bluuebunny/crossref_metadata_2025 huggingface dataset:
Nervous modulation of spontaneous contractions in bovine mesenteric lymphatics.
Authors: McHale N G , Roddie I C , Thornbury K D
Published: December 2014

1. Spontaneous isometric contractions were measured in 2 cm segments of bovine mesenteric lymphatics. 2. Field stimulation at 0.25, 1 anf 4 Hz increased the frequency of contraction. 3. Tetrodotoxin 3 x 10(‐6) M blocked the response to electrical stimulation. 4. Phenoxybenzamine 3 x 10(‐7) M converted the excitatory effect of stimulation to an inhibitory one. 5. Propranolol 3 x 10(‐7) M potentiated the excitatory response to stimulation at 1 and 4 Hz. 6. Field stimulation was without effect in the presence of propranolol and phenoxybenzamine together. 7. Cocaine potentiated the response to stimulation at 0.25 and 1 Hz. 8. Atropine 3 x 10(‐7) M failed to block the excitatory effect. 9. Field stimulation at 0.5 and 1 Hz increased the frequency of spontaneous contractions and propulsion of fluid by 8 cm cannulated segments of lymphatic. 10. The results suggest that bovine lymphatic vessels have a noradrenergic innervation which is capable of controlling lymph flow.
Physiological compensation for loss of afferent synapses in rat hippocampal granule cells during senescence.
Authors: Barnes C A , McNaughton B L
Published: December 2014

1. The effects of senescence on the input‐output characteristics of the perforant path projection to granule cells of the fascia dentata were studied in rats using extracellular techniques in vivo, and both extra‐ and intracellular recording in vitro. 2. Senescent animals exhibited a significant reduction in the perforant path excitatory synaptic field potential at all stimulus intensities tested. This was associated with a reduction in the size of the afferent fibre response, although there was no apparent change in the threshold for fibre activation. These data support the anatomical literature which indicates a loss of afferent synapses with advanced age. 3. For a given magnitude of afferent fibre response, however, the old animals exhibited a larger synaptic field potential, suggesting that the remaining synapses were in fact more powerful. Furthermore, the magnitude of the extracellular population spike, an index of the number of discharging granule cells, was greater in the old animals when plotted as a function of extracellular e.p.s.p. amplitude. 4. Intracellular recording from a total of 190 granule cells in the transverse hippocampal slice preparation revealed a 17% reduction in the voltage threshold for synaptically elicited granule cell discharge, and a 13% reduction in the latency of the action potential in old compared to young rats. Resting potentials, action potential amplitudes, whole neurone time constants, the relations between applied current and input resistance, and the discharge threshold following depolarizing current pulses, were not different between age groups. 5. These data indicate that granule cells could partly compensate for a loss of synapses during senescence by an increase in their electrical responsiveness to synaptic activation and possibly by an increase in synaptic efficacy.
Asymmetry currents in the mammalian myelinated nerve.
Authors: Chiu S Y
Published: December 2014

1. Asymmetrical displacement currents were recorded in the rabbit node of Ranvier by averaging the currents associated with depolarizing and hyperpolarizing pulses in the temperature range 15‐25 degrees C with the ends of the fibre cut in 160 mM‐CsCl. 2. The identification of the asymmetrical currents as intramembranous current is supported by the findings that (a) the "on' and "off' current transients were equal for short and small depolarizing pulses and (b) the total charge displaced reached saturation at (32‐111 x 10(‐15) C/node) when sufficiently large depolarizations were applied. 3. After a large depolarization to around 50 mV, the "off' response consisted of a fast phase followed by a slow phase. Lengthening the depolarization reduced the size of the fast response but enhanced the slow response. 4. The steady‐state rearrangement of the charges can be described by a Boltzmann distribution of charges with an effective valence of 1.86 and a midpoint potential of ‐33 mV. The time course of rearrangement of these charges following a change in membrane potential could be fitted reasonably well with a single exponential though a double exponential might have been better at large depolarizations. 5. The steady‐state activation curve for Na conductance was measured with various procedures to eliminate the effects of series resistance, which include decreasing peak Na current by TTX, and electronic compensation of the series resistance. The measured steepness of the Na‐activation curve corresponds to moving a minimum charge of about 5e to open each Na channel at 22.7 degrees C. 6. The time constant (Tm) for activation of Na current and time constant (Ton) for declining phase of the asymmetry current were of the same order of magnitude but not identical over the potential range ‐50 to +25 mV. 7. The time course of charge displacement determined from the asymmetry current occurred earlier than did Na activation. Raising the charge displacement curve to second or third power did not yield a curve that matched the time course of Na activation. 8. If all the observed asymmetrical currents are related to the Na‐gating system, an upper limit for the number of Na channels per rabbit node is 82,000 and a lower limit for the single channel conductance is 9.8 pS at 18.8 degrees C.
Beta‐bungarotoxin stimulates the synthesis and accumulation of acetylcholine in rat phrenic nerve diaphragm preparations.
Authors: Gundersen C B , Jenden D J , Newton M W
Published: December 2014

