bluuebunny/crossref_metadata_2025_split huggingface dataset:
The C fibre reflex of the cat urinary bladder
Authors: Mazières L. , Jiang C.‐H. , Lindström S. 
Published: September 2004

Reflexes evoked in bladder parasympathetic neurones by electrical stimulation of bladder C afferent fibres were studied in cats anaesthetized with α‐chloralose. The responses were compared with the ordinary micturition reflex evoked by low‐threshold Aδ afferents from bladder mechanoreceptors and mediated by a spino‐ponto‐spinal reflex pathway.
The bladder was catheterized for fluid instillations and pressure recordings. Efferent reflex discharges were recorded from the cut central end of a small distal bladder branch of the pelvic nerve. The remaining bladder pelvic nerve branches were stimulated electrically close to the bladder.
Stimulation at C afferent intensity evoked a late reflex discharge in bladder pelvic efferents in all animals. The response was centrally mediated, had a latency of 150−250 ms, and was much weaker after stimulation on the contralateral nerve.
The bladder C fibre reflex differed in several functional aspects from the ordinary Aδ micturition reflex. It could be evoked at a low rate of stimulation, with an empty bladder and no background activity from bladder mechanoreceptors. In this situation, the normal Aδ micturition reflex is not elicited. The C fibre reflex also survived an acute spinalization at a low thoracic level.
The C fibre reflex was strongly inhibited by dorsal clitoris or dorsal penis nerve stimulation, an effect that was maintained after spinalization. It was facilitated by bladder or urethra exposure to cold and menthol, stimuli that activate specific cold‐sensitive receptors associated with unmyelinated C afferents.
It is concluded that the central pathway of the C fibre reflex is spinal and partly separate from that of the ordinary micturition reflex. These observations are in keeping with the clinical finding that a bladder cooling reflex can be elicited in patients with disturbed descending control of the bladder.
Arachidonic acid increases cerebral microvascular permeability by free radicals in single pial microvessels of the anaesthetized rat
Authors: Easton A. S. , Fraser P. A. 
Published: September 2004

We have investigated the permeability‐increasing effect of arachidonic acid on pial venular capillaries in vivo using the single microvessel occlusion technique.
Permeability to Lucifer Yellow dye (476 Da) increased dose dependently when arachidonic acid was applied focally to the abluminal surface of the vessels. This was completely reversible at all but the highest dose. The permeability increase was 1.65 × 10−6± 0.247 × 10−6 cm s−1 (mean ± s.e.m.) at 0.25 mm, 3.53 × 10−6± 0.872 × 10−6 cm s−1 at 0.5 mm, 12.61 × 10−6± 3.44 × 10−6 cm s−1 at 1 mm and 18.46 × 10−6± 5.90 × 10−6 cm s−1 at 2 mm arachidonic acid. There was a similar reversible dose‐dependent permeability increase to eicosapentaenoic acid.
These permeability increases could be prevented by co‐application of a mixture of the anti‐oxidants superoxide dismutase and catalase (30 and 100 U ml−1), or by the iron chelator desferrioxamine (100 μm).
The permeability increases were also prevented by the cyclooxygenase and 5‐lipoxygenase blockers indomethacin (100 μm) and nordihydroguariaretic acid (100 μm), respectively, when applied together, but not singly.
It was concluded that the permeability response to arachidonic acid depends on the formation of free radicals and subsequent lipid peroxidation.
Synaptic potentials in respiratory neurones during evoked phase switching after NMDA receptor blockade in the cat
Authors: Pierrefiche O. , Haji A. , Foutz A. S. , Takeda R. , Champagna J. , Denavit‐Saubié M. 
Published: September 2004

