bluuebunny/crossref_metadata_2025 huggingface dataset:
Electrical activities of the muscle layers of the canine colon.
Authors: El‐Sharkawy T Y
Published: December 2014

The spontaneous electrical and mechanical activities of the circular and longitudinal muscle layers of the canine colon were studied. The smooth muscle cells of the circular muscle layer exhibited regular, omni‐present myogenic slow‐wave activity at a frequency ranging from 4 to 7 c/min. With intracellular micro‐electrodes, the slow‐wave amplitude was 21‐38 mV and its duration 3‐6 sec. The ‘resting’ membrane potential was ‐60 to ‐76 mV. Some slow waves had superimposed spike bursts on their peak depolarizations and only these were associated with phasic contractions. It is concluded that they serve a pace‐maker function similar to their counterpart in the small intestine. The longitudinal muscle layer exhibited periods of electrical activity alternating with periods of electrical quiescence. During the activity periods electrical oscillations occurred at a frequency of 13‐35 c/min with spikes on top of them. Each electrical activity period was associated with a prolonged ‘tonic’ contraction. The duration of these periods was 30‐120 sec and their frequency 0.4‐1.1 period/min. This activity is similar to that recorded from the longitudinal muscle of the guinea‐pig caecum despite the anatomical differences. The electrical activity periods of the longitudinal muscle appeared to require an excitatory input (stretch and/or acetylcholine release). Provided the strips were not excessively stretched, atropine abolished all electrical and motor activity. Stretching prolonged the electrical activity periods until they eventually fused together and the muscle developed maintained tone. Simultaneously recording from both layers showed that, although electrotonic spread between the two layers is probably insignificant, the activity of the two layers was co‐ordinated. Only those slow waves of the circular layer that occurred during the electrical activity periods of the longitudinal layer had superimposed spikes. It is suggested that this co‐ordination may indicate that the two muscle layers may be commanded by a common input from periodically active, cholinergic intramural neurones. It is proposed that the complex patterns of colonic electrical and motor activities may be explained as consisting of two major components: one arising from the longitudinal (long spike bursts, high‐frequency oscillations and tonic contractions) and the other from the circular layer (slow waves, short spike and phasic contractions). Simultaneous electrical records from the two muscle layers and the mucosa failed to show a consistent relationship between the mucosal record and the activity of either layer. Caution should be exercised in the interpretation of intraluminally derived electrical recordings.
Elimination of polyneuronal innervation in a fast muscle of normal and dystrophic mice.
Authors: Dangain J , Vrbová G
Published: December 2014

The changes in the pattern of innervation of extensor digitorum longus (e.d.l.) during post‐natal development was studied in normal and dystrophic mice. As in other mammals, individual muscle fibres of new‐born mice are supplied by more than one axon. Up to 10 days after birth there was no difference in the extent of this polyneuronal innervation between normal and dystrophic muscle fibres. During post‐natal development the polyneuronal innervation gradually disappeared. In normal e.d.l. muscles the rate of the elimination of polyneuronal innervation was faster during the first 10 post‐natal days and then slowed down. By 16 days the final value of less than 10% of muscle fibres receiving more than one input was reached. In the dystrophic muscles the rate of elimination was similar to normal up to 10 days of age, but continued to decrease rapidly so that already by 11 days of age polyneuronal innervation was reduced to its final level of less than 10%. Thus the elimination of polyneuronal innervation was completed at least 3 days earlier in the dystrophic animals. It is suggested that the increased nerve activity said to be present in dystrophic mice could account for this finding.
Responses in muscle afferent fibres of slow conduction velocity to contractions and ischaemia in the cat.
Authors: Mense S , Stahnke M
Published: December 2014

The aim of the study was to find out to what extent muscle receptors with slowly conducting afferent fibres (group III and IV) are activated by muscular contractions of moderate force, and what kind of muscle afferents could mediate the pain of ischaemic exercise. In chloralose‐anaesthetized cats, the impulse activity of single afferent units from the triceps surae muscle was recorded from dorsal root filaments during muscular contractions with intact blood supply and after occlusion of the muscle artery. Two types of responses were observed to contractions without muscular ischaemia. One was characterized by sudden onset and a graded response amplitude to contractions of increasing force. In most cases stretching the muscle was also an effective stimulus. Units showing this response behaviour were labelled c.s.m (contraction‐sensitive with mechanical mechanism of activation). The other response type had a more delayed onset and often outlasted the exercise period; because of the unknown mechanism of activation, units of this kind were labelled c.s.x. The proportion of c.s.m receptors was significantly higher amongst group III than amongst group IV units. During ischaemic contractions of comparable force the c.s.m and c.s.x receptors exhibited an unchanged or a decreased response amplitude. Under these conditions another receptor type (N, for nociceptive) was activated which did not respond to contractions with intact blood supply. Vigorous activations during ischaemic work were only observed in group IV receptors. The majority of the 131 group III and IV units tested did not respond to contractions at all. These contraction‐insensitive (c.i.) endings probably comprised different receptor populations (nociceptors, thermoreceptors, low‐threshold mechanoreceptors). It is concluded that the various central nervous effects of muscular exercise without ischaemia which are known to be due to raised activity in thin muscle afferents (e.g. cardiopulmonary adjustments, spinal locomotor reflexes) are probably produced by the c.s.m and c.s.x types. The pain of ischaemic contractions is most likely mediated by the N receptors most of which possess non‐myelinated afferent fibres.
Sensations evoked by intraneural microstimulation of single mechanoreceptor units innervating the human hand.
Authors: Ochoa J , Torebjörk E
Published: December 2014

