bluuebunny/crossref_metadata_2025 huggingface dataset:
Measurement of intracellular chloride in guinea‐pig vas deferens by ion analysis, 36chloride and micro‐electrodes
Authors: Aickin C. Claire , Brading Alison F.
Published: December 2014

1. Cl‐sensitive micro‐electrodes were used to measure the intracellular Cl activity (aCli) in smooth muscle cells of the guinea‐pig vas deferens. The values obtained were compared with those of intracellular Cl (Cli) found by both ion analysis and 36Cl efflux.

2. Various combinations of filling solution for recording membrane potential (Em), and type of micro‐electrode were tested. The most successful, which allowed continuous recording of aCli for several hours, was a double‐barrelled electrode using the reference liquid ion exchanger (RLIE; Thomas & Cohen, 1981). However, aCli measured both by simultaneous impalements of separate cells with Cl‐sensitive and conventional micro‐electrodes, and by double‐barrelled micro‐electrodes, was about 42 mM in normal Krebs solution. This is five times higher than the value from a passive distribution. ECl was about ‐24 mV, more than 40 mV positive to Em.

3. On complete removal of extracellular Cl (Clo), aCli fell to an apparent level of about 3 mM. If this represents interference from other anions, the maximum error in ECl measured in normal Krebs solution is 2·5 mV. Replacement of Clo caused a rapid increase in aCli. This must be caused by an active transport of Cl− ions into the cell against their electrochemical gradient.

4. The stabilized values of aCli measured at different levels of Clo agree surprisingly well with aCli estimated from ion analysis and 36Cl efflux, assuming that the intracellular activity coefficient was the same as measured in the normal Krebs solution. The relationship of aCli to Clo was hyperbolic.

5. It is concluded that Cl‐sensitive micro‐electrodes accurately measure aCli in smooth muscle cells. The remarkable agreement between the direct and indirect methods of measuring Cli suggests that Cl− ions are not bound to a significant extent and that the compartment seen by the micro‐electrodes is probably representative of the whole cell.
Normality of spatial resolution of retinal ganglion cells in cats with strabismic amblyopia.
Authors: Cleland B G , Crewther D P , Crewther S G , Mitchell D E
Published: December 2014

1. A convergent or divergent strabismus was induced surgically in eight kittens and a cyclotropia of about 90 deg in two additional kittens. 2. Behavioural measurements were made of the visual acuity of each eye for square‐wave gratings. All eight animals that were so tested displayed a reduction of acuity in one eye relative to the other of 1.3‐2.5 octaves. 3. The activity of retinal ganglion cells was recorded within the amblyopic eye of six cats, three with a convergent strabismus, two with a divergent strabismus and one with a cyclotropia. Measurements were made of the spatial resolution with 215 on‐centre cells for horizontal and vertical gratings. 4. In contrast to other reports, we found the spatial resolution of ganglion cells in the amblyopic eye of the strabismic animals to be comparable to those of normal cats at all retinal eccentricities. In particular there was no evidence for a loss of resolution in the vicinity of the area centralis. 5. Measurement of the cross‐sectional area of cells in the lateral geniculate nucleus (l.g.n.) revealed no evidence of cell shrinkage in laminae receiving a projection from the amblyopic eye. 6. Together, these findings lead to the conclusion that the neural deficit responsible for the strabismic amblyopia in these animals did not lie in the retina but rather at more central levels of the visual pathway.
Membrane potential responses of the mouse anococcygeus muscle to ionophoretically applied noradrenaline
Authors: Large W. A.
Published: December 2014

1. Membrane potential responses to ionophoretically applied noradrenaline and to field stimulation were studied in the mouse anococcygeus muscle using intracellular recording techniques.

2. The ionophoretic application of noradrenaline produced charge‐dependent depolarizations whose total duration was 1‐2 s at room temperature and which were characterized by a delay between the start of the ionophoretic pulse and the onset of depolarization (termed the latency of the responses). On occasion ionophoresis of noradrenaline did not depolarize the muscle even though it seemed that successful ejection of noradrenaline had occurred as small localized contractions could be seen.

3. The characteristics of these depolarizations were unaffected by tetrodotoxin (10−7 M) and could not be reproduced when the ionophoretic pipette contained 2 M‐NaCl rather than noradrenaline. Moreover noradrenaline still produced depolarizations in denervated muscle and thus it is concluded that the responses were caused by noradrenaline released from the ionophoretic micropipette and not from the intrinsic noradrenergic nerves.

4. Field stimulation of innervated muscle usually evoked excitatory junction potentials (e.j.p.s), but sometimes inhibitory junction potentials (i.j.p.s) or a mixture of e.j.p.s and i.j.p.s were observed. The time course of the e.j.p.s was slightly longer than that of the ionophoretic depolarizations which was accounted for by a smaller latency of the ionophoretically induced responses.

5. The pharmacology of the nerve‐evoked e.j.p.s and the ionophoretically induced depolarizations was similar as both types of responses were antagonized by α1‐adrenoceptor blocking agents (phentolamine and prazosin) but were unaffected by the β‐adrenoceptor antagonist, propranolol. It is probable that noradrenaline released from the intrinsic nerves and that from the ionophoretic micropipette were acting on the same adrenoceptors.

