bluuebunny/crossref_metadata_2025_split huggingface dataset:
Activity of C fibre cardiac vagal efferents in anaesthetized cats and rats
Authors: Jones James F. X. , Wang Yun , Jordan David 
Published: September 2004

Bradycardia can be evoked by stimulation of both myelinated and non‐myelinated vagal efferent fibres. The on‐going activity and synaptic inputs to cardiac vagal preganglionic neurones with myelinated axons have been studied in detail, but there is little information regarding cardiac preganglionic neurones with non‐myelinated axons. In the present study, the on‐going discharge and afferent inputs to cardiac vagal efferents with non‐myelinated axons were studied in anaesthetized rats and cats.Extracellular recordings were made from vagal preganglionic neurones in the dorsal vagal motor nucleus (DVMN) of anaesthetized rats following electrical stimulation of the cervical vagus nerve. Based on calculated axonal conduction velocities, fifty‐six neurones had non‐myelinated axons. Sixteen of these C fibre neurones had on‐going activity but this showed no relationship to central respiratory drive, lung inflation or the cardiac cycle. Activity of twenty‐one of these fifty‐six neurones was increased at short latency following right atrial injections of phenylbiguanide (PBG).Eight presumed cardiac vagal preganglionic neurones were also recorded in the DVMN. Five of these were activated by PBG administration, and the one neurone with resting activity showed no indication of respiratory‐related activity.Finally, twenty‐one single C fibres were recorded in peripheral branches of the cardiac vagus. They had a low rate of on‐going activity, and in twelve fibres this on‐going discharge was analysed in detail. On‐going activity in seven of these fibres showed no relationship to central respiratory drive, lung inflation or the cardiac cycle, whereas the other five had prominent relationships with both central respiratory drive and lung inflation, and two of these also showed a relationship to heart period. PBG administration evoked an increased activity in fourteen of the fifteen fibres tested, and the latencies of nine of these responses (1.3 ± 0.5 s) were within the pulmonary circulation time.In anaesthetized cats, extracellular recordings were made in the DVMN from thirty‐three cardiac vagal preganglionic neurones with C fibre axons. The on‐going activity of these neurones, when present, never exhibited an on‐going‐ or reflexly induced respiratory rhythm, nor any indication of an input from the arterial baroreceptors. Right atrial injection of PBG evoked a short‐latency response in four of the five spontaneously active neurones but was without effect on the eight neurones tested which did not exhibit on‐going activity.In conclusion, the majority of cardiac vagal preganglionic neurones located in the DVMN have C fibre axons, show no obvious input from central or peripheral respiratory‐ or cardiac‐related inputs, but are activated by stimulation of pulmonary C fibre afferent fibres.
Non‐linear summation of excitatory synaptic inputs to small neurones: a case study in spinal motoneurones of the young Xenopus tadpole
Authors: Wolf Ervin , Zhao Fei‐Yue , Roberts Alan 
Published: September 2004

We examined the steady‐state summation of postsynaptic potentials (PSPs) in small, electrotonically compact neurones with short dendrites, using a one‐compartment electrical equivalent model of the passive membrane with conductances to represent chemical synapses and electrotonic junctional connections to neighbouring neurones.
Our model shows that PSP summation is non‐linear and for small depolarizations is mainly determined by the increase in total neurone conductance due to the opening of synaptic channels. At bigger depolarizations the change in synaptic driving force becomes an equally important cause of non‐linearity.
Non‐linear summation of AMPA‐mediated PSPs was measured experimentally when two monosynaptic pathways to motoneurones were stimulated. The conductances underlying these PSPs were calculated relative to the resting neurone conductance using our model. These conductance ratios were hardly affected by the size of electrotonic coupling conductances. The non‐linearity in PSP summation could be predicted by the model provided that the depolarizations remained negative to potentials at which voltage‐dependent channels open.
The model was used to estimate the relative contributions of glutamatergic, cholinergic and electrotonic excitation to EPSPs measured in Xenopus tadpole spinal motoneurones during swimming. Estimates of synaptic conductances and electrotonic coupling to other motoneurones suggest that ligand‐gated conductance mediated by glutamate may be twice that due to acetylcholine.
We conclude that in small electrotonically compact motoneurones of the Xenopus tadpole, our simple model can predict the non‐linearity in PSP summation and may allow the conductances of different synaptic inputs to be compared. Furthermore, excitatory synaptic conductances can increase the resting neurone conductance significantly and limit depolarization. Our general model may also be applicable to other small neurones.
Postural after‐contractions in man attributed to muscle spindle thixotropy
Authors: Hagbarth Karl‐Erik , Nordin Magnus 
Published: September 2004