Intraneural microstimulation (i.n.m.s.) was performed in awake human volunteers, using tungsten micro‐electrodes inserted into median and ulnar nerve fascicles supplying the skin of the hand. The same electrodes were used alternatively to record impulse activity from single nerve fibres at the i.n.m.s. sites. Monitoring occasionally, with a proximal electrode, the impulse traffic evoked by i.n.m.s. distally in the same fascicle, established that the stimulation procedure could be made selective enough to activate single myelinated fibres in isolation, while also permitting multifibre recruitment. Monitoring propagated impulses also established that i.n.m.s. of a single myelinated fibre supplying a low‐threshold mechanoreceptor in the hand might evoke an elementary sensation. Such sensations were fully endowed with cognitive attributes amenable to psychophysical estimation: quality, magnitude and localized projection. Psychophysical tests were made during i.n.m.s. at intraneural sites where single‐unit activity was recorded from classified RA, PC, SA I or SA II mechanoreceptors. Changes in excitability of the nerve fibre of an identified unit, induced by further i.n.m.s., certified that the recorded unit had been stimulated during psychophysical tests. Comparing physical location of the receptive field of a recorded unit and localization of the projected field of the corresponding elementary sensation, revealed that either predicted the other accurately. This further assisted identification of the unit activated by i.n.m.s. The type of a recorded unit and the quality of the elementary sensation evoked by its activation were also reciprocally predictive. RA units evoked intermittent tapping, PC units vibration or tickle and SA I units evoked pressure. SA II units evoked no sensation when activated in isolation. Afferent impulse frequency determined magnitude of pressure in the SA I system, and frequency of vibration in the PC system. In the RA system, stimulation frequency determined frequency of tapping‐flutter‐vibration sensation at relatively low rates and subjective intensity of sensation at high rates. These findings endorse the concept that quality of sensation is coded in specific sensory systems. Further, they provide novel evidence that sensory quality, magnitude and localization can be exquisitely resolved at cognitive levels on the basis of input initiated in a single mechanoreceptor unit.
Measurement and modification of free calcium transients in frog skeletal muscle fibres by a metallochromic indicator dye.
Authors: Kovacs L , Rios E , Schneider M F
Published: December 2014

Myoplasmic free calcium transients were monitored with the metallochromic indicator dye Antipyrylazo III (AP III) in single frog skeletal muscle fibres cut at both ends, stretched so as to minimize or eliminate contractile filament overlap and voltage clamped using a double‐Vaseline‐gap system (approximately 6 degrees C). The dye entered the central fibre segment by diffusion from the solution applied to the two cut ends. The diffusion coefficient of AP III was about 20 times lower in the fibre than in solution. This very slow diffusion was not due to binding of dye since the ratio of bound to free dye obtained from analysis of the diffusion was only about 0.45. For a given depolarizing pulse, the ratio of dye‐related absorbance changes delta A at 720 and 550 nm was the same as that produced on adding calcium to dye in calibrating solution, indicating that these signals were due to changes in myoplasmic calcium. The delta A signals at 700 or 720 nm were used to monitor transient changes in concentration of calcium‐dye complex [CaD2] and of free calcium [Ca] in the myofilament space. By applying the same pulse at different times during dye entry, it was observed that increasing dye concentrations [D]T produced the following effects: (a) [CaD2] was increased; (b) [Ca] was decreased at early times during a pulse; (c) a declining phase of [Ca] observed at late times during pulses was decreased and finally reversed to a slow rising phase at high [D]T; (d) the decay of [Ca] after the pulse was slowed. Analyses of the effects of [D]T on (a) the magnitude of [CaD2] at a given early time during the calcium release produced by pulses to a given voltage and on (b) the time constant for [Ca] decay after a pulse were both consistent with a calcium: dye stoichiometry of 1:2 in the fibre as found in calibrating solution. Analysis of the effect of [D]T on the [Ca] decay time constants also revealed the presence of intrinsic rapidly equilibrating myoplasmic calcium binding sites and provided the basis for obtaining estimates of the combined concentration [Ca] of free calcium plus calcium bound to such sites. Unlike the estimates of [Ca], these estimates of [Ca] are independent of the value of the calcium‐dye dissociation constant.(ABSTRACT TRUNCATED AT 400 WORDS)
Myosin isoenzymes in fast‐twitch and slow‐twitch muscles of normal and dystrophic mice.
Authors: Fitzsimons R B , Hoh J F
Published: December 2014