6. The latency and to a lesser extent the rise‐time of the depolarizations produced by the ionophoretic application of noradrenaline was highly sensitive to changes in temperature of the bathing fluid (Q10s > 2) whereas the half‐decay time was relatively insensitive to temperature changes (Q10 ∼ 1·5). In addition the latency of the depolarizations was not altered by inhibiting the noradrenaline‐uptake mechanism with cocaine (2 × 10−6 M) or by α‐adrenoceptor blocking agents. Thus it seems likely that the latency of the responses is a property of the noradrenaline—receptor interaction rather than being caused by other phenomena such as diffusion of noradrenaline.
The role of gastric secretion in post‐diverted pancreatic hypersecretion in conscious rats.
Authors: Noda A , Magee D F , Sarles H
Published: December 2014

1. In rats prepared with chronic external pancreatic fistulae, gastric fistulae and choledocho‐enterostomy, the volume and protein secretion of pancreatic juice was measured. 2. The pancreatic secretion of water and protein after juice diversion was significantly lower when the gastric fistula was open than when closed. Secretion was abolished after atropine, with the fistula open and in animals with ligated pylori. 3. Intraduodenal HCl significantly raised juice volume and protein in animals with diverted juice when the gastric fistula was open. 4. Soybean trypsin inhibitor produced a significantly smaller elevation of juice volume and protein when the gastric fistula was open. 5. It is concluded that the initial hypersecretion of pancreatic juice and protein, following its diversion from the duodenum, is a consequence of the entry of gastric juice into the intestine.
Effects of hypercapnia on tracheal pressure, diaphragm and intercostal electromyograms in unanaesthetized fetal lambs
Authors: Dawes G. S. , Gardner W. N. , Johnston Barbara M. , Walker D. W.
Published: December 2014

1. The electromyographic (e.m.g.) activity of the diaphragm and intercostal muscles has been recorded during breathing movements of unanaesthetized lambs in utero (109‐135 days), and compared with the changes of tracheal pressure.

2. The diaphragm e.m.g. was irregular in size, shape and timing, with a variable rate of rise during inspiration, often with a flattening of integrated activity before the end of a breath and with little or no post‐inspiratory activity.

3. The diaphragm e.m.g. gave the most reliable measurements of breath interval and incidence: in eucapnia mean TI was 0.45±0.02 (S.E. of mean) and TE was 0.74±0.05 sec, and 58‐100% of the diaphragm bursts were associated with identifiable and appropriate changes of tracheal pressure.

4. During fetal hypercapnia, produced by increasing the maternal inspired CO2 in a single change or series of step changes, tracheal pressure amplitude and its rate of change during inspiration increased progressively over the Pa, CO2 range of 37‐87 mmHg.

5. In eucapnia the area, amplitude and inspiratory slope of the integrated diaphragm e.m.g. were not always correlated with tracheal pressure amplitude, and in hypercapnia they increased only in the lower part of the Pa, CO2 range. Inspiratory intercostal activity increased progressively as the Pa, CO2 was raised.

6. The frequency histograms of variables derived from the tracheal pressure, diaphragm and intercostal e.m.g.s were skewed to the left in eucapnia but became normalized during hypercapnia. The rate and depth of breathing became regular.

7. The response to mild asphyxia was a combination of the responses to hypercapnia and hypoxia.

8. The interpretation of the tracheal pressure and diaphragm e.m.g. as measures of the ‘depth’ of breathing and respiratory ‘drive’ in the fetal lamb is discussed.
Phasic bursting activity of rat paraventricular neurones in the absence of synaptic transmission
Authors: Hatton Glenn I.
Published: December 2014

1. The purpose of this study was to determine whether the phasic bursting activity, characteristic of certain magnocellular neuropeptidergic neurones in rat hypothalamus, is dependent upon chemical synaptic input.

2. Slices of hypothalamus were placed in an in vitro chamber with hippocampal slices. The synaptic response in the CA1 cell layer from Schaffer collateral stimulation was monitored before, during and after synaptic transmission was blocked by superfusion of medium containing high Mg2+ (either 18·7 or 9·3 mM) and low Ca2+ (0·05 mM). This well studied pathway was chosen as an assay of synaptic blockade because hypothalamic circuitry is relatively unknown.

3. The electrical activity of twenty‐two phasic bursting neurones in the lateral portion of the paraventricular nucleus (p.v.n.) was recorded. Nineteen of twenty‐two phasic p.v.n. neurones were recorded only after synaptic transmission was blocked. The remaining three cells were firing phasically in standard medium when first encountered and continued to display phasic bursting activity for up to 1·25 hr after synaptic blockade. Active cells in nearby hypothalamic areas did not show phasic bursting patterns either before or after synaptic transmission was blocked.

4. The phasic bursting activity of the p.v.n. neurones in this study and that of previously reported p.v.n. cells in vivo were similar in (a) firing rate within bursts (b) burst length and (c) silent period duration.

5. It is concluded that phasic bursting in p.v.n. magnocellular neuropeptidergic cells is not dependent upon synaptically mediated excitation or recurrent inhibition as has been hypothesized earlier.