It is an old observation that non‐volitional arm abduction movements accompanied by a sensation of arm lightness often occur as an after‐effect following forceful voluntary arm abductor contractions against a restraint. In the present study we have tested the hypothesis that such non‐volitional, so‐called ‘postural after‐contractions’ are tonic reflex responses to an enhanced resting discharge in primary muscle spindle afferents which in turn is a consequence of thixotropy‐dependent enhanced stiffness of intrafusal muscle fibres.
Results obtained in ten volunteers show that the arm abductor after‐contraction phenomenon in man is most readily evoked by a type of conditioning procedure which in various respects mimics the procedure proven in animal experiments to be particularly effective in producing thixotropy‐dependent excitation of primary spindle endings.
It is also shown that changes in arm abductor intramuscular temperature affect the strength of the after‐contractions in a direction predicted by the thixotropy hypothesis.
Attention is drawn to several similarities between the after‐contraction phenomenon with accompanying sensory illusions and the tonic reflex responses and illusions that can be induced when primary spindle endings are excited by muscle vibration.
The results support our hypothesis that postural after‐contractions are induced by activity in primary muscle spindle afferents as a consequence of thixotropic properties of intrafusal muscle fibres. Central excitability changes following the conditioning voluntary effort may contribute to the phenomenon.
Electrophysiological characterization of spinal neuronal response properties in anaesthetized rats after ligation of spinal nerves L5‐L6
Authors: Chapman Victoria , Suzuki Rie , Dickenson Anthony H. 
Published: September 2004

Despite a number of models of nerve injury, few studies have examined how peripheral nerve injury influences spinal somatosensory processing.
Ligation of two (L5‐L6) of the three spinal nerves that form the sciatic nerve produces a partial denervation of the hindlimb. Following ligation, rats exhibited withdrawal responses to normally innocuous punctate mechanical and cooling stimuli (acetone) applied to the lesioned hindpaw. Such mechanical and cooling allodynia was not observed in sham‐operated rats.
A significantly greater proportion of spinal neurones of ligated rats exhibited spontaneous activity at post‐operative (PO) days 7–10 (P= 0.03) and 14–17 (P= 0.0001), compared with sham controls. The frequency of the spontaneous activity was significantly higher than that of the sham controls (P= 0.03 and P= 0.02 for days 7–10 and days 14–17, respectively).
At the earlier PO period, significantly (P= 0.02) more neurones of spinal nerve‐ligated (SNL) rats responded to brush compared with the sham controls; at the later PO period the proportion of neurones of SNL rats responsive to prod was significantly (P= 0.007) reduced compared with the sham controls. The magnitude of the evoked neuronal response of SNL rats at PO days 7–10 was comparable to that of the sham controls. The magnitudes of brush‐ and prod‐evoked neuronal responses of SNL rats were significantly smaller (P= 0.05 and P= 0.002, respectively) than the sham controls at PO days 14–17. In addition, neuronal responses of SNL rats to mechanical punctate stimuli and the C fibre‐evoked neuronal responses were significantly reduced at the later PO period, compared with sham controls. Aβ‐fibre‐induced wind‐up was not observed under any conditions.
These complex changes in neuronal responses are both time and modality dependent. The plasticity of some of the neuronal and behavioural responses following nerve injury was difficult to reconcile. We suggest that an interplay between pathological peripheral and central mechanisms may account for some of the changes that could contribute to allodynia and hyperalgesia.
Efferent projection from the preoptic area for the control of non‐shivering thermogenesis in rats
Authors: Chen Xiao‐Ming , Hosono Takayoshi , Yoda Tamae , Fukuda Yutaka , Kanosue Kazuyuki 
Published: September 2004

