mV.4. At the peak of the initial fast component the rod membrane conformed closely to the behaviour of a K+ electrode with a PNa/PK ratio of 0·023. On average the amplitude of the slow component was about 35 mV in the presence of 2·6 mM‐K+ and was reduced to about 25 mV in a K+‐free Ringer.5. Addition of 100 μM‐strophanthidin to the perfusate induced several reversible changes in the electrical activity of rods. The dark resting membrane potential depolarized by about 5 mV and the kinetics of the voltage response to dim flashes of light slowed down. The voltage sensitivity initially increased by about 30%, but the peak of the response to a bright flash of light was reduced by about 13 mV.6. In rods treated with 10 mM‐Cs+ the slow component present in the bright flash response was abolished by strophanthidin with an apparent Km of 3 μM.7. The amplitude of the slow component decreased with a time lag of about 2 min when external Na+ was reduced. A previous exposure of the retina to a Na+‐free Ringer solution for at least 3 min modified the voltage photoresponse in a way similar to that observed in the presence of 100 μM‐strophanthidin.8. When external Ca2+ concentration ([Ca2+]o) was increased from 2 to 5 mM the slow component decreased by about 30%. When [Ca2+]o was reduced the slow component increased. A twofold increase was observed when [Ca2+]o was lower than 10−4 M.9. It is suggested that the slow component of the voltage response in the presence of external Cs+ is caused by an electrogenic current driven by the Na+—K+ transport system, during a voltage‐dependent block of external Cs+ of some K+ channels.