6. Alternative hypotheses, based upon acute changes in [K+]o, endogenous membrane currents and electrotonic coupling are discussed as possible explanations of phasic bursting in these magnocellular neuropeptidergic cells.
Energy expenditure of ‘cafeteria’‐fed rats determined from measurements of energy balance and indirect calorimetry.
Authors: Rothwell N J , Stock M J
Published: December 2014

1. Energy expenditure was determined in rats fed a standard laboratory diet or a varied and palatable ‘cafeteria’ diet, from metabolizable energy intake and body energy gain over a 15 d experiment. This was compared with measurements of oxygen consumption (Vo2) made over 24 h during the first and second weeks of the experiment. 2. Metabolizable energy intake was elevated by 50% in ‘cafeteria’‐fed rats and these animals gained more weight and had a higher body fat content than stock‐fed controls. Energy expenditure derived from these measurements was 45% higher in the ‘cafeteria’ group, and the net efficiency for energy gain was significantly reduced. 3. Vo2 was increased by 45% in the ‘cafeteria’ group and the daily energy expenditure, estimated from Vo2, was identical to that derived from the energy balance for controls, and differed by only 3% for the ‘cafeteria’ group. 4. These results confirm the high levels of diet‐induced thermogenesis previously seen in hyperphagic, ‘cafeteria’‐fed rats and reaffirm the validity of the carcass balance method for estimating energy expenditure.
Forestomach motility in the chronically vagotomized sheep
Authors: Gregory P. C.
Published: December 2014

1. The motility of the reticulo‐rumen and omasum in conscious sheep was studied by electromyography from chronically implanted nichrome wire electrodes. The sheep were subjected to vagotomy and were maintained totally by intragastric infusion of liquid nutrients before and after vagotomy. Before vagotomy the motility of the forestomach was essentially similar to that seen in roughage‐fed sheep.

2. Bilateral thoracic vagotomy transiently abolished all electrical activity of the reticulo‐rumen and omasum, but within 1 day some activity returned. Frequent periods of rhythmic local small group discharges were seen over the reticulo‐rumen, while the omasum showed prolonged (1‐5 min) bursts of mainly slow wave activity.

3. Within 1‐2 weeks of vagotomy strong contractions of the reticulo‐rumen were visible by radiography. Electromyographically, they comprised a rhythmic series of some two to five large group discharges recurring approximately once a minute. Each series of activity was separated from the next by a short period of quiescence. The discharges occurred almost simultaneously over the whole reticulo‐rumen and so contrasted with the progressive forward or backward spread of activity seen in the intact animal. The bursts of activity in the omasum, lasting 0·5‐2 min, were not co‐ordinated with the activity of the reticulo‐rumen as they are in the intact animal.

4. The activity in the reticulo‐rumen and omasum was not affected by bilateral section of the splanchnic nerves and removal of the coeliaco‐mesenteric ganglia. Reticulo‐rumen but not omasal activity was abolished by atropine (0·1 mg/kg) or hexamethonium (2 mg/kg), while both were stimulated by pentagastrin (3 μg/kg).

5. Following vagotomy reticulo‐rumen motility was no longer influenced by feeding, or by tactile stimulation of the buccal cavity or oesophagus. Severe distension of the abomasum caused a slight acceleration of the motility rhythm compared to the inhibition seen before vagotomy.

6. It is concluded that the reticulo‐rumen motility observed after vagotomy is an intrinsic cholinergic motility which is dependent upon the activity of the myenteric plexus. The motility of the omasum after vagotomy is similar to that seen in the intact animal and differs from that of the rumen in that it appears not to depend wholly upon cholinergic control.
Temperature‐dependence of shortening velocity and rate of isometric tension development in rat skeletal muscle
Authors: Ranatunga K. W.
Published: December 2014

1. The temperature‐dependence of the maximum velocity of shortening and of the maximum rate of isometric tension development were examined in a rat fast twitch muscle, extensor digitorum longus (e.d.l.), and a slow twitch muscle, soleus, in vitro and with direct stimulation. The temperature range was 35‐20 °C.

2. The maximum velocity of shortening and the maximum rate of tension development decreased with cooling in both muscles. The decrease was such that their logarithms were linearly related to the reciprocal of the absolute temperature over the temperature range of 35‐20 °C in e.d.l. and 35‐25 °C in soleus.

3. The calculated Arrhenius activation energy for maximum velocity of shortening was around 40‐45 kJ in both muscles. The activation energies for maximum rate of tension development were 48 kJ in e.d.l. and 56 kJ in soleus. Similar analyses made on the time to peak and time to half‐relaxation of the isometric twitch showed that their activation energies were higher, between 60‐80 kJ, in both muscles.

4. The results are examined in relation to biochemical findings and discussed in relation to A. F. Huxley's (1957) cross‐bridge theory.
Long‐term potentiation of excitatory synaptic transmission in the rat hippocampus: the role of inhibitory processes
Authors: Haas H. L. , Rose G.
Published: December 2014

1. The possibility that changes in inhibitory processes are responsible for long‐term potentiation (l.t.p.) was examined using the rat hippocampal slice preparation.

2. Inhibitory pathways were characterized using both extra‐ and intracellular recordings from the CA1 pyramidal cell layer. Stimulating electrodes were placed in either stratum radiatum or the alveus to allow orthodromic or antidromic activation of the pyramidal cells.

3. Using extracellular recordings, inhibition was studied by applying paired pulses at interstimulus intervals of 20‐500 msec through either the same or different stimulating electrodes, and quantifying the reduction in the population spike. An antidromic conditioning pulse was least effective in influencing the test response, while paired stimuli delivered through separate stimulators in stratum radiatum revealed the longest duration effects. Inhibition was either reduced or enhanced, depending upon the stimulation paradigm, with increasing stimulus intensity.

4. With l.t.p., alterations in paired‐pulse inhibition were observed corresponding to the changes in conditioning pulse amplitude. Reducing stimulus intensity to restore the initial conditioning pulse amplitude eliminated these effects.

