bluuebunny/crossref_metadata_2025 huggingface dataset:
Topography of cutaneous mechanoreceptive neurones in dorsal root ganglia of skin‐grafted frogs
Authors: Baker R. E. , Corner M. A. , Veltman W. A. M.
Published: December 2014

1. Topographical distribution patterns of dorsal root ganglion (d.r.g.) cutaneous neurones providing innervation to various body surfaces were examined in doublypithed Discoglossus pictus frogs.

2. Using electrophysiological methods, sensory neurones innervating back skin were observed to predominate on the dorsal ganglionic surfaces, while belly skin neurones were most prevalent in the caudal half of the d.r.g. ventral surfaces. Flank neurones clustered in the medial half of d.r.g. ventral surfaces.

3. Cutaneous neuronal distribution patterns within the d.r.g. of 180° skin grafted animals were indistinguishable from those observed in control frogs.

4. Sensory neurone distribution patterns were found to be altered in all animals with single skin type grafts. Projection patterns were always heaviest towards the autograft, which was on the opposite body surface (i.e. dorsally located d.r.g. sensory neurones projected to back skin on the frog's ventrum, while ventrally located neurones projected to belly skin on the frog's dorsum).

5. The results are discussed in the light of several selective outgrowth mechanisms which have been proposed as a possible underlying basis for the development of misdirected wiping reflex behaviour in skin grafted anurans. The findings indicate that none of the proposed selective growth mechanisms can account adequately for the development of misdirected wiping reflexes, at least in the species studied.

6. It is suggested that selective cell replacement, based upon competition among prespecified cutaneous neurones, might best account for the development of normal and misdirected wiping reflexes in frogs.
The effect of increasing the plasma magnesium concentration on renin release from the dog's kidney: interactions with calcium and sodium.
Authors: Wilcox C S
Published: December 2014

1. A denervated 'auto‐transplanted' dog's kidney preparation was developed to study renin release into renal plasma and lymph. The function of the 'transplant' was compared with that of its partner. In the 'basal' state it had a similar rate of plasma and urine flow, Na, Ca, Mg and Cl excretion but a lower rate of glomerular filtration and K excretion and a lower urinary osmolality. In the 'basal' state the 'transplant' did not release renin into plasma, but invariably released it into lymph. 2. Infusions of MgCl2 solutions into the renal artery which raised the renal plasma Mg concentration (PMg) by 0.1‐2 m‐mole.1.‐1 provoked a concentration‐related increase in renin release into plasma. This was due to a rise in the veno‐arterial renin difference and in the renal plasma flow rate. Blood pressure and Na excretion were unaltered. 3. In other experiments, an increase in PMg of 1.5‐2.5 m‐mole.1.‐1 was also found to increase renin release into lymph. 4. When the plasma Ca concentration was doubled by infusion of CaCl2 into one renal artery, an increase in PMg of 1.5‐2.5 m‐mole.1.‐1 no longer increased renin release into plasma or lymph. 5. When the plasma NaCl concentration was raised by 8‐15 m‐mole.1.‐1 by infusion of hypertonic saline into the renal artery, MgCl2 infusion failed to increase renin release until PMg was raised by more than 3 m‐mole.1‐1. 6. The results demonstrate that hypermagnesaemia stimulates renal renin release by a mechanism that is independent of the renal nerves, or of any changes in blood pressure or sodium excretion, but which is antagonized by concurrent hypercalcaemia or hypersalaemia. The possibility is discussed that Mg is reabsorbed from the tubular into the interstitial fluid where it antagonizes the action(s) of Ca on renin release from the juxtaglomerular cells.
Nervous release of vasoactive intestinal polypeptide in the gastrointestinal tract of cats: possible physiological implications.
Authors: Fahrenkrug J , Haglund U , Jodal M , Lundgren O , Olbe L , de Muckadell O B
Published: December 2014

1. The release of vasoactive intestinal polypeptide (VIP) into blood from the gastrointestinal tract was studied when eliciting autonomic nervous effects known to be mediated via non‐adrenergic, non‐cholinergic nerve fibres. All studies were performed on animals given atropine. 2. Electrical stimulation of the low threshold vagal fibres to the stomach did not significantly change gastric volume or VIP concentration in the venous effluent from the stomach. Stimulating the high threshold fibres, on the other hand, produced a gastric relaxation concomitant with a significant increase of venous plasma VIP concentrations. When eliciting a similar vagal relaxation of the stomach by distending a balloon the oesophagus a significant increase of venous plasma VIP concentration was also recorded. 3. Mechanical stimulation of the mucosa of the small bowel increased intestinal blood flow and a significant increase of venous plasma VIP concentration was observed. 4. Stimulation of the pelvic nerves to the colon produced a transient vasodilation and a significant increase of VIP in the venous effluent from the large bowel. A maintained vasodilation in the colon was induced by mechanically stimulating the rectal mucosa. This vascular response was accompanied by a significant raise of venous plasma VIP concentration. 5. The results demonstrate that all the studied nervous effects known to be mediated via non‐adrenergic, non‐cholinergic nerve fibres were accompanied by significant increases of the VIP concentration in the venous effluent. The possible physiological implications of these findings are discussed and it is proposed that VIP may be a neurotransmitter in the gastrointestinal tract.
Studies on neural mechanisms of the gustatory‐salivary reflex in rabbits.
Authors: Kawamura Y , Yamamoto T
Published: December 2014