An analysis of the native myosin isoenzyme composition, myosin light‐chain distribution and histochemical profile of fast‐twitch and slow‐twitch muscles of normal and dystrophic (129 REJ dy/dy) mice has been performed, and the results correlated with the known contractile abnormalities of murine dystrophic muscles. Normal mouse slow‐twitch soleus contained two isomyosins (slow myosin, SM and intermediate myosin, IM) which were electrophoretically distinct from the three major isomyosins (FM1, FM2, FM3) of fast‐twitch extensor digitorum longus (e.d.l.) muscle. The calcium‐activated ATPase activities of FM1, FM2, FM3 and IM at pH 9.2 were each much higher than that of SM, and this difference is reflected in the histochemical profile of muscle, as demonstrated with the myofibrillar ATPase reaction at alkaline pH. E.d.l. Type II fibres retained myofibrillar ATPase activity following pre‐incubation of histochemical sections at pH 4.6, and were therefore classified Type IIB, whereas soleus Type II fibres did not, and were classified Type IIA. It was concluded that Type I (slow) fibres contain SM, Type IIA (intermediate) fibres contain IM, and Type IIB (fast) fibres contain FM1‐FM3. Each electrophoretically distinct myosin contained a different combination of the five skeletal myosin light chains (LCs). Thus different normal muscles, which differed in their isomyosin profiles, differed also in their light‐chain composition. Analysis of the distribution of native myosins (FM1, FM2, FM3, IM, SM, in order of decreasing gel migration rate) in dystrophic muscles revealed increased proportions of the slower‐migrating forms, when compared with the distribution in the corresponding normal muscles. The shift in isomyosin distribution would explain the known decrease in the proportion of myosin light chain (LCf3) in murine dystrophic muscle. The abnormal isomyosin distribution in the dystrophic muscle is correlated with its altered histochemical characteristics, and with well‐established abnormalities in its isometric and isotonic properties. It is concluded that the altered isomyosin distribution in murine dystrophic muscle would result in decreased power output per unit muscle mass when compared with normal muscle. The possibility is considered that defective myelination of the innervating nerve may contribute to these abnormalities by preventing higher frequency impulses from reaching muscle.
The directional sensitivity of retinal rods.
Authors: Alpern M , Ching C C , Kitahara K
Published: December 2014

Rod field sensitivity, 10‐S(r) (i.e. the reciprocal of the radiance of a background required for 10‐fold elevation of rod threshold) was measured for monochromatic backgrounds traversing the pupil at various points (r) on three subjects. The wave‐length dependency of the directional sensitivities of the three foveal cone mechanisms of the principal subject have been reported previously (Alpern & Kitahara, 1983). Rods, as cones, are less sensitive to obliquely incident, than to normally incident backgrounds. At the pupil margin (4 mm) the effect is between 0.368 and 0.976 log10 units smaller for rods. After correction for losses by corneal reflexion and by absorption in the lens, S(r) for rods is reasonably described by the parabolic equation used by Stiles (1937) to quantify the directional sensitivity of cones. The small effect for rods precludes a description as consistently precise as this equation provides for cones. The steepness of the parabolic curve best fitting the directional sensitivity data of the rods of the principal subject was independent of background wave number. For a second subject, whose rods are supposed to be smaller, it was directly proportional to the square of that wave number. The latter is the expectation if the directional sensitivity of this subject's rods were determined by principles outlined in the diffraction theory of Simon (1970).
Neural vasodilator control in the rectum of the cat and its possible mediation by vasoactive intestinal polypeptide.
Authors: Andersson P O , Bloom S R , Edwards A V , Järhult J , Mellander S
Published: December 2014

Vascular and motor responses in the rectum to pelvic nerve stimulation are described in the anaesthetized cat and compared with corresponding effects observed in the colon. The responses comprise a cholinergic and a non‐cholinergic component, and an attempt has been made to elucidate the latter. Pelvic nerve stimulation evoked a pronounced and well maintained vasodilator response in the rectum whereas that in the colon was transient. Maximal vasodilatation occurred at much lower stimulus frequencies in the rectum (2‐4 Hz) than it did in the colon (8‐16 Hz) and maximal blood flow under these conditions was also greater in the rectum (greater than 200 ml 100 g‐1 min‐1) than the colon (less than 150 ml 100 g‐1 min‐1). Muscarinic blockade further curtailed the colonic vasodilator response to pelvic nerve stimulation, whereas the rectal dilatation was only slightly reduced in the presence of atropine. Pelvic nerve stimulation caused a substantial release of vasoactive intestinal polypeptide (VIP) from the rectum, which was related both in magnitude and duration to the vasodilatation. Intra‐arterial infusions of VIP, which reproduced this rise in rectal venous VIP concentration, caused a rectal vasodilator response which closely resembled that during pelvic nerve stimulation after cholinergic blockade. The rectal vasculature was estimated to be 50‐100 times more sensitive to VIP than the colonic vasculature. VIP therefore seems to be the most likely putative neurotransmitter responsible for non‐cholinergic rectal vasodilatation. Stimulation of the pelvic nerves also caused rapid contractile motor responses before, and more gradual motor responses after, muscarinic blockade in both the colon and rectum, in the latter preceded by a non‐cholinergic relaxation. These patterns of motor activity largely confirm previous results. Infusions of substance P effectively mimicked the non‐cholinergic contractile motor responses but failed to demonstrate significant release of this peptide during pelvic nerve stimulation in the present experiments. However, substance P is rapidly inactivated and might possibly be involved in these responses. Stimulation of the pelvic nerves in bursts at high frequencies (up to 80 Hz), simulating a discharge pattern observed electrophysiologically in vivo, was effective in eliciting all the above responses, with the exception of the colonic contraction.
A cholinergic chloride conductance in neurones of Helix aspersa.
Authors: Finkel A S
Published: December 2014