5. Using intracellular recordings, the effects of l.t.p. on inhibition were studied by examining changes in e.p.s.p.—i.p.s.p. sequences, i.p.s.p.s evoked by antidromic stimulation, and spontaneous depolarizing i.p.s.p.s observed with KCl‐filled electrodes.

6. Following l.t.p. enhanced e.p.s.p.s and slightly reduced, but prolonged, i.p.s.p.s were observed in response to orthodromic stimulation. Antidromically evoked, as well as spontaneous, i.p.s.p.s were unaffected.

7 It is concluded that alterations in inhibitory processes are not responsible for l.t.p. in hippocampal subfield CA1. However, changes in the strength of inhibitory synapses as a consequence of long‐term potentiation may modify the functional character of the hippocampal connexions.
Modulation of stretch reflexes during locomotion in the mesencephalic cat
Authors: Akazawa K. , Aldridge J. W. , Steeves J. D. , Stein R. B.
Published: December 2014

1. A cat preparation was used to study the modulation of stretch reflexes during locomotion. The brain stem was transected and locomotion was induced by electrical stimulation of the mesencephalic locomotor region below the level of transection. Three legs walked normally on a treadmill, while the fourth leg, which was denervated except for the soleus muscle, was held fixed. Brief length perturbations were applied to the soleus muscle at various phases of the stepping cycle.

2. The stretch reflex in this muscle was deeply modulated during the step cycle, and reached its peak at or before the peak in soleus e.m.g. activity associated with the locomotion. A similar variation was observed when the sciatic nerve was stimulated electrically at a strength which elicited reflex activity (H wave), but did not directly elicit motor nerve activity (M wave). Variation in the reflex during electrical stimulation could not be accounted for by cyclic variation in fusimotor activity or in the afferent volley, but must be due to post‐synaptic changes in α‐motoneurones or in the presynaptic inputs to them.

3. Large changes were also observed in intrinsic muscle stiffness during the step cycle. The maximum stiffness occurred near the time the limb would normally strike the ground during locomotion. A high stiffness would be useful in reducing the amount that the limb would yield under the weight of the body during the extension phase of the step cycle. The variation of the stretch reflex in parallel with stiffness suggests that reflexes could assist in this load compensation. The variation is not consistent with the idea that the stretch reflex is used to compensate for changes in intrinsic muscle properties, so that the total system behaves more like a spring of constant stiffness than does muscle alone.
The influence of the frequency and pattern of sympathetic nerve activity on serotonin N‐acetyltransferase in the rat pineal gland.
Authors: Bowers C W , Zigmond R E
Published: December 2014

The activity of the pineal enzyme arylamine: N‐acetyltransferase (NAT) was determined following direct stimulation of the preganglionic or post‐ganglionic nerves of the superior cervical ganglia. 1. Stimulation of the preganglionic trunks at 10 c/sec during the day or night was sufficient to increase NAT activity approximately 50‐fold, to levels comparable to those observed at night in the intact animal. The time course of this effect of nerve stimulation differed between day and night. 2. The responses of pineal NAT to certain frequencies of stimulation were similar for preganglionic and post‐ganglionic stimulation. In both cases the responses to stimulation at 5 c/sec appeared to be maximal, 10 c/sec causing no further increase. However, at 10 c/sec, stimulation was more effective post‐ganglionically than preganglionically. 3. Various patterns of preganglionic stimulation, having the same average frequency, differed in their ability to increase the activity of NAT. Some, though not all, of these differences between patterns were observed during post‐ganglionic stimulation. 4. Unilateral stimulation of the preganglionic nerves produced an increase in NAT activity that was less than half the increase produced by bilateral stimulation, suggesting that the innervation from the two ganglia interact within the pineal gland. 5. These data indicate that changes in the firing rates of sympathetic nerves innervating the pineal gland, within the range of frequencies typically observed for sympathetic neurones, would be sufficient to account for the circadian rhythm in NAT activity observed in the intact rat. Changes in the over‐all pattern of sympathetic activity, in addition to changes in the total number of stimuli, could play a significant role in the pineal response.
The effects of low calcium and background light on the sensitivity of toad rods
Authors: Bastian Bruce L. , Fain Gordon L.
Published: December 2014

1. We have examined the effects of decreases in extracellular Ca2+ concentration on the intracellularly recorded light responses of rods from the toad, Bufo marinus. In agreement with previous results (Brown & Pinto, 1974; Lipton, Ostroy & Dowling, 1977), Ca2+ concentrations below 10−6 M produced a depolarization of rod resting membrane potential of approximately 30‐40 mV and a corresponding increase in the maximum amplitude of the rod's light responses, so that saturating flashes in normal and low Ca2+ Ringer produced hyperpolarizations to approximately the same membrane potential.

2. The rod's sensitivity was reduced in low Ca2+ Ringer by an amount dependent upon the extracellular Ca2+ concentration. At 10−6 M‐Ca2+, sensitivity was approximately 0·6 log units below normal. Thereafter, it dropped nearly linearly with [Ca2+]o to a value approximately 4·0 log units below normal at 10−9 M‐Ca2+. Most of the decline occurred within 1‐2 min after the solution change as the membrane potential depolarized, but sensitivity continued to fall slowly with time at the lowest Ca2+ concentrations. Exposure to low Ca2+ solutions altered the kinetics of the receptor response to brief flashes, delaying response onset and time‐to‐peak but affecting the time course of decay very little.