1. Submandibular salivary secretion and the electrical activity of the parasympathetic preganglionic fibres innervating the submandibular gland were recorded in decerebrated rabbits in response to taste stimulation of the tongue. The electrical activity of a taste nerve (chorda tympani) responding to varying taste stimuli was also recorded in the deeply anaesthetized rabbits. These data representing input and output information were compared with each other. 2. Sucrose, quinine, tartaric acid, NH4Cl and KCl which induced a long‐lasting response in the taste nerve evoked a continuous salivary secretion, and those chemicals such as NaCl, CaCl2 and MgCl2 which induced a transient activity of the nerve evoked a transient salivary secretion. 3. The magnitude of responses of the whole taste nerve to moderate concentrations of chemical stimuli applied to the anterior part of the tongue was statistically significantly correlated with the volume of reflex submandibular salivation. 4. Parasympathetic preganglionic fibres to the salivary gland were classified into two types according to their responsiveness to taste stimuli; taste‐sensitive and taste‐insensitive fibres. The magnitude of electrical activity of the taste nerve fibres was significantly correlated with that of the taste‐sensitive preganglionic fibres to stimulation of the tongue with varying taste stimuli. 5. By calculating correlations between responses of the taste fibres to each of the four basic taste stimuli and all the stimuli tested, it was concluded that afferent inputs from the taste of sucrose and NaCl were different, while those of HCl and quinine were similar. On the other hand, it was found by the same procedure for the preganglionic fibres that sucrose and NaCl, and HCl and quinine produced a similar response profile, respectively. This result means that the afferent taste inputs are processed into appropriate outputs (perhaps on a hedonic basis) in the lower brain stem without involvement of higher central nervous mechanisms.
Transmitter release from normal and degenerating locust motor nerve terminals.
Authors: Hodgkiss J P , Usherwood P N
Published: December 2014

1. An analysis has been made of spontaneous and evoked transmitter release from terminals of 'fast' excitatory motor axons on locust muscle fibres using intra‐ and extracellular recording together with a Ca‐electrode technique for activating transmitter release from single nerve terminals on multiterminally innervated muscle fibres. 2. Spontaneous intracellular miniature excitatory junction potentials (m.e.j.p.s), recorded at active spots on these muscle fibres, occurred non‐randomly with frequent bursts of m.e.j.p.s. 3. M.e.j.p.s of subnormal amplitude were also seen but contributed only a small fraction of the minature discharge. 4. The amplitude distribution of intracellularly recorded excitatory junction potentials (e.j.p.s) evoked during ionophoretic application of Ca onto single nerve terminals was adequately predicted by Poisson statistics. 5. During the course of nerve terminal degeneration m.e.j.p.s of subnormal amplitude became more frequent and eventually formed the major part of the miniature discharge. Transmitter quanta responsible for 'small' m.e.j.p.s did not contribute to evoked release either at normal or degenerating terminals. Evoked transmitter release from degenerating axon terminals before excitation‐secretion coupling failure conformed to Poisson statistics. 6. It is concluded that more than one release mechanism operates on the transmitter pool or pools in locust motor nerve terminals.
Mobilization of colonic kallikrein following pelvic nerve stimulation in the atropinized cat
Authors: Fasth S. , Hulten L. , Johnson B. Julienne , Nordgren S. , Zeitlin I. J.
Published: December 2014

1. Pelvic nerve stimulation (p.n.s.) in cats induces atropine‐resistant colonic vasodilatation and colonic contraction. The effects of this on cat colon are mimicked by synthetic bradykinin infusions. The present study examines the effect of p.n.s. on the activation of kallikrein, the kinin‐forming enzyme present in colonic tissue and its effects on the plasma kinin system in the atropinized cat.

2. Mean level (±
S.D.) of mucosal kallikrein was found to be about 37 times higher in unstimulated colonic mucosa (300 ± 100 ng bradykinin equivalents min−1g−1) than in the underlying muscle (8·2 ± 6·3 ng bradykinin equiv min−1g−1).

3. After a p.n.s. of 5 min, mean kallikrein level in colonic muscle was 7·3 ± 3·5 ng bradykinin equiv min−1g−1, which was not significantly different from the control muscle kallikrein. However, there was an 86% fall in mucosal kallikrein to 41·3 ± 34·7 ng bradykinin equiv min−1g−1 after 5 min p.n.s., indicating a rapid activation and secretion of mucosal kallikrein.

4. Secretion of mucosal kallikrein was paralleled by specific depletion of plasma kininogen, the precursor of active kinin in blood draining the colon. The mean plasma kininogen level fell to 79 and 68% of the prestimulated value (3·1 ± 1·1
S.D. μg bradykinin equiv per ml. plasma) after 5 and 10 min p.n.s. respectively. Total plasma protein and haematocrit remained unaltered excluding non‐specific changes due to protein extravasation or haemodilution and indicating utilization of the plasma kinin precursor.

5. Following 2 hr p.n.s., raised levels of kallikrein were detected in both colonic muscle (28 ± 2·0 bradykinin equiv min−1g−1) and mucosa 434 ± 118 ng bradykinin equiv min−1g−1). Preliminary studies using a kallikrein inhibitor indicated that the increased kallikrein levels originated from plasma.