Inhibitory Cl‐ ‐mediated currents through cholinergic channels on the soma of identified neurones from the right parietal ganglion of Helix aspersa were studied under voltage clamp. Voltage‐jump relaxation analysis showed that these currents decreased with hyperpolarization. In 3 microM‐acetylcholine (ACh), the normalized fraction of channels in the open configuration (rho) decreased e‐fold with each 191 mV of membrane hyperpolarization. The steady‐state membrane conductance, G(infinity), decreased e‐fold with each 128 mV of membrane hyperpolarization. The difference in the voltage sensitivities of rho and G(infinity) arose because of the voltage sensitivity of the instantaneous membrane conductance, G(0). G(0) rectified in the direction predicted by the Goldman‐Hodgkin‐Katz conductance model. The degree of rectification decreased when the internal Cl‐ concentration was raised. The relaxing currents were composed of two exponential components. At membrane potential (Vm) = ‐160 mV, 12 degrees C, the time constants of the two components were 4.1 ms and 21 ms in 3 microM‐ACh, and 3.6 ms and 18 ms in 100 microM‐tetramethylammonium (TMA). Fluctuation analysis in neurones loaded with Cl‐ yielded spectra which were composed of two Lorentzian components. In 3 microM‐ACh the mean single‐channel conductance (gamma) appeared to rise from a low value observed in cells with normal intracellular Cl‐ to 2.7 pS in cells whose internal Cl‐ concentration was raised four‐fold. The voltage sensitivity of rho was attributed to the conformational change step of a gating mechanism having three kinetically distinguishable states.
Patterns of innervation of neurones in the inferior mesenteric ganglion of the cat.
Authors: Julé Y , Krier J , Szurszewski J H
Published: December 2014

The patterns of peripheral and central synaptic input to non‐spontaneous, irregular discharging and regular discharging neurones in the inferior mesenteric ganglion of the cat were studied in vitro using intracellular recording techniques. All three types of neurones in rostral and caudal lobes received central synaptic input primarily from L3 and L4 spinal cord segments. Since irregular discharging neurones received synaptic input from intraganglionic regular discharging neurones, some of the central input to irregular discharging neurones may have been relayed through the regular discharging neurones. In the rostral lobes of the ganglion, more than 70% of the non‐spontaneous and irregular discharging neurones tested received peripheral synaptic input from the lumbar colonic, intermesenteric and left and right hypogastric nerves. Most of the regular discharging neurones tested received synaptic input from the intermesenteric and lumbar colonic nerves; none of the regular discharging neurones received synaptic input from the hypogastric nerves. Some of the peripheral synaptic input from the lumbar colonic and intermesenteric nerves to irregular discharging neurones may have been relayed through the regular discharging neurones. Axons of non‐spontaneous and irregular discharging neurones located in the rostral lobes travelled to the periphery exclusively in the lumbar colonic nerves. Antidromic responses were not observed in regular discharging neurones during stimulation of any of the major peripheral nerve trunks. This suggests these neurones were intraganglionic. In the caudal lobes, irregular discharging neurones received a similar pattern of peripheral synaptic input as did irregular discharging neurones located in the rostral lobes. The majority of irregular discharging neurones in the caudal lobes projected their axons to the periphery through the lumbar colonic nerves. Non‐spontaneous neurones in the caudal lobes, in contrast to those located in the rostral lobes, received peripheral synaptic input primarily from the hypogastric nerves. Axons of the majority of non‐spontaneous neurones located in the caudal lobes travelled to the periphery through hypogastric nerves. The results suggest that non‐spontaneous neurones and irregular discharging neurones in the rostral lobes and the majority of irregular discharging neurones in the caudal lobes transact and integrate neural commands destined for abdominal viscera supplied by the lumbar colonic nerves. Non‐spontaneous neurones in the caudal lobes transact and integrate neural commands destined for pelvic viscera supplied by the hypogastric nerves.
Antibodies to motor nerve terminals: an electrophysiological study of a human myasthenic syndrome transferred to mouse.
Authors: Lang B , Newsom‐Davis J , Prior C , Wray D
Published: December 2014

Immunoglobulin G(IgG) prepared from the plasma of patients with a presynaptic disorder of neuromuscular transmission (Lambert‐Eaton myasthenic syndrome, l.e.m.s.), or from normal pooled control human plasma, was injected into mice (10 mg daily) for up to 99 days. Micro‐electrodes were used to record end‐plate potentials from the diaphragm muscle bathed in normal Krebs solution containing tubocurarine (1.0‐4.6 microM). At 0.5 Hz nerve stimulation frequency, the quantal content was significantly reduced (P less than 0.01‐P less than 0.001) in mice treated with six l.e.m.s. patients’ IgG each compared with paired controls. The pooled quantal content was 55 +/‐ 3 (n = 110 end‐plates) for all test animals and 131 +/‐ 9 (n = 47) for all controls (P less than 0.001). During short trains at 20 or 40 Hz nerve stimulation, control muscles showed marked depression, while test muscles showed either facilitation or less marked depression. Quantal content throughout these trains remained lower than in controls. The results indicate that IgG antibody from l.e.m.s. patients can induce a similar physiologic disorder in injected mice, and they support the view that this antibody interferes with evoked release of transmitter in l.e.m.s. by binding to nerve terminal determinants.
The distribution of small ions during the early development of Xenopus laevis and Ambystoma mexicanum embryos.
Authors: Gillespie J I
Published: December 2014