1. The effects of beta‐bungarotoxin on acetylcholine (ACh) synthesis, tissue content and release have been studied in the rat diaphragm. A gas chromatographic mass spectrometric assay was used to measure ACh and choline. 2. Within 30 min, beta‐bungarotoxin (0.14 or 1.4 micrograms/ml.) caused a significant increase in tissue ACh content. This increase was apparent prior to the final inhibition by beta‐bungarotoxin of evoked (10 Hz) ACh release. 3. The toxin enhanced the incorporation of [2H4]Ch into [2H4]ACh in both resting and stimulated preparations. 4. Hemicholinium‐3 blocked the rise in diaphragm ACh normally produced by beta‐bungarotoxin. 5. Beta‐Bungarotoxin did not directly activate choline acetyltransferase in muscle homogenates. 6. The toxin‐induced rise in tissue ACh was largely absent in Ca2+‐free solutions which contained either EGTA (1 mM) or SrCl2 (2 or 10 mM). 7. Non‐neurotoxic phospholipases A2, fatty acids and the neurotoxic phospholipase A2, notexin, did not cause ACh accumulation in the diaphragm. 8. Beta‐Bungarotoxin did not stimulate ACh synthesis in denervated muscle. 9. The extra ACh which accumulated after beta‐bungarotoxin did not contribute to enhanced release by nerve impulses even when 4‐aminopyridine was added to the medium. High K+ solution and black widow spider venom were also ineffective in increasing output from toxin‐treated diaphragms relative to controls that had not been treated with beta‐bungarotoxin. 10. Prior injection of a rat with botulinum toxin prevented the accumulation of ACh due to beta‐bungarotoxin. Tubocurarine, however, did not antagonize beta‐bungarotoxin. 11. These data indicate that beta‐bungarotoxin has a unique capacity to inhibit ACh release and stimulate ACh synthesis in diaphragm nerve endings. The results are discussed in terms of a possible action of beta‐bungarotoxin to raise the level of ionized Ca in the nerve terminal cytosol.
The tension‐depolarization relationship of frog atrial trabeculae as determined by potassium contractures.
Authors: Chapman R A , Tunstall J
Published: December 2014

1. In the presence of extracellular Na ions K contractures evoked from isolated frog atrial trabeculae show an initial phasic and a subsequent tonic contractile response. 2. The phasic response shows a steep dependence on membrane potential, persists in Na‐free fluid, but is blocked by Mn ions, D600 and tetracaine. It has an indirect dependence on the [Ca]0 and would seem to be associated with both the secondary inward current and the release of Ca2+ from intracellular stores. 3. The tonic component of the K contracture is unaffected by D600 or tetracaine, shows a shallow dependence on membrane potential but is absent in Na‐free fluid. Its tension‐depolarization curve is immediately affected by alteration of either the [Ca]0 or the [Na]0. The form of the tension‐depolarization relationship and the effects of [Ca]0 and [Na]0 are consistent with the strength of the tonic tension being determined by a 3Na+ for 1Ca2+ exchange across the cell membrane. 4. The results agree well with those obtained previously with voltage‐clamp experiments on the same tissue, and may also help with the interpretation of Ca‐flux experiments.
Interaction between motor axons from two different nerves reinnervating the pectoral muscle of Xenopus laevis.
Authors: Haimann C , Mallart A , Ferré J T , Zilber‐Gachelin N F
Published: December 2014

1. An electrophysiological and morphological study of sprouting and regeneration of motor nerves has been performed in the dually innervated pectoral muscle of Xenopus laevis. 2. Section of one of the nerves induced axon sprouting in the intact nerve. Synapse formation by the sprouting axons was slow since the intact nerve took more than 3 months to increase its field of innervation by 70%. The rate of axon regeneration was faster than that of axon sprouting since the cut nerve reinnervated its former territory in less than 1 month. 3. At early stages of synapse formation the sprouted or regenerated endings were poorly branched but any terminal branches were, as a rule, longer than normal. Signs of degeneration and replacement of endings have been observed. 4. Low levels of transmitter release persisted for several months in newly formed endings. This depression was more pronounced at the endings formed outside the normal field of innervation of the nerve. 5. Poly‐innervated muscle fibres have been observed during reinnervation by regenerated or sprouted axons. Their number decreases gradually in the months that follow the beginning of reinnervation. Synaptic efficacy was lower at poly than at mono‐innervated muscle fibres. At doubly innervated spots and at separated spots on the same fibre average end‐plate potential (e.p.p.) amplitude was 1/3 and 2/3 respectively of that recorded at singly innervated fibres. 6. Electrophysiological and morphological data have been compared at individual doubly innervated end‐plate sites. End‐plate potential amplitude was positively correlated with the degree of ending development. 7. Sprouted endings remain functional after periods of reinnervation of 30 months, although signs of regression have been observed. These are probably mediated by spontaneous degeneration of the terminals and replacement by endings from the regenerating nerve.
Drinking and changes in blood pressure in response to angiotensin II in the pigeon Columba livia.
Authors: Evered M D , Fitzsimons J T
Published: December 2014