3. The sensitivity of the rod to maintained steps of light was also reduced in low Ca2+. Furthermore, the changes in sensitivity produced by background illumination were very much smaller in low Ca2+ than in normal Ringer. In some cases backgrounds actually increased sensitivity.

4. In 10−8 M‐Ca2+, backgrounds which themselves produced no response in the rod and no changes in rod sensitivity produced large decreases in response latency for responses of all amplitudes, and pronounced changes in time‐to‐peak and time‐to‐decay for moderate and large amplitude responses.

5. Since the effects of background light and low Ca2+ on the wave form of the rod are distinct and in some cases antagonistic, and since the changes in receptor sensitivity produced by backgrounds and low Ca2+ are not additive, the decreases in sensitivity produced by exposure to low Ca2+ appear to be caused by a mechanism distinct from normal light adaptation. We suggest that they are caused by an increase in the buffering capacity of the receptor cytosol for Ca2+ and that Ca2+ is the excitatory messenger or ‘internal transmitter’, as originally suggested by Yoshikami & Hagins (1971).
Metabolism and transport of strontium in giant axons of Loligo.
Authors: Baker P F , Singh R
Published: December 2014

1. The strontium content of squid axons averages 2.9 mumol kg‐1 axoplasm and squid blood contains 75 mumol Sr l‐1. The bulk of the Sr inside axons is bound, possibly within mitochondria. Sr seems to be handled by squid axons in an essentially similar manner to Ca. 2. Sr uptake is increased by electrical activity, by lowering external Na, by depolarization with K and by poisoning with cyanide or FCCP. Uptake is unaffected by ouabain. 3. Sr efflux has a Q10 of 2.2. Efflux can be divided operationally into three components: one dependent on external Ca (or Sr), one dependent on external Na and a residual component that can be inhibited by external lanthanum or internal vanadate. 4. Poisoning an axon with cyanide or FCCP results in a large increase in Sr efflux which can be divided operationally into two components: one dependent on external Ca (or Sr) and one dependent on external Na.
Spectral sensitivity functions of post‐receptoral responses in human vision.
Authors: Hendricks I M , Ruddock K H , Waterfield V A
Published: December 2014

1. Increment threshold illumination levels, It, for visual detection of a one‐dimensional, spatially periodic test pattern (i.e. a grating) presented to the right eye have been measured following a period of adaptation to high contrast patterns. The right (test) eye was adapted to a grating, matched in bar‐width and orientation to the test grating, and the left eye was adapted to a two‐dimensional matrix array of circular spots. It is shown that the value of It is dependent on the spatial and spectral parameters of the spot matrix. 2. The variation of It with change in matrix wavelength, lambda, is greatest for matrix spots of some 10‐15 min of arc diameter. 3. Values of It were determined as a function of the matrix wavelength, lambda. Three kinds of spectral response have been observed, each associated with a different stimulus geometry, and each characterized by the wavelength, lambda, for which It is minimum. With an adaptation matrix consisting of coloured spots on a dark surround, It is minimum for values of lambda around 600 nm, whereas with a matrix of dark spots on a coloured surround, the minimum occurs for lambda around 520 nm. The third spectral response is found when a blue test grating is superimposed on a yellow background, conditions under which detection is mediated by the blue‐sensitive, pi 1‐increment threshold mechanism. In this case, It is minimum for lambda equal to about 450 nm. 4. Three subjects with normal colour vision each give similar spectral responses, but the data for two deuteranopic red‐green dichromats deviate significantly from the normal response pattern. 5. The binocular interaction mechanism through which the spot matrix influences threshold detection of the test grating is discussed in relation to electrophysiological and other psychophysical data.
Nervous release of vasoactive intestinal polypeptide from the feline uterus: pharmacological characteristics.
Authors: Fahrenkrug J , Ottesen B
Published: December 2014

1. The release of the neuropeptide, vasoactive intestinal polypeptide (VIP), from the uterus in response to electrical stimulation of the hypogastric and pelvic nerves was examined in non‐pregnant anaesthetized cats. 2. Efferent stimulation of the pelvic nerve caused an increase in the release of VIP, which was unaffected by atropine and adrenoceptor antagonists, but completely abolished by hexamethonium. 3. Efferent stimulation of the hypogastric nerves induced a marked increase in the release of VIP, which was blocked by hexamethonium. After atropine and adrenoceptor blockade the nervously induced VIP response was undiminished and accompanied by an increase in uterine venous blood flow. 4. The results suggest that the VIP‐containing neurones in the uterus are intrinsic under preganglionic influence of pelvic and hypogastric nervous activity. It is proposed that VIP is a neurotransmitter in the feline uterus involved in non‐cholinergic, non‐adrenergic mechanisms such as the uterine vasodilation observed after hypogastric nerve stimulation.
Different types of tremor in the human thumb.
Authors: Brown T I , Rack P M , Ross H F
Published: December 2014

