bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effects of reserpine on motor activity and pallidal discharge in monkeys: implications for the genesis of akinesia
Authors: Iansek R. 
Published: December 2014

1. A reversible disturbance of basal ganglia function was produced in monkeys by the intramuscular administration of reserpine.2. Pallidal discharge was then compared with that recorded in the same animals during movement performance and following passive manipulation of the limbs.3. Akinesia, loss of postural support of the trunk, head and neck and absent postural reflexes were the predominant motor abnormalities produced by reserpine administration.4. Occasionally, postural tremor and catatonia were apparent. Rigidity and resting tremor were absent.5. Recordings made in the pallidum during the presence of akinesia revealed a marked reduction in natural neuronal discharge.6. Some pallidal neurones that remained active were driven in an uncharacteristic manner by peripherally generated afferent inputs from wide territories and by a variety of peripheral stimuli.7. The findings suggest the hypothesis that the akinesia in these animals was due to the diminished pallidal activity, and that pallidal discharge is normally a prerequisite for the performance of spontaneous motor activity. Pallidal neuronal firing may provide a background excitability to motor regions involved in the maintenance and elaboration of natural motor activity.
Electrical responses of muscle fibres in a small foot muscle of Xenopus laevis
Authors: Ridge R. M. A. P. , Thomson Alex M. 
Published: December 2014

1. Extensor digitorum longus IV (EDL IV) of Xenopus laevis was isolated together with its nerve and the 8th and 9th spinal roots. Motor units were functionally isolated.2. Glass micro‐electrodes were used to penetrate the muscle fibres and to record their electrical responses to stimulation of single motor axons, or the total motor supply to the muscle.3. Three types of electrical response were recorded from muscle fibres: an action potential in response to a single nerve stimulus (type 1), an action potential following repetitive nerve stimulation but not in response to single shocks (type 2) and end‐plate potentials which summed to a plateau of depolarization during repetitive nerve stimulation without producing action potentials (type 3).4. In general muscle fibres giving type 1 responses belonged to fast motor units with high twitch: tetanus ratios; those giving type 3 responses, to small units with low twitch: tetanus ratios; and those giving type 2 responses, to units with intermediate properties.5. In many cases the several muscle fibres innervated by a single axon gave different responses to stimulation of that axon and a single muscle fibre might give different responses to stimulation of two single axons. Thus it was not possible to classify motor units or muscle fibres by electrical responses.6. Stimulation of the total motor supply to the muscle favoured the production of type 1 responses so that the proportion of muscle fibres giving type 1 responses was higher when the muscle nerve was stimulated than when single motor axons were stimulated. The proportion of fibres giving type 2 responses was lower, and the proportion of fibres giving type 3 responses was similar, in both cases. The implications of this are discussed.7. Low neuromuscular junctional efficacy is suggested as an explanation for fluctuating twitch tensions and low twitch: tetanus ratios in many motor units in this muscle, and may also affect the activity patterns imposed on the muscle fibres by the motor axons which supply them.
Functional capacities of tactile afferent fibres in neonatal kittens
Authors: Ferrington D. G. , Rowe Mark J. 
Published: December 2014