To investigate the characteristics of efferent projections from the preoptic area for the control of non‐shivering thermogenesis, we tested the effects of thermal or chemical stimulation, and transections of the preoptic area on the activity of interscapular brown adipose tissue in cold‐acclimated and non‐acclimated anaesthetized rats.
Electrical stimulation of the ventromedial hypothalamic nucleus (VMH) elicited non‐shivering thermogenesis in the brown adipose tissue (BAT); warming the preoptic area to 41.5 °C completely suppressed the thermogenic response.
Injections of d,l‐homocysteic acid (DLH; 0.5 mm, 0.3 μl) into the preoptic area also significantly attenuated BAT thermogenesis, whereas injections of control vehicle had no effect.
Transections of the whole hypothalamus in the coronal plane at the level of the paraventricular nucleus induced rapid and large rises in BAT and rectal temperatures. This response was not blocked by pretreatment with indomethacin. The high rectal and BAT temperatures were sustained more than 1 h, till the end of the experiment. Bilateral knife cuts that included the medial forebrain bundle but not the paraventricular nuclei elicited similar rises in BAT and rectal temperatures. Medial knife cuts had no effect.
These results suggest that warm‐sensitive neurones in the preoptic area contribute a larger efferent signal for non‐shivering thermogenesis than do cold‐sensitive neurones, and that the preoptic area contributes a tonic inhibitory input to loci involved with non‐shivering thermogenesis. This efferent inhibitory signal passes via lateral, but not medial, hypothalamic pathways.
Endogenous pacemaker activity of rat tumour somatotrophs
Authors: Kwiecien Renata , Robert Christophe , Cannon Robert , Vigues Stephan , Arnoux Annie , Kordon Claude , Hammond Constance 
Published: September 2004

Cells derived from a rat pituitary tumour (GC cell line) that continuously release growth hormone behave as endogenous pacemakers. In simultaneous patch clamp recordings and cytosolic Ca2+ concentration ([Ca2+]i) imaging, they displayed rhythmic action potentials (44.7 ± 2.7 mV, 178 ± 40 ms, 0.30 ± 0.04 Hz) and concomitant [Ca2+]i transients (374 ± 57 nM, 1.0 ± 0.2 s, 0.27 ± 0.03 Hz).
Action potentials and [Ca2+]i transients were reversibly blocked by removal of external Ca2+, addition of nifedipine (1 μM) or Ni2+ (40 μM), but were insensitive to TTX (1 μM). An L‐type Ca2+ current activated at ‐33.6 ± 0.4 mV (holding potential (Vh), ‐40 mV), peaked at ‐1.8 ± 1.3 mV, was reduced by nifedipine and enhanced by S‐(+)‐SDZ 202 791. A T/R‐type Ca2+ current activated at ‐41.7 ± 2.7 mV (Vh, ‐80 or ‐60 mV), peaked at ‐9.2 ± 3.0 mV, was reduced by low concentrations of Ni2+ (40 μM) or Cd2+ (10 μM) and was toxin resistant. Parallel experiments revealed the expression of the class E calcium channel α1‐subunit mRNA.
The K+ channel blockers TEA (25 mM) and charybdotoxin (10‐100 nM) enhanced spike amplitude and/or duration. Apamin (100 nM) also strongly reduced the after‐spike hyperpolarization. The outward K+ tail current evoked by a depolarizing step that mimicked an action potential reversed at ‐69.8 ± 0.3 mV, presented two components, lasted 2‐3 s and was totally blocked by Cd2+ (400 μM).
The slow pacemaker depolarization (3.5 ± 0.4 s) that separated consecutive spikes corresponded to a 2‐ to 3‐fold increase in membrane resistance, was strongly Na+ sensitive but TTX insensitive.
Computer simulations showed that pacemaker activity can be reproduced by a minimum of six currents: an L‐type Ca2+ current underlies the rising phase of action potentials that are repolarized by a delayed rectifier and Ca2+‐activated K+ currents. In between spikes, the decay of Ca2+‐activated K+ currents and a persistent inward cationic current depolarize the membrane, activate the T/R‐type Ca2+ current and initiate a new cycle.
Muscle blood flow is reduced with dehydration during prolonged exercise in humans
Authors: González‐Alonso José , Calbet José A. L. , Nielsen Bodil 
Published: September 2004