1. Angiotensin II is as potent a stimulus to drink in pigeons as it is in mammals. There are striking similarities in the action of this peptide in pigeons and mammals. 2. Angiotensin II injected intracranially, I.V. or I.P. consistently caused short‐latency and vigorous drinking in pigeons but no other behaviour. Drinking was completed rapidly and intakes were very large, sometimes in excess of 10% of the bird's body weight. 3. The latency to drink and the amount drunk were dose dependent for all routes of injection. Angiotensin II was most effective when injected directly into the brain. As little as 10(‐4) mol angiotensin II injected into the cerebral ventricles caused birds to drink. 4. The rapid cessation of drinking after intracranial injection of angiotensin II was not caused by rapid loss of activity of the peptide in the brain but by the actual ingestion of the water. 5. The brain sites most sensitive to the dipsogenic action of angiotensin II in the pigeon were the dorsal and ventral third ventricle, the tissue adjacent and anterior to these sites, and the lateral ventricles. The lateral hypothalamic area was only slightly less sensitive. Negative sites for drinking were found in the lateral forebrain and the hind brain. These findings are similar to those in mammals. 6. Pigeons drank during I.V. infusion of as little as 16 X 10(‐12) mol angiotensin II kg‐1 min‐1. This was near the threshold for increasing arterial pressure in pigeons and is near the threshold for drinking in rats and dogs. 7. The Asn1, Asp1, Val5 and Ile5 analogues of angiotensin II were equipotent as stimuli to drink but a wide range of other peptides and drugs injected into the brain failed to increase water intake. An exception was eledoisin which was, comparing molecule with molecule, only 10‐100 times less potent than angiotensin II in the pigeon. 8. Injections of angiotensin II into brain sites which caused drinking failed to alter heart rate or arterial pressure in pigeons. 9. This and other recent studies demonstrate the wide phylogenetic distribution of the dipsogenic action of angiotensin II and support the idea that the control of water intake is an important physiological function of the renin‐angiotensin system in vertebrates.
Drinking and changes in blood pressure in response to precursors, fragments and analogues of angiotensin II in the pigeon Columba livia.
Authors: Evered M D , Fitzsimons J T
Published: December 2014

1. The pigeon drank as vigorously in response to intracranial injection of synthetic renin substrate and angiotensin I as to angiotensin II. 2. Mammalian renin injected into the brain caused the water‐replete pigeon to drink but it was a less effective dipsogen than in the mammal. As in the mammal, renin‐induced drinking was slower in onset and continued for longer than angiotensin‐induced drinking. 3. The converting enzyme inhibitor SQ 20881 attenuated drinking in response to intracranial renin, synthetic renin substrate and angiotensin I but enhanced intracranial angiotensin II‐induced drinking. Therefore drinking induced by the intracranial injection of precursors of angiotensin II is mediated through local generation of angiotensin II. 4. I.V. injection of angiotensin I was as effective as angiotensin II in causing the pigeon to drink, but synthetic renin substrate was less effective. I.V. doses of angiotensin I and II had to be about 100 times greater than the intracranial doses in order to produce similar intakes. 5. Angiotensin I and II were equally effective pressor agents by I.V. injection in the pigeon but synthetic renin substrate was much less effective. I.V. SQ 20881 inhibited the pressor response to I.V. synthetic renin substrate or angiotensin I but enhanced the angiotensin II‐induced response. 6. Aliphatic position 8‐substituted analogues of angiotensin II which are competitive antagonists of angiotensin II‐induced drinking and pressor responses in the mammal in antagonist:agonist mole ratios as low as 10:1, failed to reduce drinking in response to intracranial synthetic renin substrate or angiotensin II, although not themselves agonists, nor did they prevent the pressor to infusion of angiotensin II even with antagonist:agonist mole ratios as high as 10,000:1. 7. Shortening the angiotensin octapeptide from the N‐terminus caused a progressive reduction in intracranial dipsogenic activity. Activity was completely abolished by removing the C‐terminal phenylalanine. 8. These results demonstrate that in pigeons, as in mammals, it is angiotensin II which is the biologically active peptide in the control of drinking behaviour and blood pressure by the renin‐angiotensin system. Precursors of angiotensin II can be converted to the octapeptide in the avian brain as well as in the circulation. The angiotensin receptors for drinking and blood pressure responses are similar to each other in the pigeon and they are very similar but not identical with the angiotensin receptors for the dipsogenic, pressor and myotropic actions of angiotensin II in mammals.
The dipsogenic activity of prolactin in male and female rats.
Authors: Kaufman S
Published: December 2014

1. Ovine prolactin injected intravenously in doses of 10.0, 5.0, 1.0, 0.1 and 0 mg/kg body wt. caused neither drinking nor a change in urine output in normal water replete male and female rats. 2. The water intake of male rats subjected to 48 hr water deprivation was substantially increased after injection of prolactin. 3. The water intake of male and female rats injected I.P. with a hyperoncotic solution of polyethylene glycol (20 M) was significantly increased after injection of prolactin. 4. Prolactin ws found to act synergistically with a subthreshold dose of angiotensin II amide to cause significant drinking and fluid retention. 5. The drinking responses of male and female rats injected I.V. with hypertonic saline were not modified by prolactin. 6. It is concluded that prolactin may act to increase the net water gain of animals suffering a deficit of the extracellular fluid space but is without effect on stimuli arising from deficits in the intracellular fluid space.
Longitudinal spread of adaptation in the rods of the frog's retina.
Authors: Hemilä S , Reuter T
Published: December 2014