6. Direct stimulation of the parasympathetic pelvic nerve in the atropinized cat thus produced activation of the plasma kinin system in the colon and formation of free kinins may be responsible for the mucosal vasodilatation and strong motor contraction which is not blocked by large doses of atropine. The observation that prolonged stimulation causes extravasation of plasma kallikrein, a potential inflammatory mediator, into the tissues may be of clinical significance.
Direct inhibition of gastric secretion and mucosal blood flow by arachidonic acid.
Authors: Konturek S J , Mikoś E , Pawlik W , Waluś K
Published: December 2014

1. Gastric acid and pepsin secretion stimulated almost maximally by i.v. infusion of histamine, the mucosal blood flow, and the immunoreactive prostaglandin E (PGE) content have been measured following arachidonic acid administration either intra‐arterially or topically to the mucosa of the fundic portion of a stomach kept in a Lucite chamber. 2. Arachidonic acid administered directly to the stomach produced a marked and significant inhibition of histamine‐induced gastric secretion accompanied by a reduction in mucosal microcirculation and a rise in the immunoreactive PGE content in the gastric juice. 3. These secretory and circulatory changes induced by arachidonic acid were prevented by pretreatment of the gastic mucosa with indomethacin, a potent inhibitor of the prostaglandin synthetase system. 4. Arachidonic acid infused intra‐arterially in graded doses resulted in a dose‐dependent reduction in gastric acid secretion, mucosal blood flow and cyclic AMP mucosal content. 5. These studies indicate that arachidonic acid applied directly to the stomach causes a marked gastric secretory inhibition, probably due at least in part to the enzymic transformation of arachidonic acid to prostaglandins and possibly other active lipids responsible for the changes in the gastric mucosal microcirculation and cyclic AMP mucosal content.
Extracellular potassium accumulation in voltage‐clamped frog ventricular muscle.
Authors: Cleemann L , Morad M
Published: December 2014

1. Application of voltage clamp pulses (1‐‐10 sec) to frog ventricular strips causes temporary changes in the extracellular K concentration. 2. The changes in the extracellular K concentration can be estimated from (a) slowly decaying post‐clamp after‐potentials, (b) changes in the action potential duration, and (c) measurements with a K‐selective micro‐electrode. 3. The depolarization of the resting potential and the shortening of the action potential are present in approximately the same proportions during voltage‐clamp induced extracellular K accumulation and during perfusion with a K‐ricn Ringer solution but small consistent differences are noticed. 4. The measurements of the after‐potential, the action potential shortening, and the K‐electrode response were analysed as indicators of extracellular K+ activity and it was concluded that the after‐potential provides the most convenient and reliable estimate of the absolute magnitude of the voltage‐clamp induced extracellular K accumulation. 5. The depolarizing after‐potentials decay more slowly than the hyperpolarizing after‐potentials but it is found that this reflects the selectivity of the membrane to K+ concentrations as predicted by the Nernst or the Goldman equations. 6. Analysis of the redistribution of accumulated K+ from the decay of the after‐potential suggests that the major part of the redistribution process can be described by a single time constant (2‐‐4 sec). A much longer time constant is required for a smaller component of the 'tail' in order to bring [K]o to the normal resting state. 7. N‐shaped relations similar to the 'steady state' current‐voltage relation are obtained when the post‐clamp after‐potential, the action potential shortening, and the K‐electrode response are plotted versus the clamped membrane potential. The maxima of these curves are located around ‐40 mV and the minima around ‐20 mV. 8. In spite of a significant outward membrane current (1‐‐1.5 microamperemeter) in the minimum region (‐20 mV), the post‐clamp after‐potential is often hyperpolarizing in nature suggesting extracellular K depletion. 9. These findings indicate that the K efflux is lower at ‐20 mV than at both higher and lower potentials and suggest that the N‐shape 'steady state' current‐voltage relation mainly reflects the voltage dependency of the K current. 10. A theory for K accumulation in a single compartment is presented which predicts that a simple linear RC‐circuit may describe the electrical response of the preparation in a limited potential range around the resting potential. The extracellular accumulation space was estimated to be 13‐‐16% of the total volume of the preparation. It is tentatively suggested that the accumulation space is equivalent to the subendothelial fraction of the extracellular space.
The influence of corticosteroids on the secretion of corticotrophin and its hypothalamic releasing hormone
Authors: Buckingham Julia C.
Published: December 2014

1. The effects of stress, adrenalectomy and corticosterone treatment on the functional activity of the hypothalamo‐pituitary‐adrenocortical system have been studied using highly sensitive and precise bio‐assay methods for the determination of ACTH and CRH.

2. Adrenalectomy resulted in a rise and corticosterone treatment a fall in the hypothalamic CRH content and the plasma ACTH concentration.

3. Stress caused a fall followed by a rise in the hypothalamic CRH content, a rise in the pituitary and plasma ACTH concentrations and an increase in the plasma corticosterone concentration.

4. The stress‐induced changes in hypothalamic CRH content and pituitary and plasma ACTH were exaggerated in adrenalectomized rats but normal in adrenalectomized rats treated with corticosterone. They were also normal in animals injected
I.P. with corticosterone 15 min before the stress but inhibited in those similarly treated 60 min previously.

5. The ability of adenohypophyses and hypothalami to synthesize and release in vitro ACTH and CRH respectively in response to trophic stimuli was exaggerated in glands removed from adrenalectomized rats and reduced in those removed from corticosterone‐treated rats.

6. Addition of corticosterone to the pre‐incubation medium reduced the capacities of adenohypophyses and hypothalami removed from untreated rats to synthesize and release ACTH and CRH respectively.
The transport of the lead cation across the intestinal membrane
Authors: Blair J. A. , Coleman I. P. L. , Hilburn M. E.
Published: December 2014

1. The transport of the lead cation has been investigated using the everted sac preparation of Wilson & Wiseman (1954).

2. Only a small percentage of lead was transported into the serosal compartment but there was a rapid and massive uptake onto the tissue. There was no significant difference in the amount of lead cations transported across different regions of the small intestine.