1. Responses were recorded from individual tactile afferent fibres isolated by microdissection from the median nerve of pentobarbitone‐anaesthetized neonatal kittens (1‐5 days post‐natal age). Experiments were also conducted on adult cats to permit precise comparisons between neonatal and adult fibres.2. Neonatal fibres with receptive fields on the glabrous skin of the foot pads were classified into two broad groups, a slowly adapting class (40%) which responded throughout a 1 sec period of steady indentation and a rapidly adapting or dynamically sensitive class comprising 60% of units. Fibres in these two groups had overlapping conduction velocities in the range 4·3 to 7·5 m/sec and were believed to be the developing Group II afferents of the adult.3. Neonatal slowly adapting fibres qualitatively resembled their adult counter‐parts. They displayed graded stimulus‐response relations which, over the steepest segment of the curves, had mean slopes of 15·7 impulses/100 μm of indentation. Plateau levels of response were often reached at amplitudes of skin indentation of < 0·5‐0·7 mm.4. Dynamically sensitive fibres with receptive fields on the glabrous skin were studied using sinusoidal cutaneous vibration which in the adult enables them to be divided into two distinct classes. However, in the neonate, they formed a continuum whether criteria of sensitivity or responsiveness were used.5. In response to vibration neonatal fibres differed from adult ones according to the following quantitative indices: (i) sensitivity as measured by both absolute thresholds and thresholds for a 1: 1 pattern of response, both of which were higher in the neonate than in the adult at all frequencies > 50 Hz and differed by an order of magnitude at frequencies ≥ 200 Hz; (ii) responsiveness based on the mean impulse rate evoked at a fixed amplitude of cutaneous vibration; (iii) band width of vibratory sensitivity which in the neonate was confined to approximately 5‐300 Hz whereas in the two classes of adult units it covered the range 5‐800 Hz; (iv) capacity for coding information about vibration frequency. Impulse activity of neonatal fibres was less tightly phase‐locked to the vibratory stimulus and showed a poorer reflection of the periodic nature of the vibratory stimulus than impulse patterns of adult units.6. The results reveal that tactile receptors and afferent fibres in the neonate are functionally immature. Their restricted coding capacities suggest that peripheral tactile sensory mechanisms impose limits on the ability of the new‐born animal to derive information about its tactile environment.
Effect of a ‘sickling pulse’ on calcium and potassium transport in sickle cell trait red cells
Authors: Bookchin Robert M. , Lew Virgilio L. 
Published: December 2014

1. To trace the early development of the extensive functional membrane abnormalities found in sickle cell anaemia red cells which result from polymerization of haemoglobin S, we followed the effects on Ca and K transport of an in vitro sickling pulse in sickle cell trait (SA) red cells, whose membranes are initially normal.2. Sickling induced a progressively larger uptake of Ca in fed, starved and ATP‐depleted SA cells, always substantially higher than that in normal (AA) red cells under comparable conditions. The fraction of ionized Ca within the SA cells, estimated from the equilibrium distribution of 45Ca induced by the ionophore A23187 was about 0·4 of the total Ca content and similar in SA and AA cells.3. With ATP‐depleted SA cells, Ca uptake (representing Ca permeability) was maximal during sickling and was only partially reduced towards normal after desickling. Net Ca uptake during sickling of fed or starved SA cells reverted to net Ca loss upon reoxygenation, irrespective of the Ca gradient, indicating full restoration of the low Ca permeability of the control conditions.4. Following desickling of both fed and starved SA cells, the rates of uphill extrusion of Ca gained during sickling were much smaller than those expected with normal Ca pumps operating at similar internal Ca concentrations.5. After 2 hr sickling ATP levels in starved SA cells were reduced by 50% regardless of the presence or absence of Ca in the medium; therefore sickling‐induced Ca uptake was associated with no measurable consumption of ATP due to Ca‐pump activity.6. With ATP‐depleted SA cells, a Ca uptake of 2‐3 μmole/l. cells elicited a maximal response of the K permeability system resulting in full equilibration of the K pools in the cell suspensions. Sickling of fed and starved SA cells produced a small increase in K permeability which was entirely independent of the presence or absence of Ca.7. Sickled forms persisted after reoxygenation only with ATP‐depleted SA cells and were more frequent after sickling in the presence of Ca (about 20%) than in a Ca‐free medium (about 4%).8. These findings show that initial sickling produces an increased Ca permeability whose extent and reversibility depends on the metabolic state of the cells, and a partial Ca‐pump failure, which appears to be irreversible. We confirm a small sickling‐related, reversible increase in K permeability but a Ca‐dependent increase in K permeability does not occur unless the cells are fully depleted of ATP. The implications for sequential development of related abnormalities in SS cells are discussed.
The interplay between hydrogen ions, bicarbonate ions and osmolarity in the anterior duodenum modulating gastric function in the conscious calf
Authors: Bell F. R. , Nouri M. , Webber D. E. 
Published: December 2014