1. The stimulus‐response function of the red rods in the retina of the common frog (Rana temporaria) was determined in different adaptational states by measuring aspartate‐isolated receptor responses. 2. Flash stimuli, background adaptations and bleaches were delivered through the same optical channel forming an oblique light‐beam striking the receptor side of the isolated and flat‐mounted retina at an angle of 10 degrees. 3. When the light was blue‐green and optimally polarized the absorbance of the receptor layer was about 2, from which follows that 70‐80% of the light was absorbed in the distal third of the rod outer segments, i.e. the exposure was local. Homogeneous exposures of the whole rod outer segments were obtained with orange and red lights. 4. Combinations of homogeneous and local stimuli with homogeneous and local adaptations were used to investigate the longitudinal spread of background, intermediate and opsin adaptation, i.e. the sensitivity‐reducing effect of a background light, and the transient and permanent sensitivity losses following a bleach isomerizing 3.5‐26% (usually 10%) of the rhodopsin in the retina. 5. The results obtained were related to predictions based both on the assumption that the adaptation effects spread longitudinally within the rod outer segments and the assumption that they are strictly confined to the disks absorbing the adapting lights. 6. These comparisons reveal that all three types of adaptation spread longitudinally. It is for instance clear that the sensitivity loss observed with homogeneous stimuli and local adaptation (as compared to homogeneous adaptation) is larger than that predicted by the non‐spreading hypothesis. 7. The longitudinal spread of background adaptation is largely finished within 10 sec after turning on the background light, while an efficient spread of the intermediate adaptation effect may require minutes. 8. A background light decreasing the sensitivity by about one log unit decreases the time from flash to response maximum from 5 to 1 sec (small responses). Corresponding opsin adaptation effects are accompanied by less dramatic changes in response kinetics. 9. Independent of adaptation type ‐ homogeneous or local, background, intermediate or opsin ‐ it was found that local stimuli are less efficient that homogeneous stimuli in light‐adapted retinae. This effect can be explained assuming that the sensitivity‐reducing effects are pronounced in the distal than in the proximal parts of the rod outer segments. 10. The opsin adaptation effect following 10% local bleaches decreases the sensitivity to both homogeneous and local stimuli 2‐3 times more than corresponding homogeneous bleaches. This means that the strength of the opsin effect is not related to the average percentage bleached but to the fraction bleached in the distal part of the rod, or generally to the fraction bleached in the most affected region. 11...
The uptake and transmission of protein by neonatal rat enterocytes.
Authors: Morris B , Morris R , Solari R
Published: December 2014

1. Proximal enterocytes transmitted intact immunoglobulin G (IgG) preferentially in the order rat, human, sheep and bovine; the removal from the vascular compartment of these transmitted molecules occurred at about the same rate. 2. Heterologous IgGs are processed similarly to rat IgG: they are either transmitted intact or broken down to less than 1000 mol. wt. fragments. 3. All of the human transferrin removed from the intestine was broken down to less than 1000 mol. wt. fragments, but a small amount of bovine serum albumin (BSA) was transmitted intact. 4. The IgGs and BSA are relatively indigestible molecules whereas human transferrin is relatively digestible. 5. These observations are discussed in the context of receptor‐mediated transmission.
Studies on the atropine‐resistant sacral parasympathetic vascular and motility responses in the cat colon.
Authors: Fasth S , Hultén L , Nordgren S , Zeitlin I J
Published: December 2014

1. Pelvic nerve stimulation in atropinized cats elicits a sustained contraction of the proximal colon and a relaxation of the rectum. Concomitantly there is an immediate but transient vasodilatation which is followed by recurrent increases and a slight post‐stimulatory hyperaemia. Direct stimulation of the pelvic nerve produces secretion of colonic kallikrein and activation of the plasma kinin system. The present study examines whether Trasylol, which inhibits the kinin system, affects the atropine‐resistant responses observed on pelvic nerve stimulation. 2. After I.V. or close I.A. administration of Trasylol, the initial vasodilatation on pelvic nerve stimulation was markedly reduced and in a few experiments completely blocked. The recurrent blood flow increases and the post‐stimulatory hyperaemia observed on prolonged stimulation were completely abolished. In contrast the proximal colonic contraction and the rectal relaxation appeared unchanged after Trasylol. 3. The reactivity of the vascular bed after Trasylol injection was studied by recording the changes of vascular resistance following sympathetic vasoconstrictor fibre activation and infusion of bradykinin before and after Trasylol injection. The responses were quantitatively unchanged excluding an unspecific interference with nervous transmission or vascular smooth muscle reactivity. 4. The results show that the atropine‐resistant vasodilatation in the cat colon as elicited by pelvic nerve stimulation is partly abolished by a kallikrein inhibitor. This observation lends further support to the hypothesis that kinins might be involved in this response. The motor response, however, appears not be dependent on such a mechanism.
Some effects of n‐pentane on the sodium and potassium currents of the squid giant axon.
Authors: Haydon D A , Kimura J E
Published: December 2014