3. Both the rate of transport into the serosal compartment and the tissue uptake increased linearly with increasing concentration of the lead cation, from 10−7
M to 5 × 10−5
M. Little evidence for saturation of serosal transport or tissue uptake was found.

4. Lead transport into the serosal compartment appeared to be related to water movement, but was little affected by changes in glucose concentration and temperature.

5. It is concluded that lead is transported into the serosal space by a process of passive diffusion linked to water transport.

6. The interaction between lead ions and the intestinal tissue was extremely tenacious and displayed characteristics of covalent bonding.

7. It is suggested that the lead cation interacts with tissue phosphate ions thus removing lead ions from the transport pool. Chelation of lead to form a neutral species reduces this interaction and also promotes transport.
Non‐electrolyte permeability of trout gills: effect of temperature and adrenaline
Authors: Isaia J.
Published: December 2014

1. The gill permeability to various non‐electrolytes (Ps) was measured in fresh‐water and sea‐water adapted trout (Salmo gairdneri). This study was performed in vitro using a ‘head‐perfused’ preparation. The influence of temperature and adrenaline (10−6
M) on permeability to non‐electrolytes was also investigated.

2. During salt adaptation Pbutanol and Pwater decrease, Pmannitol rises and Pdextran stays constant. In view of recently acquired morphological data these results back up the hypothesis of different pathways across the gill epithelium (transcellular, vesicular and paracellular) according to the physico‐chemical characteristics of the molecules. The low selectivity of the gill epithelium as a function of the liposolubility of the molecules used testifies to the hydrophilic nature of diffusion across this epithelium, a feature becoming more pronounced during salt adaptation.

3. The activation energies are about 4 kcal/mol, an energy comparable to diffusion in water for most of the substances tested, exceptions being butanol for fresh‐water adapted gills and water for fresh‐water and sea‐water adapted gills. Arrhenius plots for butanol in fresh water gills show a transition temperature at 15 °C, suggesting an increased membrane lipid fluidity above this temperature.

4. Adrenaline has no effect on Pmannitol and Pdextran, but increases Pbutanol and Pwater selectively according to the adaptation medium (+ 160% and + 100% in fresh water and + 25% and + 20% in sea water respectively). These results point to an effect of this catecholamine on the membrane lipid fluidity.
The effect of nutritional state on neuromuscular transmission in the rat.
Authors: Kelly S S
Published: December 2014

1. Evoked end‐plate potentials (e.p.p.s) were recorded in phrenic nerve‐hemidiaphragm preparations from rats which had been subjected to periods of dietary restriction. 2. The mean quantum content of the first e.p.p. of trains of e.p.p.s was significantly increased after 1 week of dietary restriction in 30‐day‐old but not in 110‐day‐old rats. 3. The mean quantum content of plateau e.p.p.s elicited at a frequency of 10 Hz was not significantly affected by brief periods of dietary restriction in either 30‐day‐old or 110‐day‐old rats. 4. In the younger animals there was found to be a decrease in the safety factor of neuromuscular transmission following dietary restriction when this parameter was calculated using previously reported values for the amplitude of spontaneous miniature end‐plate potentials (m.e.p.p.s) after such a restricted diet. 5. Such rapid changes in neuromuscular transmission following brief periods of dietary restriction indicate that great care is required in the choice of adequate control animals when food intake is altered by experimental procedures.
Characteristics of the internal anal sphincter and the rectum of the vervet monkey.
Authors: Rayner V
Published: December 2014

1. The physiology of the internal anal sphincter of the vervet monkey was investigated. 2. Strips of sphincter in vitro contracted to noradrenaline and adrenaline; adrenoceptors were mainly alpha‐excitatory. Strips of rectal circular muscle relaxed to noradrenaline and contained both inhibitory alpha‐ and beta‐adrenoceptors. 3. All strips contracted to acetylcholine. After hyoscine or atropine, high doses of acetylcholine relaxed all strips by stimulating intramural inhibitory neurones as relaxations were blocked by tetrodotoxin and hexamethonium. Nicotine and DMPP gave relaxations with similar characteristics. 4. It was concluded that relaxations to acetylcholine, nicotine and DMPP were not adrenergic as relaxations still occurred in strips from sympathetically denervated or reserpinized animals. The block of these relaxations by propranolol and guanethidine was considered to be unrelated to their actions as adrenergic blocking drugs. 5. All strips relaxed to field electrical stimulation (1‐‐5 Hz) through stimulation of intramural inhibitory neurones as tetrodotoxin blocked these relaxations. Adrenergic blocking drugs, prior reserpinization or prior section of the hypogastric nerves did not block these responses. The relaxations were not therefore adrenergic. 6. 5‐Hydroxytryptamine relaxed all strips but was not the transmitter in relaxations to acetylcholine, DMPP or nicotine, nor to field electrical stimulation, as desensitization of strips of 5‐HT did not alter these responses. 7. The circular smooth muscle of the internal anal sphincter had a dense terminal adrenergic innervation which rapidly decreased orad. 8. In vivo, hypogastric nerve stimulation relaxed the rectum but contracted the sphincter. Sacral nerve root stimulation caused an after‐contraction in both rectum and sphincter. In vivo, a close arterial injection of adrenaline or noradrenaline inhibited the spontaneous contraction waves of the rectum, but contracted the sphincter. Both these responses were blocked by phentolamine. 9. It was concluded that the internal anal sphincter is a discrete high pressure zone which was excitatory cholinergic and adrenergic innervations and an inhibitory non‐adrenergic innervation.
Diffusional inhomogeneity: gas mixing efficiency in the new‐born lung.
Authors: Bolton D P
Published: December 2014