The free ion concentrations of Na+, K+ and Cl‐ have been measured in the cells and intercellular spaces of developing amphibian embryos using ion‐sensitive microelectrodes. Ca2+, H+ and buffering capacity have also been measured in the intercellular spaces. The free intracellular Na+ and K+ concentrations in the early cleavage stages remain approximately constant at 21 mM and 90 mM respectively. The free intracellular Cl‐ concentration, approximately 60 mM during the egg to 4‐cell stage, falls during development to around 30 mM by the 128‐cell stage. Embryos from different batches show a wide variation in intracellular free ion content. A strong correlation was observed between the ion content, particularly of K+, and the viability of the embryo. If the intracellular K+ concentration was less than 60 mM, embryos invariably died between late blastula and early gastrula stages; if greater than 80 mM the embryo generally survived. The intercellular free Na+, K+, Cl‐ and Ca2+ concentrations in Xenopus mid‐blastula embryos are 91 mM, 4 mM, 59 mM and 1.5 mM respectively. The intercellular potential at late neurula stages is +3.5 mV when the embryo is bathed in 5% Ringer solution; changing to Ringer solution reduced the potential to ‐4 mV. Before gastrulation the intercellular Ca2+ concentration in Xenopus falls to approximately 0.5 mM, where it remains throughout gastrulation before returning to its mid‐blastula value during neurulation. In Xenopus, the intercellular Na+ concentration falls to around 75 mM and the intercellular K+ concentration rises to around 17 mM at the end of gastrulation. These changes are not maintained and both Na+ and K+ concentrations return to their earlier values. In Ambystoma, the intercellular K+ concentration falls steadily from 7 mM at the mid‐blastula stage to 2 mM at the end of neurulation. The Na+ concentration is constant at approximately 93 mM up to stage 14; between stages 14 and 16 the measurements show some scatter (minimum value 60 mM, maximum value 100 mM), and beyond stage 16 the Na+ concentration increases to 123 mM.
Spatial contrast sensitivities of X and Y type neurones in the cat's dorsal lateral geniculate nucleus.
Authors: Troy J B
Published: December 2014

The discharges of X and Y type neurones were recorded extracellularly from the binocular segment of the A laminae of the dorsal lateral geniculate nucleus of anaesthetized, paralysed cats. X type geniculate cells are referred to as XG cells and Y type geniculate cells as YG cells. They were differentiated on the basis of a test of linear spatial summation and the relatively higher spatial resolution of the XG type. Contrast sensitivities of these cells were measured for a series of spatial frequencies at 5.2 Hz. Sensitivity measurements took account of the variability inherent in the cells’ maintained discharges. Maintained discharges of XG and YG cells were found to be similarly noisy and the level of noise was stable in the time range of seconds to hours. The noise level was greater than in corresponding ganglion cells, suggesting that an extra source of noise is added at the geniculate level. The criterion set routinely to measure ‘threshold’ contrast corresponded to a level of reliability of about two false positives in fifty. YG cells had higher contrast sensitivities at low spatial frequencies and XG at high. YG cells were found also to have higher peak sensitivities. The optimum spatial frequency of XG cells was found to be higher than that of YG cells. YG cells also show less attenuation in contrast sensitivity for gratings of spatial frequencies below their optima. Contrast sensitivities of both XG and YG cells were found to be lower than those of corresponding ganglion cells. The optimum spatial frequencies and spatial resolutions of XG and YG cells decreased as the retinal eccentricities of their receptive fields increased. XG cells were found to have higher spatial resolution in lamina A than lamina A1. No difference was found between on‐ and off‐centre types of either cell class. Although individual YG cells are more sensitive to low spatial frequencies than individual XG cells, the ensemble of XG cells of one centre‐type which overlaps a particular YG cell receptive field of the same centre‐type has a contrast sensitivity at optimum spatial frequency very close to that of the YG cell. This leads one to believe that XG cells could by themselves account for the contrast sensitivity of the cat's visual system.
The regulation of extrajunctional acetylcholine receptors in the denervated rat diaphragm muscle in culture.
Authors: Kallo J R , Steinhardt R A
Published: December 2014

The regulation of the number of extrajunctional acetylcholine (ACh) receptors was assayed by 125I‐labelled alpha‐bungarotoxin binding sites in denervated rat diaphragm muscle in culture. Sustained K depolarization does not eliminate extrajunctional ACh receptors. In fact, muscle cultured in high‐K medium (normal Cl) for 3 days exhibits a greater binding capacity than controls. Under conditions in which the intracellular Cl concentration is unaltered (high‐K‐low‐Cl medium) this effect of high‐K medium on the number of extra‐junctional ACh receptors is blocked. The number of extrajunctional receptors increases 24‐48 h after exposure to high‐K‐normal Cl medium, similar to the time course of the initial appearance of extrajunctional receptors in the denervated diaphragm muscle in vivo or in organ culture in normal media. High‐K‐normal Cl medium did not alter the rate of receptor degradation. Electrical stimulation of denervated muscle strips cultured in low‐Ca medium containing D‐600 eliminated extrajunctional receptors as efficiently as stimulation of muscles in control medium. Electrical stimulation did not reduce the extrajunctional ACh receptor population in glycerol‐treated uncoupled muscles to the same extent as in untreated muscles. The extrajunctional ACh receptor content of denervated muscle cultured for 3 days in 2 and 5 mM‐caffeine was reduced by about half respectively. Denervated muscle cultured in 0.3 mM‐caffeine did not differ from control denervated muscle. Other agents which may alter intracellular cyclic nucleotide levels: dibutyryl cyclic GMP, dibutyryl cyclic AMP, papaverine, and sodium nitroprusside, did not mimic the effect of caffeine or electrical stimulation in lowering the levels of extrajunctional ACh receptors. We conclude that intracellular Ca release from the sarcoplasmic reticulum is necessary for the elimination of extrajunctional ACh receptors in denervated muscle. The levels of intracellular Cl also influence the population of extrajunctional receptors. Conditions which lead to higher levels of intracellular Cl result in greater rates of synthesis of ACh receptors.
Secretion control for active and inactive renin: effects of calcium and potassium on rabbit kidney cortex slices.
Authors: Ginesi L M , Munday K A , Noble A R
Published: December 2014