1. Sodium and potassium currents have been recorded in intracellularly perfused squid giant axons before, during and after exposure to solutions of n‐pentane in artificial sea water. 2. The currents were fitted with equations similar to those proposed by Hodgkin & Huxley (1952) and the changes in the parameters of these equations in the presence of pentane were calculated. 3. In the range of membrane potential ‐40 to 40 mV, the time constants for activation (tau m) and inactivation (tau h) of the Na current, and for activation (tau n) of the K current were all reduced by the pentane. 4. The curve of the steady‐state inactivation parameter (h infinity) for the Na current against membrane potential was shifted by the pentane in a hyperpolarizing direction (at h infinity = 0.5 this shift was approx. ‐15 mV in 275 microM‐pentane) and the slope at all potentials was reduced. 5. The curve of the steady‐state activation parameter (m infinity) for the Na current against membrane potential was also shifted by the pentane in a hyperpolarizing direction (in 153 microM‐pentane, 10 mV at m infinity = 0.5). 6. The maximum Na and K conductances gNa and gK were lowered by the pentane, though not usually completely reversibly. 7. The changes in position and slope of the steady‐state inactivation curve have been tentatively accounted for in terms of an increase in membrane thickness.
The effects of chloride substitution on intracellular pH in crab muscle.
Authors: Sharp A P , Thomas R C
Published: December 2014

1. Intracellular pH (pHi) was measured in crab muscle fibres using pH‐sensitive micro‐electrodes. The mean stable pHi was 7.19 +/‐ 00.2 (S.E. of mean) and the corresponding mean membrane potential was ‐64.6 +/‐ 0.4 mV (S.E. of mean) at an external pH of 7.5. 2. The effects on pHi of replacing 20% (100 mM) of the external NaCl by the Na salts of various anions were examined. The anions of weak acid (pK'a greater than 4.5) caused large internal acidifications. The anions of strong acids (pK'a less than 2.6) caused little or no change in pHi. The anions of acids with an intermediate pK'a had varied effects on pHi. In particular salicylate (pK'a = 2.97) was found to cause a large fall in pHi. 3. Increasing the external pH reduced the effects of the anions of weak acids on pHi. It is argued that these effects are the result of the entry and subsequent dissociation of undissociated acid molecules. 4. The results with propionate were quantified by comparing them with the effects of 5% CO2 and were found to be smaller than expected. It is suggested that this is the result of substantial membrane permeability to the propionate anion.
Release of glutamate from the crayfish neuromuscular junction.
Authors: Kawagoe R , Onodera K , Takeuchi A
Published: December 2014

1. The superficial abdominal flow flexor muscle was isolated from the crayfish (Cambarus clarkii) and placed in a bath solution of 100 microliters. The concentration of glutamate in this solution was measured by mass fragmentography using a gas chromatograph‐mass spectrometer. 2. The excitatory post‐synaptic potential (e.p.s.p.) of the slow flexor muscle and its sensitivity to L‐glutamate were similar to those observed in the opener muscle of the dactyl in the walking leg or claw of the crayfish. 3. The background efflux of glutamate during control rest periods was about 20 p‐mole/10 min. Nerve stimulation caused a significant increase in the efflux of glutamate. The net release of glutamate above the background was 11.9 p‐mole/100 microliters. at 10 Hz stimulation and 21.1 p‐mole/100 microliters. at 20 Hz stimulation. 4. When the amplitude of e.p.s.p. was decreased by streptomycin, thereby reducing the muscle contraction, the net release of glutamate by nerve stimulation was not changed. Streptomycin depressed the e.p.s.p. by its action on the post‐synaptic membrane. 5. When the external concentration of Ca was lowered, the amplitude of e.p.s.p. and the net release of glutamate were decreased. 6. It is concluded that L‐glutamate is released from the nerve terminals of the crayfish neuromuscular junction.
The kinetics of post‐vibration tension recovery of the isolated rat portal vein.
Authors: Klemt P , Peiper U , Speden R N , Zilker F
Published: December 2014

1. The kinetics of post‐vibration tension recovery have been examined during electrical, noradrenaline or KCl stimulation of the isolated rat portal vein. 2. Inhibition of isometric contractions produced by a combination of noradrenaline (20 microM) and KCl (53 mM) by longitudinal, 100 Hz sinusoidal vibration increased with increasing vibration amplitude up to a maximum of 78.7% of the active tension. This inhibition was little affected by a decrease in temperature from 37 to 25 degrees C. Recovery of tension after the end of vibration was complete and took place exponentially. The time constant for this recovery was little affected by changes in vibration amplitude, but increased from 1.72 +/‐ 0.09 to 4.35 +/‐ 0.33 sec, for large amplitude vibrations, when the temperature was lowered from 37 to 25 degrees C. 3. The increase in isometric tension during 50 Hz a.c. electrical field stimulation was exponential, apart from a minor initial activation component, and took place with a time constant of 1.25 +/‐ 0.17 sec. Neither delaying nor interrupting development of this contraction with inhibitory vibration altered the time constant for this exponential increase in tension. There was no correlation between the time constant and the maximum active tension achieved after vibration was stopped. 4. Post‐vibration tension recovery during electrical, noradrenaline (20 microM) or KCl (120‐130 mM) stimulation was independent of the nature of the stimulus at comparable times of stimulation, but the time constant increased during exposures of more than 10 sec to either noradrenaline or KCl. With noradrenaline, the increase was from 1.45 +/‐ 0.10 sec after 50 sec of stimulation to 2.24 +/‐ 0.16 sec after 336 sec of stimulation (P less than 0.0005). Such an increase in the time constant may reflect slower cycling of cross‐bridges with an improvement in the efficiency by which contraction is maintained. 5. The kinetics of post‐vibration tension recovery were those of a monomolecular or, as is more likely, a pseudo‐monomolecular chemical reaction. A cross‐bridge attachment model based on such a reaction has been used to interpret the observations.
Effects of bleaching and backgrounds on the flash response of the cone system
Authors: Geisler Wilson S.
Published: December 2014