The present study examined whether the blood flow to exercising muscles becomes reduced when cardiac output and systemic vascular conductance decline with dehydration during prolonged exercise in the heat. A secondary aim was to determine whether the upward drift in oxygen consumption (V̇O2) during prolonged exercise is confined to the active muscles.
Seven euhydrated, endurance‐trained cyclists performed two bicycle exercise trials in the heat (35 °C; 40–50% relative humidity; 61 ± 2% of maximal V̇O2), separated by 1 week. During the first trial (dehydration trial, DE), they bicycled until volitional exhaustion (135 ± 4 min, mean ± s.e.m.), while developing progressive dehydration and hyperthermia (3.9 ± 0.3% body weight loss; 39.7 ± 0.2 °C oesophageal temperature, Toes). In the second trial (control trial), they bicycled for the same period of time while maintaining euhydration by ingesting fluids and stabilizing Toes at 38.2 ± 0.1 °C after 30 min exercise.
In both trials, cardiac output, leg blood flow (LBF), vascular conductance and V̇O2 were similar after 20 min exercise. During the 20 min‐exhaustion period of DE, cardiac output, LBF and systemic vascular conductance declined significantly (8–14%; P < 0.05) yet muscle vascular conductance was unaltered. In contrast, during the same period of control, all these cardiovascular variables tended to increase. After 135 ± 4 min of DE, the 2.0 ± 0.6 l min−1 lower blood flow to the exercising legs accounted for approximately two‐thirds of the reduction in cardiac output. Blood flow to the skin also declined markedly as forearm blood flow was 39 ± 8% (P < 0.05) lower in DE vs. control after 135 ± 4 min.
In both trials, whole body V̇O2 and leg V̇O2 increased in parallel and were similar throughout exercise. The reduced leg blood flow in DE was accompanied by an even greater increase in femoral arterial‐venous O2 (a‐vO2) difference.
It is concluded that blood flow to the exercising muscles declines significantly with dehydration, due to a lowering in perfusion pressure and systemic blood flow rather than increased vasoconstriction. Furthermore, the progressive increase in oxygen consumption during exercise is confined to the exercising skeletal muscles.
Respiratory modulation of carotid and aortic body reflex left ventricular inotropic responses in the cat
Authors: de Burgh Daly M. , Jones James F. X. 
Published: September 2004

The reflex changes in the inotropic state of the left ventricle, measured as the dP/dtmax(maximum rate of change of pressure), occurring in response to selective stimulation of the carotid and aortic body chemoreceptors by sodium cyanide, were studied in the cat anaesthetized with a mixture of chloralose and urethane.The animals were artificially ventilated with an open pneumothorax. The heart rate and mean arterial blood pressure were maintained constant.With on‐going central respiratory activity, stimulation of the carotid bodies caused an increase in respiratory movements. Variable changes in left ventricular dP/dtmaxoccurred, the predominant response being an increase. The mean change was 8.3 ± 2.9 % from a control value of 6850 ± 450 mmHg s−1. Stimulation of the aortic bodies resulted in a smaller increase in respiration or no effect, but a significant increase occurred in left ventricular dP/dtmaxof 19.6 ± 2.9 % from a control value of 6136 ± 228 mmHg s−1. No significant changes in left ventricular end‐diastolic pressure occurred in response to stimulation of either group of chemoreceptors.Tests of chemoreceptor stimulations were repeated during temporary suppression of the secondary respiratory mechanisms: the central respiratory drive was suppressed reflexly by electrical stimulation of the central cut ends of both superior laryngeal nerves and lung stretch afferent activity was minimized by stopping artificial respiration. Carotid body stimulation again evoked variable responses, the predominant now being a reduction in left ventricular dP/dtmaxof 3.1 % from a control value of 5720 ± 320 mmHg s−1, which was significantly different to that occurring during on‐going spontaneous respiration. Aortic body stimulation caused an increase in left ventricular dP/dtmaxsimilar to the response during on‐going spontaneous respiration.The positive inotropic responses were mediated via the sympathetic nervous system, as indicated by their abolition as a result of intravenous injections of the β‐adrenoceptor blocking agent, propranolol.It is concluded that the carotid bodies exert a small variable effect on left ventricular dP/dtmax, the predominant positive inotropic response being due to the concomitant neurogenic effects of the increase in respiration. In contrast, the positive inotropic response to excitation of the aortic chemoreceptors is not respiratory modulated.
Selective lesioning of the cat pre‐Bötzinger complex in vivo eliminates breathing but not gasping
Authors: Ramirez J. M. , Schwarzacher S. W. , Pierrefiche O. , Olivera B. M. , Richter D. W. 
Published: September 2004