Release of active and inactive renin by rabbit kidney cortex slices was investigated. Inactive renin was estimated as the increase in renin activity after acidification (pH 2.8) of slice supernatant solutions. In Ca2+‐free media, release of both active and inactive renin was increased but the changes in inactive renin were more marked. The percentage of total renin released which was inactive ranged from 8.3% ([Ca2+] = 9.2 mM) to 34.5% (zero [Ca2+]) with a linear relationship (r = ‐0.96) over the range of [Ca2+] studied. Depolarizing media ([K+] = 20 mM) suppressed release of inactive renin more than release of the active form. This effect, for both forms of renin, was lost when Ca2+ ions were omitted from the incubation media. This suggests that influx of Ca2+ ions was responsible for the reduced renin secretion following depolarization of the juxtaglomerular cells. Reducing the [K+] of the incubation buffer from 5.7 mM (control) to 1.0 mM did not alter active renin but increased release of inactive renin. Low [K+] media abolished the stimulatory effect of low [Ca2+] on release of both forms of renin. In incubation media with low [Ca2+] or with low [K+] the mixture of renins released by the kidney cortex slices correlated with that found in extracts of non‐incubated kidney: that is, about 35% of the total renin was in the inactive form. Mechanisms controlling the secretion of active and inactive renins by the kidney are at least partially independent. Differential secretion of the two forms, perhaps linked to regulation of the activation of inactive renin before release, appears to be the basis of a control step in the over‐all expression of the renin‐angiotensin system. This may be coupled in some way to juxtaglomerular cell Na+ ion flux.
Sensitivity to stationary flashing spots of the brisk classes of ganglion cells in the cat retina.
Authors: Cleland B G
Published: December 2014

The responses of brisk‐sustained (X) and brisk‐transient (Y) cat retinal ganglion cells to small stationary spots flashing on and off in their receptive fields were recorded. Response magnitudes were determined as the amplitude of the fundamental frequency component. At 0.5 and 8 Hz the sensitivity of brisk‐sustained cells is independent of the size of their receptive field centre, with the mean sensitivity at 0.5 Hz being 16% lower than at 8 Hz. At 8 Hz the sensitivity of brisk‐transient cells is inversely proportional to the centre diameter of their receptive fields. The relationship is quite different from that found in brisk‐sustained cells. The ratio of the sensitivity at 0.5 Hz to the sensitivity at 8 Hz can be used as a measure of the ‘sustainedness’ of a ganglion cell. Using this measure brisk‐sustained cells show no change in their sustained nature as a function of eccentricity. In contrast, brisk‐transient cells appear to become increasingly transient with eccentricity. Within the area centralis the sensitivities of brisk‐transient cells at 0.5 and 8 Hz are very similar to the sensitivities of brisk‐sustained cells, and hence they have a very obvious sustained component to a light flashed on and off at low frequency. These brisk‐transient units meet all other criteria of their class and so there can be no question as to their classification.
Vagal influences on the jejunal ‘minute rhythm’ in the anaesthetized ferret.
Authors: Collman P I , Grundy D , Scratcherd T
Published: December 2014

Spontaneous jejunal motility in the urethane‐anaesthetized ferret shows a cyclical pattern of contraction bursts alternating with quiescent periods described as ‘minute rhythm’ in conscious animals. Cooling the cervical vagi to below 4 degrees C or acute vagotomy abolished this pattern of motility. On re‐warming the vagi there was a return to cyclical motility after a latency which depended upon the contractile state at the time vagal conduction was restored. Electrical vagal stimulation produced bursts of contractions at the same frequency as the spontaneous motility. Longer periods of stimulation gave rise to bursts of contractions interrupted by periods of relative quiescence, mimicking the spontaneous motility, despite the continuous stimulation. Following atropinization all spontaneous motility was abolished, but electrical stimulation of the vagi revealed a non‐cholinergic, non‐adrenergic response whose characteristics differed from that of the cholinergic response. It is concluded that the vagus plays a permissive role in regulating the jejunal ‘minute rhythm’ via a cholinergic pathway and that there is a second excitatory vagal pathway which innervates non‐cholinergic post‐ganglionic neurones whose functional significance and transmitter mechanism is unknown.
Stimulation of electrolyte secretion in rabbit colon by adenosine.
Authors: Grasl M , Turnheim K
Published: December 2014

