bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nucleus Z, the medullary relay in the projection path to the cerebral cortex of group I muscle afferents from the cat's hind limb
Authors: Landgren S. , Silfvenius H. 
Published: December 2014

1. The medullary relay of hind limb muscle afferents was studied in cats anaesthetized with chloralose. Evoked potentials were recorded from the dorsal surface of the medulla oblongata and from the depth of the medulla with penetrating micro‐electrodes. Graded electrical stimulation of the muscle nerves was used. The afferent volley was monitored by recordings from the lumbar dorsal roots or from the peripheral nerves.2. Group I muscle afferents from the ipsilateral quadriceps, posterior biceps‐semitendinosus and gastrocnemius‐soleus nerves evoked potentials in the nucleus Z of Brodal & Pompeiano (1957a). Focal and unitary potentials were recorded within 2·7–3·8 mm rostral to the obex and 2·8–4·1 mm lateral to the mid line. The recording positions were checked histologically.3. Focal and unitary responses appeared at threshold strengths of the afferent volleys. The latencies of the focal potentials varied between 4·5 and 7·0 msec, those of the unitary ones between 5·1 and 11·0 msec. Group II muscle afferents and low threshold cutaneous afferents also projected to nucleus Z.4. An antidromic discharge was evoked in the relay cells of nucleus Z by electrical stimulation of the contralateral thalamus.5. A lesion of nucleus Z abolished the response evoked in the contralateral post‐sigmoid gyrus of the cerebral cortex by the Group I muscle afferents of the hind limb.6. A superficial transection of the ipsilateral dorsolateral fascicle at the 1st cervical segment abolished the potentials evoked in nucleus Z.7. Results of lumbar cord transections showed that most of the primary afferents of the Group I hind limb path supplying nucleus Z enter the dorsolateral fascicle at L3 level.8. The relation of the Group I hind limb path to the dorsal spinocerebellar tract is discussed.
Responses of vibration‐sensitive receptors in the interosseous region of the duck's hind limb
Authors: Dorward Patricia K. , McIntyre A. K. 
Published: December 2014

1. Responses of receptors with fibres in the interosseous nerve of the duck's leg have been studied by recording unit discharges in filaments dissected from the sciatic nerve.2. Seventy‐two of the ninety‐four units examined served highly phasic, vibration‐sensitive mechanoreceptors in the interosseous region interpreted as being Herbst corpuscles. Receptor types for most of the other units could not be determined, but some were slowly adapting mechanoreceptors.3. Rheobase threshold values for the most sensitive vibration‐receptors were similar to those of mammalian Pacinian corpuscles.4. Threshold—frequency relationships for the vibration receptors showed a wider range of low frequency cut‐off values, and a greater capacity to signal high frequencies, than is the case with Pacinian corpuscles.5. Fibres of the vibration‐receptors had calculated diameters ranging from 5 to 10 μm and account for the bulk of the larger fibres in the interosseous nerve.6. It is suggested that Herbst corpuscles in the legs of birds might act as a warning device by detecting vibratory disturbances of the ground or other supporting surface.
Development of isometric tension in simian extraocular muscle
Authors: Fuchs A. F. , Luschei E. S. 
Published: December 2014

1. Isometric tension resulting from electrical stimulation of the abducens nerve was measured in the lateral rectus muscle of anaesthetized monkeys.2. The lateral rectus showed no increase in maximum tension at stimulus frequencies greater than 400/sec.3. However, at frequencies between 400 and 600/sec, the rate of change of tension increased so that maximum tension was achieved more rapidly.4. Rates greater than 600/sec caused no further increases in the rate of change of tension and actually resulted in a decrease of maximum tension.5. Since, in addition, single fibre recordings from ocular motor nerves reveal maximum discharge rates of less than 600/sec, units in the abducens nucleus that fire at greater than 600/sec are likely interneurones.6. Stimulation at rates of 30/sec, the frequency at which feline slow or slow twitch fibres produce fused contraction, produced no measurable tonic component of tension. Therefore, the force contributed by slow muscle fibres probably plays an insignificant role during eye movements.
Ultrastructure and contractures of the pigeon iris striated muscle
Authors: Pilar G. , Vaughan P. C. 
Published: December 2014