1. The upper limbs of normal subjects were immobilized in a way that allowed measurement of forces and movements at the thumb interphalangeal joint without significant movement elsewhere in the limb. 2. When the subject attempted to maintain a steady flexing force at the joint against a rigid stop, the actual force showed the irregular 8‐11 Hz fluctuations characteristic of a ‘physiological tremor'. This force fluctuation increased when the mean flexing force increased. 3. If the subject exerted his flexing force against a light complaint spring, there was an analogous irregular 8‐11 Hz movement at the joint. 4. When, however, an extra inertial load was added to the terminal phalanx, flexion against a complaint spring was often accompanied by a different type of tremor. This was a more regular oscillation, of lower frequency (3‐6 Hz), and of much larger amplitude. 5. The precise frequency and amplitude of this type of tremor depended on the characteristics of the added inertia and spring, in a way that could have been predicted from the responses of the joint to an imposed sinusoidal movement (Brown, Rack & Ross, 1982a). The movement appeared to arise from re‐excitation within stretch reflex pathways. 6. The irregular 8‐11 Hz tremor at this joint could not be attributed to reflex re‐excitation, since the responses to sinusoidal movement indicated a stretch reflex whose timing would not support a movement at that frequency. It is, however, emphasized that other joints of the hand and fingers may behave in different ways.
Pharmacological inhibition of the M‐current
Authors: Adams P. R. , Brown D. A. , Constanti A.
Published: December 2014

1. The effects of muscarinic agonists, luteinizing hormone‐releasing hormone (LHRH) analogues, uridine triphosphate (UTP) and divalent cations on K+‐currents in voltage‐clamped bullfrog sympathetic neurones have been studied.

2. Muscarine (1‐10 μM), D‐ala6 LHRH (1‐5 μM), UTP (50‐100 μM) and Ba2+ (1‐4 mM) selectively depressed the M‐current (IM), without appreciable effect on the delayed rectifier, Ca2+‐activated or transient outward currents (IK, IC or IA).

3. IM‐inhibition was characterized by: (a) elimination of slow current relaxations accompanying voltage jumps in the membrane potential range ‐30 to ‐60 mV; (b) reduced voltage‐dependent chord conductance over this range with no change in the voltage‐independent chord conductance at more negative membrane potentials; (c) suppression of outward rectification in the steady‐state current—voltage curve between ‐70 and ‐25 mV; and (d) development of an inward current which increased in amplitude between ‐70 and ‐20 mV in proportion to the decrease in steady‐state IM. The kinetics and voltage sensitivity of residual IM were unchanged.

4. The magnitude of the inward current produced by muscarine or LHRH could be accounted for quantitatively by the reduction in steady‐state IM. No increase in leak current could be detected in the range ‐60 to ‐30 mV. In two cells muscarine (10 μM) increased the leak current and conductance at ‐70 to ‐100 mV, but not at more depolarized levels.

5. IM was not modified by removing extracellular Ca2+, adding a selective Ca2+‐channel blocker (Cd2+), adding 1 mM‐dibutyryl cyclic AMP or 8′Br cyclic GMP, or by intracellular ionophoresis of Ca2+, 8′Br cyclic GMP, dibutyryl cyclic AMP, GTP‐γ‐S or S‐adenosylmethionine.

6. It is concluded that the principal effects of these agents in unclamped neurones — depolarization, increased input resistance, reduced outward rectification and increased excitability — are due entirely to a selective inhibition of IM. The intracellular transduction mechanism for IM inhibition is unknown.
An analysis of voltage noise in rod bipolar cells of the dogfish retina.
Authors: Ashmore J F , Falk G
Published: December 2014

1. The power spectral density of voltage noise in depolarizing rod bipolar cells was analysed during darkness and steady illumination. 2. The variance of the voltage fluctuations increased nearly linearly with dim light but was suppressed by bright light. 3. The spectrum in darkness and during illumination could be resolved into two components. One component was attributed to random quantal events arising from spontaneous or light‐induced isomerization of rhodopsin in the bipolar cell's rod pool. 4. The second component had a peaked spectrum and was attributed to synaptic noise. 5. A significant fraction of the noise variance in the dark arose from spontaneous thermal isomerization of rhodopsin, with a rate constant of 6 X 10(‐12) s‐1 or a half‐life for rhodopsin of 3700 years at 17 degrees C. 6. The peak amplitude of the single‐photon signal in the bipolar cell was about 200 microV, associated with a peak conductance increase of 200 pS. The spectral data suggest that there may be a random delay in the generation of these events. 7. It was concluded that the limitation to single‐photon detection in the dark‐adapted state may be the rate of spontaneous rhodopsin isomerization. Synaptic noise at the rod‐bipolar cell level would not seriously degrade the signal‐to‐noise ratio.
The rate of rise of alveolar carbon dioxide pressure during expiration in man.
Authors: Cochrane G M , Newstead C G , Nowell R V , Openshaw P , Wolff C B
Published: December 2014

1. The purpose of the study was to see whether the rate of rise of alveolar PCO2 (PA, CO2) in expiration was directly proportional to the rate of pulmonary elimination of CO2 (VCO2) in man in the steady state. 2. Alveolar ventilation at rest and during exercise in man was calculated from the difference between total ventilation and dead space ventilation, and from the ratio of the rate of pulmonary CO2 elimination to the mean expired alveolar CO2 (total) fraction. The results were indistinguishable. In agreement with other workers’ findings alveolar ventilation changed in direct proportion to the rate of carbon dioxide elimination, confirming the isocapnia of exercise ventilation in man. 3. The rate of rise of expiratory alveolar PCO2 in individual breaths has been obtained by two methods. In the first, a pattern of respiration with constant expiratory flow in each breath brought expiratory alveolar profiles to the outermost end of the airway. In the second method, the early part of the alveolar PCO2 during normal expiration was calculated from airway PCO2 and expired volume. 4. The data obtained with both methods show that, in the steady state, expiratory alveolar PCO2 rises at a rate which is directly proportional to the rate of CO2 production.
Muscarinic synaptic potentials in guinea‐pig myenteric plexus neurones.
Authors: North R A , Tokimasa T
Published: December 2014