Serosal addition of adenosine after inhibition of adenosine deaminase with deoxycoformycin increases short‐circuit current (Isc) and tissue conductance of isolated epithelia of rabbit descending colon. In the presence of Cl this increase in Isc results from a reversal of electrically neutral Cl absorption to rheogenic Cl secretion. When Cl is absent the stimulating effect of adenosine on Isc is reduced to one‐third and appears to be brought about by HCO3 secretion. Under all conditions active Na transport remains unaltered. Adenosine‐induced electrolyte secretion is markedly decreased by serosal addition of furosemide and depends on the presence of Na on the serosal side of the tissue. The stoichiometry of the interaction of Na and Cl with the basolateral Cl entry mechanism appears to be 1:1. Under Na‐free conditions adenosine elicits a current transient which is carried by Cl ions and which is not inhibited by furosemide. Hence this current transient seems to be brought about by rheogenic apical Cl efflux. All these findings suggest that the conductive step in transepithelial Cl secretion resides in the apical membrane. Hyperpolarization of the Na‐transporting cells by luminal addition of amiloride does not enhance electrolyte secretion. The site of action of adenosine is the extracellular surface of the basolateral membrane, because (a) luminal addition of adenosine is ineffective, (b) nitrobenzylmercaptopurineriboside, a blocker of cellular nucleoside uptake, augments the effect of serosal adenosine, and (c) the intracellular metabolites of adenosine do not mediate the effect. From the rank‐order of potency of adenosine and its analogues 5'‐N‐ethylcarboxamide adenosine and N6‐cyclohexyladenosine it is concluded that the adenosine receptors involved in electrolyte secretion are of the Ra subtype. Theophylline partially inhibits the secretory effect. The intracellular mediator of adenosine appears to be cyclic AMP and/or cyclic GMP, since the tissue levels of both compounds are rapidly elevated after addition of adenosine and both cyclic AMP and cyclic 8‐bromo‐GMP are able to mimic the adenosine action.
On the mechanism by which adenosine receptor activation inhibits the release of acetylcholine from motor nerve endings.
Authors: Silinsky E M
Published: December 2014

The process by which adenosine receptor agonists inhibit the evoked release of acetylcholine (ACh) was studied at motor nerve endings to frog skeletal muscle. Adenosine and 2‐chloroadenosine were employed as agonists. Each agonist reduced the mean number of ACh packets released synchronously in response to a nerve impulse (m). Adenosine was from one to two orders of magnitude less potent than 2‐chloroadenosine as an inhibitor of this release. Focally recorded nerve terminal action potentials were unaffected by either adenosine receptor agonist. In normal Ca (1.8 mM), addition of sufficient Mg to reduce m to less than half the control value did not alter the degree of inhibition produced by adenosine receptor agonists. ACh release evoked by methods that do not require Ca entry through Ca channels (Ca‐containing liposomes, La) was inhibited by either 2‐chloroadenosine or adenosine. In Ca‐free solutions containing Ba, the magnitude of neurally evoked asynchronous ACh release (miniature end‐plate potential frequency = m.e.p.p.f) was depressed by either adenosine receptor agonist without change in the rate constant of decay of m.e.p.p.f; the m.e.p.p.f decay is thought to reflect the rate of clearance of Ba from regions of ACh release. Agents which displace Ca from storage sites and also inhibit phosphodiesterases increased m.e.p.p.f in the virtual absence of extracellular Ca and increased the level of inhibition produced by adenosine receptor agonists. RMI 12,330A (7 X 10(‐6) to 7 X 10(‐5) M), an adenylate cyclase inhibitor, occluded the effects of adenosine receptor agonists on ACh release. The results are consistent with the hypothesis that activation of extracellular adenosine receptors on adenylate cyclase inhibits evoked ACh release by reducing the affinity for Ca of an intracellular component of the secretory apparatus.
Milk production and consumption and growth of young of wild mice after ten generations in a cold environment.
Authors: Barnett S A , Dickson R G
Published: December 2014

Three classes of wild house mice, Mus musculus, were studied: (a) mice of the tenth generation in captivity in an environment kept at 23 degrees C (controls); (b) a similar stock kept at 3 degrees C (Eskimo); (c) offspring of controls transferred at mating to 3 degrees C (immigrants). For analysis of chemical composition, samples of milk were drawn from lactating females after they had been injected with oxytocin. For estimates of milk yield, lactating females were injected with tritiated water, and yield was calculated from the tritium content of young aged 10 days, over a 24 h period. The milk of Eskimo females had a much higher proportion of both fat and protein than had milk of other classes. The milk of immigrant females had more fat but less protein than that of controls. Eskimo females were heavier than immigrant females; control females were the lightest. Eskimo young at 10 days were heavier than those of the other classes. Their body fat was much higher; but their fat‐free body weight was also above that of the others. Young of both classes in the cold drank more milk than the controls, and the Eskimo more than the immigrant young. Maternal body weight, milk intake by the young and body weight of the young were intercorrelated, but milk intake was the principal determinant of the body weight of the young. There was no evidence of differences in the growth potential of the young of different classes.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of hormonal and electrical stimulation of sodium transport on metabolism of toad urinary bladder.
Authors: McLaughlin C W
Published: December 2014