1. Gastric emptying, gastric acid and pepsinogen secretion were assessed simultaneously in the conscious calf using the test meal and duodenal perfusion technique (Bell & Mostaghni, 1975).2. Duodenal infusion of NaCl at a constant osmolality of 300 m‐osmole/kg, but with pH ranging from 2·0 to 12·0, did not alter the high level of gastric emptying and secretion already reported for isotonic NaCl or NaHCO3 alone (Bell & Mostaghni, 1975; Bell & Webber, 1979). Gastric function, therefore, is either unaffected by gastric chyme at pH 2·0‐12·0 entering the duodenum, or else isotonicity is dominant over pH in activating duodenal receptors which increase motor activity.3. When the pH of the isotonic NaCl was reduced by the addition of HCl to below pH 2·0, inhibition of gastric function occurred in direct proportion to the amount of titratable acid present in the infusate. The H+ moiety of isotonic duodenal infusates of pH < 2·0 dominates activation of osmoreceptors and so inhibits motor activity.4. When the same amount of acid but at differing concentrations and infusion rates was introduced into the duodenum uniform inhibition of gastric function occurred. This result indicates that duodenal acid receptors respond to acid concentration and flow rate to produce an integrated response in proportion to the amount (concentration × volume) of acid present.5. Isotonic NaHCO3 solutions adjusted to pH 8·1‐12·0 by the addition of NaOH, like isotonic NaCl infusions, did not affect gastric function until pH 11·0‐12·0, when significant inhibition occurred. This inhibitory effect of isotonic NaHCO3 at high pH is probably due to CO32−, since Na2CO3 and Li2CO3, but not LiCl, produce a similar inhibitory effect on gastric function.6. The inhibitory effect of carbonate gives some support to the existence of a CO2‐sensor as suggested by Hunt & Knox (1972), whereby increased PCO2 produced by intracellular or intercellular neutralization of CO32- by duodenal H+ activates acid receptors. But other experiments reported here, where simultaneous perfusion of HCl and excess NaHCO3 produced a rise in intraluminal PCO2, did not inhibit gastric function, which is contrary to the idea of a direct intraluminal effect of CO2 on duodenal receptors.7. The pH, PO2, PCO2, HCO3− and base excess of venous blood showed no detectable change during duodenal infusion of either acidic or alkaline solutions. Metabolic acidosis or alkalosis, therefore, cannot be considered to play any part in controlling gastric function. The results thus corroborate the notion that the receptors controlling gastric function are localized in the intestinal mucosa.8. Our results suggest that interplay between acid and osmolality of gastric chyme occurs in the rostral part of the duodenum to produce a graded inhibitory effect which by negative feedback modulates the gastric effectors that normally activate smooth muscle, parietal cells and zymogen cells.
The effect of the red cell membrane and a diffusion boundary layer on the rate of oxygen uptake by human erythrocytes
Authors: Huxley Virginia H. , Kutchai Howard 
Published: December 2014

1. This paper deals with the contributions of the red cell membrane and an external diffusion boundary layer (‘unstirred layer’) to the resistance to O2 entry into the red cell. Bovine serum albumin (BSA) was added to the extracellular fluid to enhance the effect of the diffusion boundary layer by diminishing both the solubility and the diffusivity of O2. The rate of O2 uptake by human red cells at various extracellular BSA concentrations was determined with a stopped‐flow rapid‐reaction apparatus.2. The initial rate of O2 uptake by the red cells was directly proportional to the diffusion coefficient of O2 in the extracellular fluid.3. If the diffusion boundary layer and the plasma membrane are considered as resistors in series, we estimate that 82‐100% of the total resistance to O2 entering the cell is due to the diffusion boundary layer. Our best estimate is that 95% of the resistance resides in the diffusion boundary layer.4. Our best estimate of the O2 permeability of the red cell membrane is 3·15 × 10−6 m‐mole/(cm2 sec mmHg). With this permeability the membrane would account for only 5% of the total resistance to O2 entering the cell. Partly because the membrane O2 diffusion resistance is a small fraction of the total resistance our estimate of the membrane resistance has a large standard deviation. Taking our estimate of the membrane resistance plus and minus its standard deviation we find that the membrane may account for 0‐18% of the total resistance to O2 entering the cell.5. The effective thickness of the diffusion boundary layer immediately after mixing is about 1·93 μm according to our analysis.
A study of desensitization of acetylcholine receptors using nerve‐released transmitter in the frog
Authors: Magleby K. L. , Pallotta B. S. 
Published: December 2014