1. Increment‐threshold functions for flashed backgrounds were measured in the human fovea under several conditions: (1) during dark adaptation following full bleaches, (2) in the presence of steady adapting backgrounds and (3) 500 msec following extinction of adapting backgrounds.

2. To prevent the intense flashed backgrounds from interfering with the course of dark adaptation the inter‐trial interval was continuously increased during dark adaptation. This technique may prove generally useful for presenting suprathreshold stimuli during dark adaptation.

3. All the increment‐threshold functions measured during dark adaptation were found to be roughly shape invariant and continuously accelerating when plotted in log—log co‐ordinates. Furthermore, in order to translate a function obtained at any given time into coincidence with a function obtained at any other time, it had to be translated vertically and horizontally the same number of log units. This is equivalent to adding or removing neutral density filters from in front of the eye.

4. The increment‐threshold functions obtained with steady adapting backgrounds were also continuously accelerating, but could not be brought into coincidence by equal vertical and horizontal translation. However, this became possible again if the adapting background was extinguished during presentation of the flashed background.

5. These results contradict the equivalent‐background hypothesis. None the less, they suggest that under present conditions the effects of bleaches and backgrounds may be similar except that steady backgrounds provide additional quanta which drive the visual system part of the way up its intensity—response function.

6. The conclusions above were supported by applying a simple model based on the equation R = Rmax. In / (In + I1n), which has frequently been used to describe the peak responses of retinal neurones to flashed stimuli. Virtually all of the data reported here were fitted by this simple model with Rmax held constant.

7. The parameters estimated from the model imply that the flash responses measured in the present experiments differ in at least one fundamental way from receptor responses. Even after taking into account changes in the half saturation constant I1, steady backgrounds were found to be much less effective than flashed backgrounds in driving the visual system up its intensity—response function. A subtractive inhibitory network prior to the non‐linear stages responsible for threshold saturation could explain this result.
Activation delays in frog twitch muscle fibres.
Authors: Close R I
Published: December 2014

1. The length dependence of the mechanical latent period and early tension development, uncomplicated by latency relaxation, was determined from responses of single muscle fibres to restimulation at the peak of the isometric twitch at 15 degrees C. 2. The onset of the reactivation response showed little (less than 1.5 X 10(‐7) N) or no latency relaxation. 3. Reactivation latency was minimal (2.8 msec) and constant at 1.9‐2.1 micrometers sarcomere length and it increased by about 3 msec with sarcomere extension to 3.2 micrometers. 4. Reactivation responses showed two stages of early tension development, an initial phase in which tension acceleration increased, and a phase of maximum responsiveness in which tension acceleration was constant; the transition between the two phases occurred about 4.5 msec after the start of the stimulus at 2.2 micrometers sarcomere length and was delayed about 4 msec with increase in sarcomere length to 3.2 micrometers. 5. The square root of the maximum tension acceleration was directly proportional to the degree of overlap of thick and thin filaments in the sarcomere length range 2.3‐3.2 micrometers. 6. It is proposed that the onset of the phase of constant tension acceleration marks the end of the period during which the activator, calcium, is distributed throughout the sarcomere. 7. Analysis of early tension transients in relation to myofibril structure showed that length‐dependent changes in reactivation latency and time of onset of constant tension acceleration were probably brought about mainly by alteration of the kinetics of distribution of activator within the myofibril and by changes in the diffusion distance between activator‐release sites ner the end of the sarcomere and the tension‐generating sites. 8. There was a 2 msec myofibril priming delay in the rise of tension in twitch responses that was not seen in reactivation responses; the possible origin of that delay is discussed in relation to structural changes accompanying activation and to competition between calcium‐binding structures. 9. The onset of twitch latency relaxation occurred within about 250 microseconds after the time corresponding to latency of the earliest reactivation responses and appeared to signal the start of a process that took place after the arrival of calcium among the myofilaments. The origin of latency relaxation is discussed.
Brain stem sites mediating specific and non‐specific temperature effects on thermoregulation in the pekin duck.
Authors: Martin R , Simon E , Simon‐Oppermann C
Published: December 2014