1. The results of 105 nitrogen washouts on seventy‐six new‐born babies are presented; the mean lung volume (functional residual capacity, FRC) of the seventy‐six babies measured at more than 1 hr of age was 77.5 +/‐ 2.9 (S.E. of mean; S.D. = 25.4). 2. The mean gas mixing efficiency was 0.466 +/‐ 0.0097 (S. E. of mean; S.D. = 0.096). The reasons for the difference between this figure and the normal for adults of 0.66‐‐0.76 are discussed, and it is suggested that the very much greater turnover rate of gas within the lungs is responsible for diffusion inefficiency. 3. Calculations indicate that there is a tenfold fall in diffusion inefficiency for every 9.8 sec turnover time (the time for VE to equal VFRC). In the baby the turnover time is 5‐‐6 sec on average but with a very wide spread; in the adult it is of the order of 30 sec, so that diffusion inefficiency of gas in the lung would be only 0.001 or 0.1%. 4. The significance of this is that the effective alveolar ventilation of the average neonate is less than half the total ventilation (as opposed to two‐thirds if deadspace only is considered), becoming a smaller fraction of VE on hyperventilation. This would explain discrepancies in the calculation of alveolar carbon dioxide levels from the output of that gas and the non‐deadspace ventilation.
Mechanics of the trachea and behaviour of its slowly adapting stretch receptors.
Authors: Mortola J P , Sant'Ambrogio G
Published: December 2014

1. The trachea is constructed by a series of U‐shaped cartilaginous rings supporting a membranous posterior wall. We have studied separately the pressure‐volume relationships of the two components. 2. The motion of the membranous posterior wall contributes most to the tracheal volume change caused by any given transmural pressure change; the cartilaginous rings provide a semi‐rigid support to the posterior wall and have a far greater compliance with negative than positive transmural pressure. 3. The response of tracheal stretch receptors to transmural pressure can be explained by the mechanical coupling between cartilages and posterior wall. They respond both to positive and negative transmural pressure, they are active at zero transmural pressure and have a point of least activity with small negative transmural pressures. 4. The stress‐strain relationship of the posterior wall has been studied in static and dynamic conditions in control situations and after removal of either the tunica fibrosa or the trachealis muscle. Each of these two components contributes to the stiffness of the posterior wall, with the trachealis muscle providing most of its viscosity. 5. The response of tracheal stretch receptors to transverse traction of the posterior membranous wall has been studied in both static and dynamic conditions before and after removal of the tunica fibrosa. The behaviour of these receptors reflects the visco‐elastic properties of the trachealis muscle in which they have been localized.
Mossy and climbing fibre mediated responses evoked in the cerebellar cortex of the cat by trigeminal afferent stimulation.
Authors: Cody F W , Richardson H C
Published: December 2014

1. The trigeminal input to the cerebellar cortex was studied by recording mass and unitary resonses evoked by electrical stimulation of individual trigeminal cutaneous and muscle nerve branches, in cats lightly anaesthetized with sodium thiopentone. 2. The trigeminal projection area of the cerebellar cortex comprised essentially lobule HVI, but included adjacent folia of lobules HV and HVIIA. 3. Each trigeminal branch had a 'patchy' representation throughout the projection area and there was extensive convergence of individual afferents at each site. Exact combinations of convergent inputs varied between loci, the projection from the muscle nerve being weaker. No other differential representation of individual trigeminal branches was evident. 4. Responses were evoked by stimulation of both ipsi‐ and contralateral trigeminal afferents but contralateral projections were present at fewer sites. 5. Mass responses to stimulation of individual trigeminal branches comprised mossy fibre and climbing fibre‐mediated potentials, although both components were not always present. Latencies for mossy and climbing fibre responses, evoked by ipsilateral nerve stimulation, were in the ranges 5‐‐8 msec and 11‐‐29 msec respectively. 6. Unitary responses of Purkinje cells activiated by trigeminal inputs also revealed convergence from individual ipsilateral afferent sources (28% influenced by one ipsilateral trigeminal branch, 48% by two branches, 17% by three branches and 7% by four branches). 7. Response patterns comprised one or more of the following: short latency (3‐‐8 msec) simple, mossy fibre‐mediated spikes, 'delayed' (10‐‐25 msec) simple spikes and climbing fibre‐mediated multiple spike bursts (9‐‐35 msec).
On the time course of the electrical response of salivary gland cells of Nauphoeta cinerea to ionophoretically applied dopamine.
Authors: Blackman J G , Ginsborg B L , House C R
Published: December 2014

1. An attempt has been made to account for the latency and slow time course of the electrical responses of salivary gland cells of Nauphoeta cinerea (Olivier) to nerve stimulation and ionophoretically applied dopamine from a pipette placed as close as possible to the acinar surface. 2. The effects have been investigated on the time course of the ionophoretic response of changes in the distance of the pipette from the acinar surface and of the amount of dopamine ejected. 3. The observed changes were smaller than those predicted by models in which the rate limiting step was assumed to be diffusion or slow receptor kinetics. Indirect evidence suggests that the time course of the response is determined by processes subsequent to receptor activation.
Dark‐adaptation of the aspartate‐isolated rod receptor potential of the frog retina: threshold measurements
Authors: Donner K. O. , Hemilä S. O.
Published: December 2014

1. The dark‐adaptation of the aspartate‐isolated rod receptor potential of the isolated and perfused frog retina has been measured after bleaching about 5‐10% of the rhodopsin. The fraction bleached (ΔR) and the decay of rhodopsin photoproducts were determined using alternating measurements with a photometric technique (Donner & Hemilä, 1975).