1. The ultrastructure of adult pigeon iris muscle fibres has been described with emphasis on the distribution of the sarcoplasmic reticulum (SR). Contractures due to superfusion with solutions of different [K+] (3–150 m
M) and acetylcholine (ACh) and their modification by alteration of external [Ca2+] and [Mg2+] were studied in isolated pigeon iris.2. The arrangement of the contractile myofilaments was like that of vertebrate skeletal fibres. The SR is well developed in the I‐band and sparse at the A‐band level.Tubular elements (T‐system) which form triads with the SR were seen at all levels of the sarcomere though usually adjacent to the A—I junction.3. K+ contractures developed monotonically to a steady level which was maintained for the duration of the high [K+] superfusion. The response to a standard [K+] stepwise change was not altered by conditioning the preparation with various [K+].4. Decreasing external [Ca2+] from 20 m
M to Ca2+‐free (i.e. no Ca2+ added), enhanced iris contractures at all [K+] and in ACh enriched solutions. The K+ response was abolished when the iris was superfused with Ca2+ free solution plus EDTA (2 m
M) for 45 min. Increasing [Mg2+] had little or no effect on iris contracture.5. Reducing external [Ca2+] from 3 to 0·3 m
M caused a reduction of 3‐7 mV in resting membrane potential and an increase from 3 to 10 m
M‐Ca2+ caused 3 to 7 mV membrane hyperpolarization. Muscle fibre input resistance was not affected.6. It is concluded that in the pigeon iris, Ca2+ required for contractile activation is obtained from internal stores, that membrane potential determines the degree of contractile activation and that the maintenance of the contracture is dependent on the failure of the Ca2+ releasing mechanism to inactive. In addition, it is speculated that because the iris muscle has only sparse SR at the A‐band level of the sarcomere, there may be slow Ca2+ reaccumulation.
Afferent discharges from arterial mechanoreceptors in the kidney of the rabbit
Authors: Niijima Akira 
Published: December 2014

1. Afferent discharges were observed in dissected filaments or single nerve fibres of renal nerves in the rabbit.2. Increasing the arterial perfusion pressure in excised kidney preparations caused an increase in afferent discharge rate. Increasing the venous pressure was without effect. Receptor discharge patterns were compatible with those of the slowly adapting type.3. In vivo, increasing the systemic blood pressure by means of the sinus reflex caused an increase in afferent discharge rate. Afferent discharge patterns showed no synchronicity with heart beat, irrespective of the blood pressure levels.4. It is suggested that mechanoreceptors are present around the arterial walls in the kidney and that they send information about blood pressure levels in the renal artery to the central nervous system.
The action of phospholipases on the inner and outer surface of the squid giant axon membrane
Authors: Abbott N. Joan , Deguchi T. , Frazier D. T. , Murayama K. , Narahashi T. , Ottolenghi A. , Wang C. M. 
Published: December 2014

1. The effects of phospholipases on resting potential, action potential and membrane ionic conductances of squid giant axons have been studied by means of internal perfusion and voltage clamp techniques. The sample of phospholipases used exhibited both phospholipase A and B activities.2. When applied externally, phospholipases had no effect on the resting and action potentials at a concentration of 100 μg/ml.3. When applied internally, the enzymes effectively suppressed the amplitude and maximum rate of rise of the action potential at a concentration of 100 μg/ml. The resting potential started decreasing appreciably only after the action potential had been suppressed to a considerable extent.4. Under voltage clamp conditions, the peak transient current was suppressed following internal perfusion of phospholipases, 150 μg/ml. The steady‐state current began to decrease, and the leakage current to increase only after the transient current had been suppressed to a considerable extent.5. The time course of sodium inactivation was not significantly slowed by internal perfusion of the enzymes.6. The curve relating the peak transient conductance to the membrane potential was shifted in the direction of depolarization after internal perfusion of phospholipases. No appreciable shift of the steady‐state conductance curve was observed.7. These experimental results are discussed in connexion with the possible role of membrane phospholipids in the conductance changes associated with excitation.
The depolarizing action of acetylcholine or carbachol in intestinal smooth muscle
Authors: Bolton T. B. 
Published: December 2014