1. Thermodes were chronically implanted into various levels of the brain stem of sixteen Pekin ducks. The effects of local thermal stimulation on metabolic heat production, core temperature, peripheral skin temperature and respiratory frequency were investigated. 2. Four areas of thermode positions were determined according to the responses observed and were histologically identified at the end of the investigation. 3. Thermal stimulation of the lower mid‐brain/upper pontine brain stem (Pos. III) elicited an increase in metabolic heat production, cutaneous vasoconstriction and rises in core temperature in response to cooling at thermoneutral and cold ambient conditions and, further, inhibition of panting by cooling and activation of panting by heating at warm ambient conditions. The metabolic response to cooling this brain stem section amounted to ‐0.1 W/kg. degrees C as compared with ‐7 W/kg. degrees C in response to total body cooling. 4. Cooling of the anterior and middle hypothalamus (Pos. II) caused vasodilatation in the skin and did not elicit shivering. The resulting drop in core temperature at a given degree of cooling was greater than the rise in core temperature in response to equivalent cooling of the lower mid‐brain/upper pontine brain stem. 5. Cooling of the preoptic forebrain (Pos. I) and of the myelencephalon (Pos. IV) did not elicit thermoregulatory reactions. 6. It is concluded that the duck's brain stem contains thermoreceptive structures in the lower mid‐brain/upper pontine section. However, the brain stem as a whole appears to contribute little to cold defence during general hypothermia because of the inhibitory effects originating in the anterior and middle hypothalamus. Cold defence in the duck, which is comparable in strength to that in mammals, has to rely on extracerebral thermosensory structures.
Critical bands in cat spatial vision.
Authors: Blake R , Martens W
Published: December 2014

1. The ability of cats to detect sinusoidal grating patterns superimposed on one‐dimensional visual noise was assessed using behavioural methods. 2. The magnitude of elevation in contrast threshold due to noise increased monotonically within limits with increasing noise contrast. 3. Visual noise was filtered using various techniques (band‐reject, low‐pass, high‐pass and band‐pass noise); filtered noise resulted in threshold elevation only when it contained frequencies similar to the test frequency. 4. In all cases the masking functions indicated that the band widths of the channels mediating detection ranged from +/‐ 0.50 to +/‐ 0.75 octaves across three spatial frequencies and that the channel sensitive to low spatial frequencies was asymmetrical in its tuning. 5. The spatial properties of these psychophysical detecting channels closely resemble the spatial frequency selectivity exhibited by some cat cortical neurones, both in the general narrowness of tuning and the asymmetry in tuning at lower, but not higher, spatial frequencies.
Calcium‐mediated inactivation of the calcium conductance in caesium‐loaded giant neurones of Aplysia californica.
Authors: Eckert R , Tillotson D L
Published: December 2014

1. The intracellular potassium in giant neurones of Aplysia californica was replaced with caesium by a method utilizing the ionophore nystatin. Because caesium ions have low permeability through potassium channels outward currents during voltage‐clamp depolarization were strongly curtailed after the caesium loading procedure and the subsequent wash‐out of the ionophore. 2. The calcium current elicited by a test voltage‐clamp depolarization (pulse 2) was depressed following the entry of calcium elicited by a prior depolarization (pulse 1). 3. The percentage depression of the test current was a linear function of the pulse 1 current‐time integral, and thus appears to be related linearly to the amount of calcium carried into the cell during pulse 1. This linear relation was maintained when calcium entry was varied by changes in external calcium concentration, by altered pulse 1 amplitude and altered pulse 1 duration. Depression was substantially reduced by injection of EGTA, and by substitution of barium for extracellular calcium. 4. The calcium current was unaffected by prior hyperpolarization of the membrane or by prior depolarizations to about ECa. Depression of the current was not altered by addition of extracellular 50 mM‐TEA or by a strong hyperpolarization between the conditioning and test pulses. 5. The rate relaxation of the inward current during a given depolarization depended on the rate of entry and accumulation of free calcium. Relaxation under a given command potential became slower when calcium was partially replaced with magnesium so as to produce a smaller calcium current, or when accumulation of intracellular free calcium was retarded by injected EGTA or by barium substitution for extracellular calcium. 6 Evidence is considered that accumulation of calcium ions at the cytoplasmic surface of the membrane leads to inactivation through an action upon the calcium conductance. Reduced driving force and intracellular surface‐charge neutralization do not adequately account for the observed depression of the calcium current resulting from intracellular accumulation of calcium ions.
Transport of cholecystokinin‐octapeptide‐like immunoreactivity toward the gut in afferent vagal fibres in cat and dog.
Authors: Dockray G J , Gregory R A , Tracy H J , Zhu W Y
Published: December 2014

1. The distributions of gastrin‐ and cholecystokinin‐like immunoreactivities in the dog and cat vagus nerves have been studied after nerve section and ligation. 2. In dogs, there was an increase in cholecystokinin‐octapeptide‐like immunoreactive material on the cranial side of ligatures on the thoracic or cervical vagi. When pairs of ligatures were tied on the cervical vagi there was accumulation proximal, and a slight decrease distal to, the upper ligature. There was also a modest increase distal to the lower ligature. 3. In cats, section of the vagus above the nodose ganglion, and hence degeneration of the efferent fibres, did not prevent increases in cholecystokinin‐octapeptide‐like immunoreactivity on the cranial side of ligatures which were later tied below the ganglion. Removal of the superior cervical ganglion had no effect on the accumulation of immunoreactive material above the ligatures. Section of the vagus below the nodose ganglion, and hence degeneration of both afferent and efferent fibres, abolished the accumulation on the cranial side of ligatures which were later tied below the section. Cholecystokinin‐octapeptide‐like material is therefore localized to afferent fibres with cell bodies in the nodose ganglion. 4. Immunoreactive forms were characterized by gel filtration and ion exchange chromatography, and the use of region‐specific antisera. In all cats, and all but one dog, a molecule with the properties of sulphated cholecystokinin octapeptide was found to predominate. In some cats (30%) and dogs (26%) a molecule with the properties of heptadecapeptide gastrin (G17) was identified; concentrations of G17 were generally low compared with cholecystokinin octapeptide. In three dogs (20%) there was an accumulation of heptadecapeptide gastrin above the ligatures. 5. Axonal transport of cholecystokinin octapeptide in the vagus is consistent with a neuro‐regulatory role for this peptide. However, the functional significance of its localization in afferent fibres, and transport towards the periphery, remains to be determined.
Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.
Authors: Tyce G M , Yaksh T L
Published: December 2014