1. Intracellular recordings were made from neurones in the myenteric plexus of the guinea‐pig ileum in vitro. 2. A single pulse stimulus to the presynaptic fibres entering a myenteric ganglion elicited a fast excitatory post‐synaptic potential (e.p.s.p.) in type 1 (S) cells: in about one‐quarter of cells this was followed by a slow e.p.s.p. 3. The slow e.p.s.p. had a latency of 122 ms and a total duration of 3‐15 s. It was reversibly abolished by hyoscine (1 microM). 4. Both the fast e.p.s.p. and the slow e.p.s.p. could be mimicked by ionophoretic application of a single brief pulse of acetylcholine (ACh) to the neurone soma. The depolarization which mimicked the fast e.p.s.p. was reversibly blocked by hexamethonium. The depolarization which mimicked the slow e.p.s.p. was reversibly blocked by hyoscine. 5. Type 2 (AH) neurones did not show fast or slow e.p.s.p.s in response to a single pulse stimulus. Stimuli comprising many pulses (typically 10 Hz for 3 s) evoked a slow e.p.s.p. in which the initial portion was partly blocked by hyoscine, but which was predominantly non‐cholinergic.
The effects of hydrostatic pressure on the spontaneous release of transmitter at the frog neuromuscular junction.
Authors: Ashford M L , MacDonald A G , Wann K T
Published: December 2014

1. The effects of hydrostatic pressure (0.1‐15.55 MPa) on the spontaneous release of transmitter at the frog neuromuscular junction were investigated. 2. The major effect of high pressure is on the release mechanism, pressure (0.1‐10.40 MPa) producing an exponential decrease in frequency of the miniature end‐plate currents in normal Ringer solution. The frequency decreases to 0.52 and 0.24 of the control value at 5.25 and 10.40 MPa respectively. This effect is reversible on decompression. 3. The sensitivity of the release process to high pressure is unaltered in 10 mM‐K+, 6 mM‐ and 10 mM‐Ca2+ and hypertonic (165 mM‐NaCl) Ringer solution, although the high Ca2+ media shift the threshold for the pressure effect to higher pressures. 4. Higher pressure (10.40‐15.55 MPa) produces a small increase in the time constant of decay (tau D) of m.e.p.c.s with no effect on the growth phase. A pressure of 15.55 MPa increases tau D to 1.35 of the control value. 5. The possible actions of high pressure on both the pre‐ and post‐synaptic processes are briefly discussed.
Neurotransmitter release and nerve terminal morphology at the frog neuromuscular junction affected by the dye Erythrosin B
Authors: Augustine George J. , Levitan Herbert
Published: December 2014

1. The quantal release of neurotransmitter and the fine structure of frog neuromuscular junctions has been examined in the presence of the xanthene dye Erythrosin B.

2. At concentrations of 10 μM or greater, Erythrosin B produced time‐ and dose‐dependent increases in transmitter release from presynaptic nerve terminals.

3. Miniature end‐plate potential (m.e.p.p.) frequency increased in an exponential manner during continuous exposure to the dye. The rate constant for this exponential was dose‐dependent, increasing with concentrations from 10 μM to 1 mM.

4. The amplitude of evoked end‐plate potentials (e.p.p.s) also increased exponentially during dye treatment, primarily due to an increase in quantal content. Rate constants for this effect were also dose‐dependent, and were approximately 1/5 as large as those for m.e.p.p.s.

5. While the frequency of m.e.p.p.s was increasing, their amplitude distribution did not qualitatively change. Thus the dye has little effect on the size of individual quanta.

6. The presynaptic effects of Erythrosin B were irreversible under these experimental conditions. Brief exposure to the dye caused increases in m.e.p.p. frequency and e.p.p. amplitude which were maintained at steady levels during extensive rinsing with dye‐free Ringer solution.

7. Prolonged exposure to the dye caused an eventual decrease in m.e.p.p. frequency and abolition of e.p.p.s. Coincident with this decline ‘giant’ m.e.p.p.s as large as 40 mV were observed.

8. At dye concentrations greater than approximately 200 μM, Erythrosin B rapidly and reversibly increased the membrane potential and input resistance of muscle fibres. This post‐synaptic effect was small and variable in normal saline, but was pronounced in low potassium solutions.

9. During the period that release was enhanced by Erythrosin B, presynaptic nerve terminals contained the normal complement of synaptic vesicles and other organelles. Mitochondria were swollen in this condition.

10. After m.e.p.p. frequency declined below normal levels and ‘giant’ m.e.p.p.s appeared, the number of synaptic vesicles within nerve terminals declined and dilated cisternae were present. Mitochondria were swollen further.