1. The membrane potential of the longitudinal muscle of the guinea‐pig ileum was recorded intracellularly with glass micro‐electrodes.2. Acetylcholine or carbachol depolarized the membrane. The depolarization produced by 1·4 × 10−6
M carbachol was only 3·6 mV less than that produced by 5·5 × 10−5
M.3. When the change in size of the electrotonic potential was used to estimate the increase in membrane conductance produced by different concentrations of carbachol, the increase in conductance was about tenfold at 1·4 × 10−6
M and about 100‐fold at 5·5 × 10−5
M. There was a significant (P < 0·025) regression of the change in size of the electrotonic potential on the logarithm of the concentration of carbachol over this dose range. This and other observations suggest that it is not the availability of receptors which curtails the depolarization produced by concentrations of carbachol in excess of 1·4 × 10−6
M.4. Reducing the external sodium concentration shifted the level of peak depolarization produced by carbachol negatively, and increasing the external sodium concentration shifted it positively.5. Reducing the external chloride from 134 to 13 m
M had no significant effect on the level of peak depolarization produced by carbachol. Reducing the external chloride to 7 m
M shifted the level of peak depolarization 3·1 mV in a positive direction.6. Increasing the external potassium concentration had little effect on the level of peak depolarization produced by carbachol, and decreasing the external potassium shifted the level of peak depolarization positively.7. It was possible to account for the observed relationship between membrane potential and membrane conductance if the assumption was made that carbachol opens additional ion channels in the membrane which have an equilibrium potential of about −9 mV. It is suggested therefore that the depolarizing action of carbachol on this smooth muscle is limited by its equilibrium potential, and that the equilibrium potential and the membrane potential in the presence of large concentrations of carbachol (e.g. 5·5 × 10−5
M) are very close. Hence changes in the level of peak depolarization produced by varying the ionic composition of the external solution probably reflect changes in the equilibrium potential fairly closely.8. A simple model in which carbachol opens conductances to sodium, potassium and chloride ions and in which these conductances are independent of external ion concentrations (and voltage) could account for the effects on the equilibrium potential of varying [Na+]0 and [Cl−]0 but not [K+]0.9. It is suggested that carbachol increases the conductance to sodium, potassium and possibly other cations, and that, if it increases chloride conductance, then the increase produced is small relative to the increase in conductance to cations.
Site of action of 2‐deoxy‐D‐glucose mediating gastric secretion in the cat
Authors: Kadekaro Massako , Timo‐Iaria C. , Valle L. E. R. , Velha L. P. E. 
Published: December 2014

1. Site of action of 2‐deoxy‐
D‐glucose (2‐DG) responsible for its effect on gastric secretion was investigated in cats prepared with polyethylene or nylon cannulae chronically implanted in the antrum.2. The patterns of their basal secretion and secretory response to slow intravenous administration of 60 mg 2‐DG/kg body wt. were determined. After being subjected to selective neural lesions the cats were tested again and the secretory response was compared with the control.3. The normal response to 2‐DG in the cat is equivalent to that obtained in the dog. Volume, pH, acid concentration and output, chloride concentration and pepsin output attain peak values in 45–60 min.4. After intercollicular transection of the mid‐brain no secretory response occurred except for a tendency of acid concentration to increase. Large lesions of several diencephalic structures did not suppress the secretory response. Only those cats with a circumscribed lesion of the lateral area of the medial and posterior hypothalamus were unresponsive to 2‐DG. Acid secretion, as in the decerebrate animals, showed a slight tendency to increase after 2‐DG. Lesions immediately rostral, medial and dorsal to the territory of the medial forebrain bundle were ineffective in preventing augmentation of secretion. Destruction of structures contributing fibres to the medial forebrain bundle at hypothalamic levels, such as the neocortex, amygdala, fornix, septal and preoptic areas, did not change the secretory response.5. Intrafascicular neurones of the medial forebrain bundle are suggested as the main site of action of 2‐DG on gastric secretion.
Degeneration of sympathetic nerves in vitro and development of smooth muscle supersensitivity to noradrenaline
Authors: Geffen L. B. , Hughes Chris C. 
Published: December 2014