1. Desensitization of acetylcholine (ACh) receptors was studied at the frog neuromuscular junction under voltage clamp.2. ACh was applied directly to junctional receptors by stimulating the motor nerve with trains of impulses. End‐plate currents (e.p.c.s) were used to estimate the total number of channel openings by the junctional ACh receptors, and miniature end‐plate currents (m.e.p.c.s) were used to measure changes in post‐synaptic sensitivity. Under the conditions of these experiments the changes in m.e.p.c. amplitudes were shown to be post‐synaptic in origin and thus provided a measure of desensitization.3. When the acetylcholinesterase was inhibited with diisopropylfluorophosphate, neostigmine, or collagenase treatment to prolong the duration of the nerve‐released ACh in the synaptic cleft, desensitization developed during repetitive stimulation of 1000 impulses at 5‐33 impulses/sec and then recovered after the conditioning trains, with a time constant of about 25 sec.4. When the acetylcholinesterase was active so that the duration of ACh in the synaptic cleft resulting from each nerve impulse was brief (< 300 μsec), desensitization developed in response to 300‐500 pairs of nerve stimuli if the interval between the impulses of each pair was 25 msec or less. When the interval was 30 msec or greater, however, measurable desensitization did not occur, even if the total number of channel openings was many times greater than in the experiments with shorter intervals or inhibited esterase where desensitization readily occurred.5. The desensitization observed to pairs of impulses was enhanced by chlorpromazine and decreased when the post‐synaptic membrane was depolarized, properties similar to those described previously for desensitization to bath and ionophoretic application of ACh.6. These results indicate that desensitization to nerve‐released transmitter is not a simple consequence of receptor activation, is not due to blockade of the open receptor channels by ACh, and does not result from ACh binding directly to desensitized receptors with a resulting shift in the receptor population towards the desensitized state.7. We suggest that the desensitization observed to nerve‐released transmitter is a two‐step process with both steps initiated by ACh. In the first step ACh converts some receptors into a desensitizable state which has an apparent lifetime of less than 30 msec; in the second step ACh desensitizes the desensitizable state.
Pattern of ‘non‐reciprocal’ inhibition of motoneurones by impulses in group Ia muscle spindle afferents in the cat
Authors: Jankowska Elżbieta , McCrea David , Mackel Robert 
Published: December 2014

1. Inhibitory post‐synaptic potentials (i.p.s.p.s) evoked by adequate stimulation of group Ia muscle spindle afferents of triceps surae and plantaris and by near‐threshold electrical stimulation of quadriceps and hamstring nerves were recorded in a number of motoneurone species. The aim of the study was to compare the pattern of non‐reciprocal Ia inhibitory actions on hind‐limb motoneurones with the pattern of inhibition evoked from group Ib tendon organ afferents.2. In all the motoneurone species analysed in which i.p.s.p.s were evoked by electrical stimulation maximal for both group Ia and Ib afferents of triceps surae and plantaris, they were also evoked when these muscles were stretched and the amplitude of the stretch (10‐35 μm) was below threshold for Ib afferents; 70‐100% of motoneurones with Ib i.p.s.p.s showed stretch‐evoked i.p.s.p.s. The stretch‐evoked i.p.s.p.s appeared with latencies compatible with disynaptic and trisynaptic linkage. Since these latencies were too short to allow their mediation by group II afferents the i.p.s.p.s are attributed to a selective action of Ia afferents. The i.p.s.p.s did not appear after the nerves to triceps surae and plantaris had been cut.3. Electrical stimulation of quadriceps and hamstring nerves which was near threshold for Ia afferents and well below threshold for either the Ib component of the incoming volley or group II afferents, similarly evoked non‐reciprocal i.p.s.p.s. They were found in those motoneurones in which inhibition was evoked by stimulation maximal for group I afferents. Such Ia i.p.s.p.s were evoked both in homonymous motoneurones and in motoneurones of four other hind‐limb muscles. Their latencies corresponded to di‐ and trisynaptic coupling.4. In some motoneurones of the pretibial flexors (anterior tibial, extensor digitorum longus and peroneus longus), disynaptic i.p.s.p.s evoked from triceps surae and/or plantaris which were depressed by a conditioning ventral root stimulation (i.e. Ia reciprocal i.p.s.p.s) were followed by trisynaptic i.p.s.p.s which were not depressed in this way (Ia ‘non‐reciprocal’ i.p.s.p.s). It thus appears that the same motoneurones may be inhibited by impulses in group Ia afferents via different spinal pathways.5. The study leads to the conclusion that the non‐reciprocal inhibition from group Ia muscle spindle afferents operates in parallel with the inhibition from group Ib tendon organ afferents in all motoneurone species tested.
Calcium current‐dependent and voltage‐dependent inactivation of calcium channels in Helix aspersa
Authors: Brown A. M. , Morimoto K. , Tsuda Y. , Wilson D. L. 
Published: December 2014