11. These results do not reveal any mechanism to explain the ability of Erythrosin B to increase transmitter release, but the decline in release may be caused by partial depletion of synaptic vesicles. The ‘giant’ m.e.p.p.s could be due to the discharge of acetylcholine from cisternae.
Electrophysiological and chemical determination of acetylcholine release at the frog neuromuscular junction.
Authors: Miledi R , Molenaar P C , Polak R L
Published: December 2014

1. Mass fragmentography was used to measure the tissue content and release of acetylcholine (ACh) by frog sartorius muscles, which had been previously treated with an irreversible cholinesterase inhibitor. The frequency of miniature end‐plate currents (m.e.p.c.s) was also measured. 2. Exposure of muscles for 15 min to 2 mM‐LaCl3 resulted in a large release of ACh which subsided to low levels after 1 h. About 4 h later treatment with 50 mM‐KCl, or with the calcium ionophore A 23187, or with a second dose of LaCl3, all failed to augment ACh release, notwithstanding the fact that the ACh content of La3+‐treated muscles was about the same as that of controls. 3. Hypertonic NaCl or raised KCl concentrations were used to increase m.e.p.c.s and this also increased ACh release; it was estimated that each quantum corresponded to the release of 12 000 molecules of ACh. 4. ACh release by nerve stimulation was greatly potentiated by 10 mM‐tetraethylammonium chloride, and this enabled the ACh released by ten, and even single, stimuli to be detected; it was calculated from the ACh released and the quantal content that each quantum contained on the average 13 000 molecules. 5. ACh released by nerve stimulation at 0.2/s in the absence of tetraethylammonium was about half that expected on the basis of previous estimates of quantal content; it was increased about two‐fold by alpha‐bungarotoxin. 6. It is concluded that chemical and electrical stimulation of the nerve evoked quantal ACh release, without influencing non‐quantal ACh leakage. The results are consistent with the view that ACh quanta are derived from synaptic vesicles. They also show that resting ACh release is not due to leakage of ACh ions along an electrochemical gradient in the membrane.
An evaluation of the plethysmographic method of measuring cranial blood flow in the new‐born infant.
Authors: Cowan F , Eriksen M , Thoresen M
Published: December 2014

Cranial blood flow values obtained plethysmographically in the human new‐born infant have been very variable and frequently very low. We have used a doppler ultrasound velocitymeter and skull compliance measurements to investigate whether the technique itself affects the cranial arterial inflow and whether the methods of calculation used introduce bias. Blood velocities were measured in intracranial and extracranial arteries during plethysmography, i.e. before, during and after jugular vein compressions of short duration. Skull expansion after tilting was used to estimate skull compliance. In about 10% of jugular vein compressions, arterial velocities decreased immediately, due to direct pressure on the carotid artery. In the remaining compressions a fall in arterial velocities was seen four or five heartbeats after the onset of the compression. This was probably caused by a decrease in the cranial perfusion pressure consequent on rising venous pressure. Some babies demonstrated very poor skull compliance and these babies had correspondingly low estimates of cranial blood flow. We conclude that jugular venous occlusion plethysmography is not a suitable method for use in the clinical field and is only useful as a research tool in carefully selected situations.
Anoxia and endothelium‐dependent reactivity of the canine femoral artery.
Authors: De Mey J G , Vanhoutte P M
Published: December 2014

Experiments were designed to determine the role of the endothelium in the responsiveness of the arterial wall to anoxia. Paired rings of canine femoral arteries were mounted for isometric tension recording in organ chambers filled with aerated Krebs‐Ringer bicarbonate solution (37 degrees C). One ring served as control; in the other the intimal layer was removed mechanically. Anoxia was induced by gassing the organ chamber with 95% N2/5% CO2. In control rings anoxia augmented contractile responses to noradrenaline, KCl and BaCl2. On return to O2 the contractile responses were transiently depressed. Removal of the endothelium reduced the anoxic augmentation, but did not affect the post‐anoxic inhibition. Indomethacin did not affect the response to anoxia. Anoxia abolished the endothelium‐dependent inhibitory effect of acetylcholine and thrombin, reduced that of adenosine triphosphate, but augmented that of arachidonic acid. These experiments indicate that endothelial cells may contribute to anoxic facilitation of the responsiveness of the canine arterial wall.
Actions on gamma‐motoneurones elicited by electrical stimulation of group II muscle afferent fibres in the hind limb of the cat.
Authors: Appelberg B , Hulliger M , Johansson H , Sojka P
Published: December 2014

The reflex effects elicited by electrical stimulation of group II muscle afferent fibres were recorded with micro‐electrodes in ninety‐eight hind‐limb gamma‐motoneurones of cats anaesthetized with chloralose. Eighty‐one of the gamma‐cells were classified as either static or dynamic by means of stimulation in the mesencephalic area for dynamic control known to influence dynamic gamma‐motoneurones selectively. A high responsiveness to activity in group II muscle fibres was found for the whole sample of gamma‐cells. Group II muscle action on dynamic gamma‐motoneurones was found to be more frequent than that on static ones. Excitation from group II fibres outweighed inhibition. This was clear cut for flexor gamma‐motoneurones. In extensor gamma‐cells, excitation prevailed by a small margin only. However, for both static and dynamic extensor gamma‐cells, excitation prevailed from both posterior biceps‐‐semitendinosus and the gastrocnemius‐‐soleus nerves, whereas inhibition was more frequent from the deep peroneal and quadriceps nerves. All the reflex effects studied were likely to be mediated via oligosynaptic pathways. The shortest latencies of excitatory effects were compatible with a disynaptic coupling. The fastest inhibitions were presumably trisynaptic. The present findings, supported by a parallel study of reflexes evoked by group III muscle afferents, strongly suggest that the reflexes on gamma‐motoneurones are not organized in accordance with the concept of flexion reflex afferents as conceived for alpha‐motoneurones. The interpretation of the results suggests a particularly independent position for dynamic gamma‐cells in relation to alpha‐ and static gamma‐motoneurones. Hence, the results also furnish an argument against the concept of alpha‐gamma linkage.