1. The sequence of events involved in degeneration of sympathetic nerve terminals has been studied in vitro in the expansor secundariorum muscle of the chicken.2. The muscle underwent a degeneration contraction due to abrupt release of noradrenaline stores from the nerves about 18 hr after isolation. The tension reached its peak within 6 hr at about 44% of the maximum tension developed to added noradrenaline.3. Responses to nerve stimulation were transiently potentiated by 35% on average just before the onset of the degeneration contraction and then failed abruptly.4. Degeneration release of noradrenaline was Ca2+‐dependent. Development of the degeneration contraction was delayed by temporary withdrawal of Ca2+ from the medium and was accelerated by a twofold increase in Ca2+ concentration when applied at a critical period close to the onset.5. Neither continuous nerve stimulation nor alterations in the length of the nerve stump influenced the course of the degeneration contraction in vitro.6. When the muscle was left in situ after denervation, the degeneration contraction occurred between 2 and 3 days later depending on the length of the distal portion of nerve. Cutting the nerve supply 5 cm closer to the muscle in vivo hastened the loss of transmission and the onset of the degeneration contraction by 24–48 hr.7. Supersensitivity to noradrenaline occurred soon after the degeneration contraction but the full development of a sevenfold supersensitivity to noradrenaline, equivalent to that produced by cocaine, took up to 48 hr. No further increase in sensitivity to noradrenaline could be detected in vitro after chronic denervation in vivo for up to 30 days.8. It is concluded that the degeneration contraction and failure of transmission was precipitated by an abrupt increase in the Ca2+ permeability of the axon causing discharge of transmitter from vesicles. This was probably the result of depletion of essential factors normally transported somatofugally in the axon at 1–2 mm/hr. The supersensitivity to noradrenaline that develops subsequently appears to be due to a loss of the uptake mechanism of the nerve terminals.
The role of post‐synaptic neurones in the biochemical maturation of presynaptic cholinergic nerve terminals in a mouse sympathetic ganglion
Authors: Black I. B. , Hendry I. A. , Iversen L. L. 
Published: December 2014

1. The role of post‐synaptic adrenergic neurones in the biochemical maturation of presynaptic cholinergic nerve terminals has been investigated in mouse superior cervical ganglion in vivo.2. Selective destruction of ganglion adrenergic neurones chemically, with 6‐hydroxydopamine (6‐OH‐DA), or immunologically, with nerve growth factor antiserum (NGF‐antiserum) prevented the normal maturation of choline acetyl transferase (ChAc) activity in presynaptic endings during development. Enzyme activity remained depressed for at least 2 months.3. 6‐OH‐DA treatment failed to alter ChAc activity in the developing duodenum or diaphragm, organs in which cholinergic fibres do not synapse with adrenergic neurones, suggesting that destruction of post‐synaptic neurones per se inhibited presynaptic maturation.4. Similarly, NGF‐antiserum, which does not destroy adrenergic neurones in the adult did not alter ChAc activity in adult mouse ganglia.5. These observations suggest that post‐synaptic adrenergic neurones regulate the biochemical development of presynaptic cholinergic nerve terminals.
An analysis of volume changes in the T‐tubes of frog skeletal muscle exposed to sucrose
Authors: Birks R. I. , Davey D. F. 
Published: December 2014