1. Inactivation of the Ca channels has been examined in isolated nerve cell bodies of Helix aspersa using the suction pipette method for voltage clamp and internal perfusion.2. Satisfactory suppression of outward currents was essential. This was achieved over most of the voltage range by substitution of Cs ion for K ion and by the use of TEA intra‐ and extracellularly and 4‐AP extracellularly. A small time‐ and voltage‐dependent non‐specific current remained at potentials above +60 mV.3. In these solutions, Ca current approaches ECa but cannot be detected in the outward direction. The Ca channel appears to be impermeable to Cs and Tris ions.4. Inactivation of Ca currents occurs as a bi‐exponential process. The faster rate is 10‐20 times the slower rate and is about one twentieth the rate of activation. The development of inactivation during a single voltage‐clamp step and the onset of inactivation produced by prepulses followed after brief intervals by a test pulse, have roughly similar time courses.5. The rates of inactivation increase monotonically at potentials more positive than about ‐25 mV. The amount of steady‐state inactivation increases with membrane depolarizations to potentials of about +50 mV. At more positive potentials, steady‐state inactivation is reduced.6. Intracellular EGTA slows the faster rate of inactivation of ICa and reduces the amount of steady‐state inactivation measured with a standard two pulse protocol. The effect is specifically related to Ca chelation and hydrogen ions are not involved. This component of inactivation is referred to as Ca current‐dependent inactivation and is consistent with observations that increased Cai inactivates the Ca channel. The process does not depend upon current flow alone since Ba currents of comparable or greater magnitude have smaller initial rates of inactivation. Furthermore, application of Ba ion intracellularly in large concentrations has no effect on steady‐state inactivation.7. The bi‐exponential inactivation process that persists in the presence of EGTAi is similar to that occurring when extracellular Ba ion carries current through the Ca channel. Steady‐state inactivation also persists and is similar in the two cases. Therefore it is concluded that inactivation is voltage‐dependent as well as Ca current‐dependent.8. Diffusion models that included reasonable values for the effect of binding on diffusion, even when combined with declining influxes, did not account for this ‘mixed’ form of calcium‐ and voltage‐dependent inactivation. A compartmental model in which the particular kinetic model of voltage‐dependent inactivation was not critical described the Ca current‐dependent inactivation.
Ouabain and regulation of cellular volume in slices of mammalian renal cortex
Authors: Cooke K. R. 
Published: December 2014

1. The effect of ouabain on cellular volume recovery in rabbit, guinea‐pig and rat renal cortical slices was studied. A concentration of ouabain that is maximally effective in inhibiting slice potassium accumulation was determined for each species. Slices from each species were either freshly prepared and then incubated, or leached and then incubated, or preincubated in oxygenated ordinary medium (equilibrated), leached and then reincubated in media with and without this concentration of ouabain. All incubations were at 25 °C.2. Potassium loss produced by ouabain was greater in rabbit and guinea‐pig slices than in rat slices.3. With slices that were freshly prepared and then incubated, and with slices that were leached and then incubated, cellular volume recovery was inhibited by ouabain in rabbit and guinea‐pig slices, but not in rat slices.4. After equilibration, swelling during leaching was less, especially in rabbit and guinea‐pig slices. However, on subsequent reincubation, significant differences in tissue water and cation contents that were consistent with inhibition of cellular volume recovery by ouabain, were seen in slices from these two species, but not in rat slices.5. Slices from all three species, when incubated with concentrations of ouabain that were maximally effective in inhibiting potassium accumulation, appeared to approach a steady‐state tissue potassium content that was greatest in rat slices and least in rabbit slices. Rat slices, previously depleted of potassium, reaccumulated potassium in the presence of 10 m
m‐ouabain to reach this steady‐state potassium content.6. Despite superficial appearance to the contrary (especially in the case of rat slices) these results are consistent with a major role for the conventional pump in controlling cortical cell volume. They do not provide evidence for the postulate that renal cortical cells possess a separate, ouabain‐insensitive mechanism regulating cell volume.