1. Superfusates taken from spinal cords of cats anaesthetized with chloralose and urethane were assayed for endogenous serotonin and noradrenaline by high‐pressure liquid chromatography with electrochemical detection. 2. Stimulating the dorsolateral funiculus, caudal to a spinal transection, enhanced in a frequency‐dependent manner the levels of monoamines in the spinal superfusate. 3. Tyramine added to the superfusate enhanced the release of noradrenaline and serotonin. 4. In cats with intact neuraxes, stimulation of the sciatic nerve at high, but not low intensities produced a 2‐ to 3‐fold increase in the levels of monoamines in the spinal superfusate. This evoked monoamine efflux was attenuated by cold block of the cervical spinal cord. 5. Stimulation of the infraorbital branch of the trigeminal nerve evoked the release of noradrenaline and serotonin from the lumbar cord in animals with intact neuraxes. Cold block of the cervical cord blocked trigeminal‐evoked release of lumbar serotonin and noradrenaline. 6. That the monoamine efflux was not due to elevations in blood pressure was indicated by the failure of vasoxyl, an alpha‐agonist producing hypertension, to evoke any changes in spinal monoamine levels. 7. The monoamine release was not dependent upon either an opiate‐sensitive link or upon the activation of the sympathetic ganglia, because systemic administration of naloxone (an opiate antagonist) and chlorisondamine (a ganglionic blocking agent) failed to antagonize the evoked release of amines. 8. These results suggest the existence of a spinopetal monoamine system which is activated by peripheral stimuli. The modulatory influence associated with increasing monoamine tone in the spinal cord clearly indicated that somatic stimuli may activate a descending monoamine pathway which serves to modulate the magnitude of the ascending sensory message.
A comparison of the recurrent inhibition of alpha‐ and gamma‐motoneurones in the cat.
Authors: Ellaway P H , Murphy P R
Published: December 2014

1. The degree of recurrent inhibition of tonically firing alpha‐ and gamma‐motoneurones to triceps surae muscles was assessed in decerebrated cats by measuring the change in probability of firing caused by an antidromic volley in other motoneurone axons. 2. In nine cats 91% (thirty‐one out of thirty‐three) of alpha‐ and 54% (twenty‐five out of forty‐six) of gamma‐motoneurones could be inhibited by antidromic volleys in alpha‐motoneurone axons. 3. The degree of recurrent inhibition, expressed as the average reduction in probability of firing during the response, was typically in the range of 59‐95% for alpha‐motoneurones compared to 20‐85% for gamma‐motoneurones. 4. The duration of recurrent inhibition was 20‐50 msec for alpha‐motoneurones and 5‐40 msec for gamma‐motoneurones. The duration was dependent upon the frequency of firing of a neurone, being shorter at high frequencies than at low frequencies. When alpha‐ and gamma‐motoneurones had similar frequencies of discharge the durations of their recurrent inhibition were comparable. 5. Raising the strength of electrical stimulation to elicit an antidromic volley in gamma‐ as well as alpha‐motoneurone axons never produced or increased recurrent inhibition in either type of motoneurone. 6. The quantitative differences in recurrent inhibition of alpha‐ and gamma‐motoneurones are discussed in relation to the control of firing frequency.
Spatial contrast sensitivity of cells in the lateral geniculate nucleus of the rat.
Authors: Lennie P , Perry V H
Published: December 2014

1. The responses to visual stimuli of cells in the dorsal lateral geniculate nucleus of the rat were recorded with micro‐electrodes. 2. Maps made with small spots of light showed that most units had concentrically organized receptive fields. Some units gave ‘on‐off’ responses to spots flashed anywhere within the receptive field. These units were not directionally selective. 3. By the use of grating patterns as stimuli, units with concentrically organized receptive fields could be divided into groups that showed linear or non‐linear spatial summation. Those unit showing linear spatial summation behaved like the ‘X’ cells of the cat, those showing non‐linear summation like ‘Y’ cells. 4. ‘On‐off’ units showed non‐linear spatial summation of a kind that readily distinguished them from Y cells. 5. Measurements of spatial contrast sensitivity made with moving gratings showed, for both X and Y cells, peak sensitivities for spatial frequencies between 0.05 and 0.09 c/deg X and Y cells were not distinguished by their preferred spatial frequencies at any eccentricity.