The volume responses of the T‐system of frog skeletal muscle to isotonic solutions of altered ionic composition, as studied by electron microscopic examination of osmium‐fixed tissue, have been re‐investigated using aldehyde fixatives.1. In confirmation of the earlier work we find that the T‐tubes swell in frog sartorius muscles which have been soaked in Ringer solution in which the sodium chloride concentration has been reduced to 40 m
M and tonicity maintained with sucrose before fixation in osmium.2. The swelling does not occur in muscles similarly treated, but fixed with acrolein or glutaraldehyde.3. Swelling of the T‐tubes, which has been reported for osmium‐fixed muscle following exposure to Ringer in which chloride is replaced by acetate, or reduced and sulphate substituted, does not occur when fixation is by acrolein.4. Analysis of the data from the earlier work with sucrose substitution shows that the degree of T‐tube swelling is proportional to the sucrose concentration of the soaking medium, whether the solution be isotonic or anisotonic.5. It is concluded that the increase in T‐tube volume arises in muscles which have been exposed to certain impermeant solutes during fixation by osmium, and a possible mechanism to account for the effect is described.6. The relevance of these observations to the hypothesis that the sarcoplasmic reticulum is an extracellular compartment in muscle and to the proposal that the T‐tubes may represent an intermediate compartment for potassium fluxes is discussed.
The effects of bile salt and raw bile on the intestinal absorption of micellar fatty acid in the rat in vitro
Authors: Rampone Alfred J. 
Published: December 2014

1. The uptake, esterification and transport of [14C]oleic acid were studied using sacs of rat everted small intestine incubated in 25 ml. of a buffered mixture of sodium taurocholate, glyceryl mono‐oleate and 14C‐labelled oleic acid in micellar form.2. Intestine obtained from bile fistula rats (bile duct cannulated 48 hr previously) showed elevated rates of 14C uptake into the tissue total lipid compared with sham‐operated controls.3. Nearly all of the excess 14C uptake in the bile fistula group was in the form of free fatty acid. Both groups showed similar rates of [14C]oleic acid incorporation into tissue triglyceride and also similar, though small, amounts transported into the serosal fluid.4. In further experiments using intestine from bile fistula rats the addition of 1 ml. of fresh rat bile to the incubation mixture reduced the 14C uptake to approximately control levels. The addition of 2‐3 ml. of fresh bile similarly reduced the uptake and increased 14C incorporation into the triglycerides of mucosal tissue and serosal fluid.5. These responses were not entirely the result of the bile salts contained in fresh bile since increasing the taurocholate concentration per se caused uptake, esterification and transport all to increase. In the presence of the higher taurocholate concentration the addition of fresh bile still caused a decrease in 14C uptake.6. There was no significant effect of either fresh bile or taurocholate on the transport of the 3‐O‐methyl analogue of
D‐glucose under comparable conditions.7. It is concluded that raw bile contains one or more components other than bile salts which may be important in determining fatty acid absorption.
Eating caused by 6‐hydroxydopamine‐induced release of noradrenaline in the diencephalon of the rat
Authors: Evetts K. D. , Fitzsimons J. T. , Setler Paulette E. 
Published: December 2014

1. Although it is well established that exogenous noradrenaline injected into the diencephalon causes the satiated rat to eat, it is not known whether eating may be induced by release of endogenous diencephalic noradrenaline. In the present experiment 6‐hydroxydopamine was injected into the diencephalon of the rat to release catecholamines and produce degeneration of catecholamine‐containing neurones.2. Injection into the preoptic area of 0·01–16·0 μg of 6‐hydroxydopamine caused satiated rats to eat.3. All doses of 6‐hydroxydopamine above 0·01 μg produced long‐lasting partial depletion of noradrenaline and dopamine in the region of the brain composed of septum, preoptic area and hypothalamus.4. Repeated injections of 8 μg 6‐hydroxydopamine at intervals of several days caused progressively less eating.5. Eating in response to 6‐hydroxydopamine was inhibited by pre‐treatment with desmethylimipramine, or by pre‐treatment with the adrenergic blocking agents phentolamine or MJ‐1999.6. Water intake after 6‐hydroxydopamine was reduced by pre‐treatment with desmethylimipramine or MJ‐1999 but was enhanced after pre‐treatment with phentolamine.7. It is concluded that release of diencephalic catecholamines by injection of 6‐hydroxydopamine causes eating in rats and that the catecholamine responsible for eliciting eating is noradrenaline.