2. The dark‐adaptation time course of the log threshold elevation is exponential, log It/I0 = W exp (‐t/τ)+P, where W is the extrapolated value for log It/I0‐P at t = 0 and P is log It/I0 for t = ∞. When ΔR increases from 2 to 10% W increases from ca. 2·6 to ca. 5. The time constant τ is about 13 min at 9 °C and 7 min at 14 °C (ΔR = 5‐10%).

3. When the bleaching period is extended, keeping the amount bleached (I×t) constant, dark‐adaptation is completed earlier.

4. The time course of dark‐adaptation and the decay of the photoproduct ‘retinal’ are similar, as is also their dependence on temperature (Q10 ≈ 3).

5. The permanent log threshold rise P is approximately proportional to ΔR after small bleaches; when more than about 10% is bleached the slope of the curve P(ΔR) decreases. P is considerably larger (about 2·5‐fold) for the same fraction bleached in experiments at 14 °C as compared to experiments at 9 °C.

6. A comparison with previously obtained corresponding values for dark‐adaptation after small bleaches at the ganglion cell level shows a close agreement between the time constants for the dark‐adaptation curve, its range and the dependence of threshold on the fraction of rhodopsin bleached.
Dark‐adaptation in frog rods: changes in the stimulus‐response function.
Authors: Bäckström A C , Hemilä S O
Published: December 2014

1. Aspartate‐isolated photoresponses of the frog's rods to weak and strong flashes have been recorded during dark‐adaptation after bleaching a fraction of rhodopsin (generally 4‐‐30%). Stimulus‐‐response functions were measured before the bleach and in the steady state after dark‐adaptation. 2. The movements of the operating curve, i.e. the stimulus‐‐response function plotted in a log‐log diagram, are interpreted in terms of a model of outer segment adaptation, where the adaptation processes are associated with the transmitter release (Q‐adaptation), the number of active sodium channels and leakage channels in the plasma membrane of the outer segment (M‐adaptation), and the transmitter background (c1‐adaptation). 3. A small bleach in a fully dark‐adapted, non‐bleached retina brings about a displacement of the operating curve predominantly to the right. The shift back to the left is approximately exponential, typical time constants being 6‐‐12 min. 4. A strong exposure (bleaching 15‐‐30% of rhodopsin) in a previously partially bleached retina brings about a nearly vertical displacement of the operating curve: after the bleach the maximum photoresponse is strongly reduced, and during intermediate adaptation the operating curve returns mainly upwards. 5. Cumulatively increasing permanent displacements of the operating curve are observed in the steady states after successive dark‐adaptation transients. The permanent displacements are predominantly to the right and they increase with increasing temperature. 6. The experimental results, as interpreted according to the model, indicate that the Q‐adaptation process is dominant in physiological conditions (small or moderate bleaches), whereas the M‐adaptation becomes important only after rather large bleaches and especially after several successive bleaches in an isolated retina.
The role of diffusion in the photoresponse of an extraretinal photoreceptor of Aplysia.
Authors: Andresen M C , Brown A M , Yasui S
Published: December 2014

1. Membrane currents produced by flashes and steps of light (photo‐current) were recorded from the ventral photoresponsive neurone of Aplysia californica. The effects of background illumination and changes in temperature were also examined. 2. The falling phase of the response wave form may be separated into two components with time constants of 10‐‐12 sec and 50 sec. 3. Background illumination reduced the response amplitude to light impulses without appreciably altering the response wave form. 4. Lowering the temperature greatly reduced the amplitude of the photo‐current with a Q10 of 2.91 (25‐‐15 degrees C) and greatly prolonged the duration of the response. 5. Because of the relatively large distance between the plasma membrane and the pigmented cytoplasmic lipochondria where light is absorbed, a diffusion‐based model with Ca as the internal‐transmitter (Andresen & Brown, 1979) was developed. 6. In this model diffusion of Ca2+ released from the lipochondria upon photon absorption is slowed by the reversible uptake of Ca2+ at cytoplasmic binding sites. Ca2+ interacts with sites at the plasma membrane to increase GK and Ca2+ levels are subsequently restored by irreversible uptake processes. Ca2+ release and its adsorption and desorption from the more numerous plasma membrane binding sites were assumed to be instantaneous with respect to the duration of the light‐evoked response. 7. The linearized model equations adequately predict the experimental response wave forms, the effects of temperature, and saturation of the steady‐state amplitude‐‐stimulus relationship. Aside from amplitude scaling, no curve‐fitting was used. 8. The model also gives realistic values for the cytoplasmic diffusion coefficient of Ca and the net rate of Ca efflux required to restore dark Ca activity.
Phosphate efflux and oxygen consumption in small non‐myelinated nerve fibres at rest and during activity
Authors: Ritchie J. M. , Straub R. W.
Published: December 2014

1. The oxygen consumption and the movements of labelled phosphate were measured in garfish olfactory nerve at rest and during activity.