The carbon dioxide produced by toad urinary bladders bathed on their mucosal surfaces by sodium Ringer solution and on their serosal surfaces by modified Leibovitz tissue culture medium was analysed by multiple regression on both sodium transport and time. The fractions contributed by metabolism related to transport and by basal metabolism were assessed, and the extent to which these might vary with time was determined. This analytical method, which improves the accuracy with which suprabasal metabolism is estimated, was used to examine the effects on metabolism of vasopressin, aldosterone, and mucosa‐positive voltage‐clamping. Vasopressin (0.05 u./ml), which on average increased sodium transport 2.9 times and concurrently increased the rate of carbon dioxide production in these transporting tissues, also altered the carbon dioxide production of non‐transporting, amiloride‐treated control hemibladders. For each hemibladder the ratio of sodium transported to suprabasal carbon dioxide produced after vasopressin was compared with that observed before vasopressin. Differences between the ratios were much reduced when the carbon dioxide productions of the paired transporting hemibladders were corrected for the effects of vasopressin on basal carbon dioxide production. With such analysis, it was confirmed that vasopressin did not alter the stoichiometry of sodium transport. A 30 mV, mucosa‐positive voltage clamp, applied near the peak of the response to vasopressin, further increased both sodium transport and carbon dioxide production. No alterations of the ratio of sodium to suprabasal carbon dioxide were seen under these conditions where the maximal rate of active sodium transport in this tissue must have been approached. Active sodium transport was more than doubled some 4 h after adding aldosterone (10(‐7) M). However, the related increase in suprabasal carbon dioxide production was greater than threefold. Therefore, whereas the stimulation resulting from vasopressin and voltage clamping had no effect on the ratio of sodium transported to suprabasal carbon dioxide produced, this ratio was reduced significantly by aldosterone. When the sodium transport of aldosterone‐treated bladders was increased further by voltage clamping, the ratio of sodium transported to suprabasal carbon dioxide production remained at the reduced value. Sodium transport was increased by approximately 35% more when aldosterone‐treated hemibladders were voltage clamped after vasopressin, the control paired hemibladders being exposed to vasopressin and voltage clamping alone.(ABSTRACT TRUNCATED AT 400 WORDS)
Electric current flow in a two‐cell preparation from Chironomus salivary glands.
Authors: Metzger P , Weingart R
Published: December 2014

Conventional micro‐electrode techniques were used to study the passive electrical properties of salivary glands from Chironomus nuditarsis insect larvae of the fourth instar stage. Linear cable analysis performed on intact glands revealed the following constants: axial intracellular resistance, Ri = 2730 omega cm; membrane resistance per unit apparent cylindrical area, Rm = 1350 omega cm2; membrane capacitance per unit apparent cylindrical area, Cm = 17.6 microF cm‐2. The multicellular glands were reduced to intact two‐cell preparations by destroying neighbouring cells mechanically. Each cell of a coupled cell pair was impaled with two micro‐electrodes, one to pass rectangular current pulses and the other to monitor the resulting voltage deflexions. Internal consistency tests revealed that the experimental data under steady‐state conditions may be described accurately by an equivalent circuit consisting of a delta configuration of three resistive elements: the resistances of the non‐junctional membrane of cell 1 and cell 2 (r1 and r2), and the resistance of the gap junctional membrane connecting the two cells (rg). The current‐voltage relation of the non‐junctional membrane was found ohmic over a membrane potential ranging from ‐40 mV to + 10 mV. The mean value of Rm was 2020 omega cm2. The resistance function of the gap junctional membrane was also ohmic. There was no dependence of gap junctional resistance on voltage or direction of current flow, at least over the relatively narrow range of potentials tested (approximately +/‐ 10 mV). Individual values of rg varied from 20 to 3800 k omega, with an over‐all mean of 1100 k omega. The lower values are thought to represent the physiological state of cellular coupling, whereas the higher ones may reflect partial uncoupling caused by local damage. The proposed cell pair is a suitable preparation for studying problems related to intercellular coupling.
Trigeminal‐baroreceptor reflex interactions modulate human cardiac vagal efferent activity.
Authors: Eckberg D L , Mohanty S K , Raczkowska M
Published: December 2014

Instantaneous levels of vagal cardiac inhibition reflect integrated responses of vagal motonuclei to multiple sensory neural inputs. We studied how two of these inputs, from trigeminal cutaneous receptors and carotid arterial baroreceptors interact to influence human vagal cardiac outflow. Nine healthy young men voluntarily maintained breathing rates and tidal volumes within narrow limits. Carotid baroreceptors were stimulated with brief periods of moderate neck suction. Volunteers were studied prone, breathing through a snorkel, before and during face immersion in cold water, and before and after an intravenous injection of a very low dose of atropine sulphate (which increases vagal cardiac efferent activity in dogs). Face immersion raised blood pressure slightly, increased heart period, and augmented baroreflex bradycardia and respiratory sinus arrhythmia significantly. Low‐dose atropine together with face immersion further augmented blood pressure, heart period, baroreflex responses and sinus arrhythmia. These results suggest that one input to the central nervous system (from trigeminal cutaneous receptors) which increases vagal cardiac outflow, augments vagal responses to another input (from arterial baroreceptors). Since the initial pathways of these two inputs are anatomically separate, it is likely that the influences of respiration and low doses of atropine on vagal motonuclei are exerted down‐stream from the termination of primary trigeminal and baroreceptor afferent fibres.