To examine the functional importance of the pre‐Bötzinger complex for breathing we micro‐injected, under in vivo conditions, the calcium channel blocker ω‐conotoxin GVIA and the sodium channel blocker tetrodotoxin (TTX) into the ventrolateral medulla of adult cats, while monitoring respiratory rhythmic motor output in the phrenic nerve.
ω‐Conotoxin GVIA caused a highly localized synaptic ablation by blocking presynaptic N‐type calcium channels. When injecting 5–60 fmol ω‐conotoxin GVIA unilaterally, the amplitude of phrenic nerve activity decreased bilaterally and sometimes disappeared, indicating central apnoea. These effects were reversible and could only be induced in a very localized area of the pre‐Bötzinger complex. By injecting ω‐conotoxin GVIA several times during an experiment and analysing the areas where injections affected respiratory activity, it was possible to map exactly the anatomical extent of the area critical for respiratory rhythm generation.
Following the precise localization of the pre‐Bötzinger complex with ω‐conotoxin GVIA, we injected TTX to induce an irreversible inactivation of this region. TTX injected unilaterally into the pre‐Bötzinger complex irreversibly reduced the amplitude of phrenic nerve activity. Bilateral TTX injections eliminated respiratory rhythmic activity, causing a persistent central apnoea.
After bilateral lesioning of the pre‐Bötzinger complex, it was still possible to induce gasping during hypoxia or asphyxia, indicating that respiration and gasping are generated by two different neuronal networks.
We propose that ω‐conotoxin GVIA as employed in this study to investigate the functional role of the pre‐Bötzinger complex can also be used as a general pharmacological approach to map other neuronal networks. We call this the ‘ω‐conotoxin GVIA tracing’ method.
Mesenteric, coeliac and splanchnic blood flow in humans during exercise
Authors: Perko M. J. , Nielsen H. B. , Skak C. , Clemmesen J. O. , Schroeder T. V. , Secher N. H. 
Published: September 2004

Exercise reduces splanchnic blood flow, but the mesenteric contribution to this response is uncertain.
In nineteen humans, superior mesenteric and coeliac artery flows were determined by duplex ultrasonography during fasting and postprandial submaximal cycling and compared with the splanchnic blood flow as assessed by the Indocyanine Green dye‐elimination technique.
Cycling increased arterial pressure, heart rate and cardiac output, while it reduced total vascular resistance. These responses were not altered in the postprandial state. During fasting, cycling increased mesenteric, coeliac and splanchnic resistances by 76, 165 and 126%, respectively, and it reduced corresponding blood flows by 32, 50 and 43% (by 0.18 ± 0.04, 0.42 ± 0.03 and 0.60 ± 0.04 l min−1). Postprandially, mesenteric and splanchnic vascular resistances decreased, thereby elevating regional blood flow, while the coeliac circulation was not influenced. Postprandial cycling did not influence the mesenteric resistance significantly, but its blood flow decreased by 22% (0.46 ± 0.28 l min−1). Coeliac and splanchnic resistance increased by 150 and 63%, respectively, and the corresponding regional blood flow decreased by 51 and 31% (0.49 ± 0.07 and 0.96 ± 0.28 l min−1). Splanchnic blood flow values assessed by duplex ultrasound and by dye‐elimination techniques were correlated (r= 0.70; P < 0.01).
During submaximal exercise in humans, splanchnic resistance increases and blood flow is reduced following a 50% reduction in the hepato‐splenic and a 25% reduction in the mesenteric blood flow.
Coupling of sympathetic and somatic motor outflows from the spinal cord in a perfused preparation of adult mouse in vitro
Authors: Chizh Boris A. , Headley P. Max , Paton Julian F. R. 
Published: September 2004

The relationship between sympathetic and somatic motor outflows from thoraco‐lumbar spinal cord was investigated in a novel arterially perfused trunk‐hindquarters preparation of adult mouse.
Ongoing activity was present in both somatic motor (obturator, sciatic or femoral nerves) and sympathetic outflows (either renal nerve or abdominal sympathetic chain). Sympathetic activity was rhythmic with bursts frequencies of 0.6‐2.2 Hz. No obvious rhythmic activity was found in the somatic motor outflow. There were periods during which sympathetic and somatic motor activity were correlated.
Addition of NMDA (20‐80 μM) to the perfusate elicited repetitive burst discharges in the somatic motor outflow which were sometimes rhythmic. The frequency of these burst discharges/rhythmic activity varied between preparations but in all cases increased with increasing NMDA concentration.
NMDA induced burst discharges in the sympathetic outflow. This bursting activity was of the same frequency as the somatic motor outflow and the two were coupled as revealed by correlation analysis. Periods of coupling persisted for up to 3 min.
Administration of hexamethonium (300 μM), to block sympathetic ganglionic transmission, had no effect on the somatic motor activity but severely attenuated sympathetic nerve discharge.
The thoraco‐sacral cord therefore has the neuronal machinery necessary for generating and coupling activity in somatic motor and sympathetic outflows. Our findings indicate a dynamic control over the degree of coupling. We discuss that the synchronization of these neural outflows reflects either coupling between two independent mechanisms or the presence of a common synaptic driver impinging on both somatic motor and sympathetic neurones.