2. In solutions with 2·5 m
M‐K and 0·2 m
M‐phosphate the resting oxygen consumption was 0·206 m‐mole/kg.min; activity at 2 sec−1 produced an extra oxygen consumption of 2·46 μmole/kg.impulse. The extra oxygen consumption declined exponentially with a time constant of 2·62 min at 22‐26 °C.

3. The phosphate efflux, measured simultaneously, had a resting efflux rate constant of 1·24 × 10−3 min−1; activity at 2 sec−1 produced an extra fractional loss of 9·38 × 10−6 impulse−1. The increase in phosphate efflux followed almost the same time course as the increase in oxygen consumption.

4. Increasing the frequency of stimulation from 2 sec−1 to 3 or 5 sec−1 decreased both the extra oxygen consumption and the extra fractional loss of phosphate. When the frequency was decreased to 0·5 or 1 sec−1 the extra oxygen consumption per impulse increased, while the extra phosphate liberation was lowered.

5. Changing the phosphate concentration did not much affect the extra oxygen consumption; on the other hand, lowering or increasing the phosphate from the standard 0.2 m
M decreased both the resting and the stimulated phosphate efflux.

6. Lowering the K from the standard 2·5 m
M did not affect the extra oxygen consumption, but increased both the resting and the extra loss of phosphate. At higher K concentrations the extra oxygen consumption and the extra fractional loss of phosphate decreased without much change in the resting phosphate efflux.

7. Application of 1‐20 μ
M‐strophanthidin produced a transient decrease in the resting phosphate efflux without much change in resting oxygen consumption. With 10 or 20 μ
M‐strophanthidin the extra fractional loss of phosphate and the extra oxygen consumption were both lowered in approximately the same proportions.

8. The findings are consistent with the hypothesis that the increase in intracellular inorganic phosphate that results from increased break‐down of ATP after activity, is the main cause for the increased phosphate efflux. A fraction of the increase in intracellular phosphate only appears to be liberated to the outside, the value of the fraction depending on the resting phosphate efflux before activity.

9. The initial increase in intracellular inorganic phosphate after an impulse, estimated from the oxygen consumption or the phosphate fluxes, appears to be about 12‐19 μmole/kg nerve, remarkably close to the value known from chemical analysis.
Voluntary activation of spindle endings in human muscles temporarily paralysed by nerve pressure.
Authors: Burke D , Hagbarth K E , Skuse N F
Published: December 2014

1. In normal human subjects, the afferent activity from muscle spindle endings in the pretibial muscles was recorded while a pressure block was applied to the peroneal nerve proximally in the popliteal fossa. 2. In five of ten blocks, spindle activity increased in attempted isometric voluntary contractions when the receptor‐bearing muscles were completely paralysed. In the remaining five blocks, voluntary effort still increased spindle activity when maximum voluntary power was reduced by more than 90%, but the ability to activate spindles voluntarily was lost with or slightly before block of the last motor units. When the ability to activate spindle endings in an attempted voluntary contraction was lost sympathetic efferent fibres remained unblocked. 3. It is concluded that the fusimotor effects seen during a voluntary contraction are mediated by myelinated fibres of small calibre which probably innervate intrafusal structures exclusively (gamma fusimotor fibres). There is no necessity to postulate that skeleto‐fusimotor (beta) fibres are responsible for the tight 'alpha‐gamma co‐activation' seen in man during voluntary contractions.
Dual effects of ether on end‐plate currents.
Authors: Gage P W , Hamill O P , Van Helden D
Published: December 2014

1. The effects of diethyl ether (ether) on miniature end‐plate currents (m.e.p.c.s) and on acetylcholine‐activated end‐plate channels were measured in toad sartorius muscle fibres with voltage‐clamp and extracellular recording techniques. 2. At low concentrations (less than 20 mM) either made m.e.p.c.s decay faster than normal. At high concentrations (greaster than 40 mM), the decay of m.e.p.c.s was slower than normal. With all concentrations, the cecay remained exponential with single time constant, tau D. 3. At low concentrations ether did not affect the growth phase of m.e.p.c.s and only slightly reduced the amplitude of m.e.p.c.s. At the higher concentrations, the growth phase was slowed and m.e.p.c.s were significantly reduced in amplitude. 4. Ether at all concentrations (5‐‐70 mM) reduced end‐plate channel lifetime, the effect increasing with ether concentration. Ether did not significantly alter the elementary channel conductance or the actylcholine null (reversal) potential. 5. Curare reduced tau D which had been prolonged by high concentrations of ether. Ether itself at high concentrations caused a reduction in tau D increased by neostigmine. It is proposed that high concentrations of either inhibit acetylcholine hydrolysis by acetylcholinesterase. 6. The effect of ether in reducing end‐plate channel lifetime and reducing m.e.p.c. amplitude, without significantly altering the normal voltage and temperature sensitivity of channel lifetime, is consistent with the proposal that either reduces the stability of open end‐plate channels.
The effects of histamine, acetylcholine and 5‐hydroxytryptamine on lung mechanics and irritant receptors in the dog.
Authors: Dixon M , Jackson D M , Richards I M
Published: December 2014

1. The ability of histamine, acetylcholine, acetylcholine (ACh) and 5‐hydroxytryptamine (5‐HT) given I.V. and by aerosol to induce reflex bronchoconstriction and to activate lung irritant receptors has been studied in dogs anaesthetized with chloralose. 2. Histamine (four breaths of an aerosol from 0.0625%, 0.125% and 0.25% solutions and 5, 10 and 20 microgram kg‐1 I.V.), 5‐HT (four breaths of an aerosol from 0.5% or 1.0% solutions and 10, 20 and 40 microgram kg‐1 I.V.) produced significant relex changes in RL (total lung resistance). The changes in RL produced by ACh (four breaths of an aerosol from 0.25%, 0.5% and 1.0% solutions, of 5, 10, 20 and 40 microgram kg‐1 I.V.) were unaffected by vagal cooling. 3. The falls in Cdyn (dynamic compliance) produced by ACh given by aerosol or I.V. were unaffected by vagal cooling. The falls in Cdyn produced by histamine (10 microgram kg‐1 and 40 microgram kg‐1 I.V.) and 5‐HT (four breaths of an aerosol generated from a 0.5% solution and 20 microgram kg‐1 and 40 microgram kg‐1 I.V.) were significantly reduced by vagal cooling. 4. Histamine, 5‐HT and ACh given by aerosol and I.V. increased lung irritant receptor discharge. Irrespective of the route of administration, for a given change in RL histamine produced a greater increase in irritant receptor discharge than did ACh or 5‐HT, which produced similar increases. 5. For a given change in RL, histamine, ACh and 5‐HT were more effective in activating lung irritant receptors when given I.V. than by aerosol. 6. The mechanisms of irritant receptor activation by histamine, ACh and 5‐HT and the relationship between irritant receptor discharge and reflex bronchoconstriction are discussed.
Pepsin secretion in anaesthetized cats stimulated by pentagastrin and gastrin II in the presence or absence of secretin.
Authors: Beswick F B , Braganza J M , Howat H T
Published: December 2014

1. In fasting anaesthetized cats pentagastrin and gastrin II, infused alone in doses which evoked a large acid response, did not stimulate the secretion of pepsin. However, peptic secretion increased significantly when either acid stimulant was infused simultaneously with a dose od Boots' secretin, in itself below the threshold for peptic stimulation. 2. The potentiation by pentagastrin and gastrin II of the peptic response to secretin was similar to the potentiation observed when caerulein, histamine and N‐methyl histamine are given with secretin, an effect we have attributed to a non‐specific increase of gastric mucosal blood flow which accompanies the infusion of these acid stimulants and effectively increases the concentration of secretin delivered at the site of the chief cell in the gastric mucous membrane.
The effect of pentagastrin on peptic secretion in man
Authors: Braganza Joan M. , Herman K. , Hine Pauline , Kay G.
Published: December 2014

1. We have studied the peptic responses of the intact human stomach to stimulation by doses of pentagastrin which elicit a maximal acid response.

2. In twelve patients an intramuscular injection of pentagastrin (6 μg/kg) was followed by a prompt increase in acid output which attained a peak value eight times higher than the basal value in the period 15‐30 min after stimulation. The pattern of the peptic response was similar, but the peak output of pepsin was only three times the output in unstimulated juice.

3. In ten subjects the acid and peptic responses to
I.V. infusion of pentagastrin (1·2 μg/kg per hr) were studied using a gastric perfusion technique with 14C‐labelled polyethylene glycol as non‐absorbable marker. In seven of these ten subjects the pH of duodenal contents exceeded 6, and less than 0·5 m‐mole HCl per 15 min entered the duodenum throughout the tests. In this subgroup pentagastrin evoked a strong acid response but no peptic response.

4. In three subjects the pH of duodenal juice was less than 5·5 at times when more than 1 m‐mole HCl per 15 min entered the duodenum. The acid response to pentagastrin differed considerably in the three subjects, but in each individual the output of pepsin increased each time an excess of HCl entered the duodenum.

5. Since pentagastrin infused in a dose which maximally stimulates acid did not significantly increase the output of pepsin provided no HCl entered the duodenum we conclude that pentagastrin does not stimulate the secretion of pepsin in man. The transient insignificant peptic response to pentagastrin infusions, and the small but significant response to bolus injections of pentagastrin, can be explained as a wash‐out phenomenon.
Loss of extrasynaptic acetylcholine sensitivity upon reinnervation of parasympathetic ganglion cells.
Authors: Dennis M J , Sargent P B
Published: December 2014

1. The extrasynaptic acetylcholine sensitivity of frog cardiac ganglion cells was measured both after denervation and during the early stages of reinnervation by preganglionic axons. Sensitivity was measured by ionophoretic application of acetylcholine (ACh) to randomly chosen sites on ganglion cell bodies. 2. Extrasynaptic sensitivity rose gradually following denervation and after 3 weeks reached a mean value of approximately 1000 mV/nC. 3. Reinnervation of the cardiac ganglion began about 3 weeks after nerve crush. The ACh sensitivity of ganglion cells fell markedly during the 23‐‐31 day period, to a mean of 184 mV/nC. None of forty‐three neurones studied during that period received synaptic inputs sufficient to generate action potentials. 4. Twenty‐nine of the forty‐three neurones examined 23‐‐31 days after nerve crush had not yet received detectable synaptic inputs, yet even these cells had markedly reduced ACh sensitivity. 5. When reinnervation of cardiac ganglia was delayed by resecting the preganglionic nerves, ACh sensitivity was reduced slightly (43%) between 14‐‐21 and 23‐‐31 days after surgery. Thus, most of the sixfold reduction in sensitivity that occurs during this time after nerve crush is a specific effect of reinnervation. 6. We conclude that loss of extrasynaptic receptors coincides with, or may even precede, the earliest physiological signs of synapse formation. Restoration of action potential activity in the ganglion cells is not essential to initiate this loss.