Blockade of NMDA receptors by dizocilpine impairs the inspiratory off‐switch (IOS) of central origin but not the IOS evoked by stimulation of sensory afferents. To investigate whether this difference was due to the effects of different patterns of synaptic interactions on respiratory neurones, we stimulated electrically the superior laryngeal nerve (SLN) or vagus nerve in decerebrate cats before and after i.v. administration of dizocilpine, whilst recording intracellularly.
Phrenic nerve responses to ipsilateral SLN or vagal stimulation were: at mid‐inspiration, a transient inhibition often followed by a brief burst of activity; at late inspiration, an IOS; and at mid‐expiration, a late burst of activity.
In all neurones (n= 16), SLN stimulation at mid‐inspiration evoked an early EPSP during phase 1 (latency to the arrest of phrenic nerve activity), followed by an IPSP in inspiratory (I) neurones (n= 8) and by a wave of EPSPs in post‐inspiratory (PI) neurones (n= 8) during phase 2 (inhibition of phrenic activity). An EPSP in I neurones and an IPSP in PI neurones occurred during phase 3 (brief phrenic burst) following phase 2.
Evoked IOS was associated with a fast (phase 1) activation of PI neurones, whereas during spontaneous IOS, a progressive (30‐50 ms) depolarization of PI neurones preceded the arrest of phrenic activity.
Phase 3 PSPs were similar to those occurring during the burst of activity seen at the start of spontaneous inspiration.
Dizocilpine did not suppress the evoked phrenic inhibition and the late burst of activity. The shapes and timing of the evoked PSPs and the changes in membrane potential in I and PI neurones during the phase transition were not altered.
We hypothesize that afferent sensory pathways not requiring NMDA receptors (1) terminate inspiration through a premature activation of PI neurones, and (2) evoke a late burst of phrenic activity which might be the first stage of the inspiratory on‐switch.
Modification of activity‐dependent increases of cerebral blood flow by excitatory synaptic activity and spikes in rat cerebellar cortex
Authors: Mathiesen Claus , Caesar Kirsten , Akgören Nuran , Lauritzen Martin 
Published: September 2004

Mechanisms of activity‐dependent increases in cerebral blood flow (CBF) were examined in rat cerebellar cortex using the laser Doppler flow technique and extracellular recordings of single unit activity and field potentials.
Stimulation of the monosynaptic climbing fibre system evoked long‐lasting complex spikes in Purkinje cells, and extracellular field potentials with a characteristic profile that indicated contributions from both passive and active membrane mechanisms. The concomitant CBF increases were reproducible at fairly short intervals, and suggest that both synaptic activity and spikes may contribute to increased CBF.
Stimulation of the disynaptic parallel fibre system inhibited the spiking activity in Purkinje cells, while the postsynaptic activity increased as indicated by the simultaneously recorded field potential. Nevertheless, CBF always increased. The inhibition of spike firing activity was partly dependent on GABAergic transmission, but may also relate to the intrinsic membrane properties of Purkinje cells.
The CBF increases evoked by parallel or climbing fibre stimulation were highly correlated to the sum of neural activities, i.e. the negativity of field potentials multiplied by the stimulus frequency. This suggests a robust link between extracellular current flow and activity‐dependent increases in CBF.
AMPA receptor blockade attenuated CBF increases and field potential amplitudes, while NMDA receptor antagonism did not. This is consistent with the idea that the CBF responses are of neuronal origin.
This study has shown that activity‐dependent CBF increases evoked by stimulation of cerebellar parallel fibres are dependent on synaptic excitation, including excitation of inhibitory interneurones, whereas the net activity of Purkinje cells, the principal neurones of the cerebellar cortex, is unimportant for the vascular response. For the climbing fibre system, not only synaptic activity but also the generation of complex spikes from Purkinje cells contribute to the increases in CBF. The strong correlation between CBF and field potential amplitudes suggests that extracellular ion fluxes contribute to the coupling of brain activity to blood flow.
Two neural mechanisms for respiration‐induced cutaneous vasodilatation in humans?
Authors: Wallin B. Gunnar , Båtelsson Karin , Kienbaum Peter , Karlsson Tomas , Gazelius Bertil , Elam Mikael 
Published: September 2004

In humans, a deep breath is known to induce cutaneous vasoconstriction in the warm state, and vasodilatation in the cold state. To investigate whether vasodilatation in the cold state is related to reduction of sympathetic vasoconstrictor nerve traffic, we studied the effect of a deep breath on vascular resistance in a skin area on the dorsum of the hand, in which release of noradrenaline from sympathetic nerves was blocked by iontophoretic pretreatment with bretylium tosylate. Simultaneous measurements were made in two control areas. In eight healthy subjects, data were obtained from deep breaths taken before bretylium in the warm state, after general cooling to a finger skin temperature below 25 °C and after rewarming to above 32 °C.
In the warm state before bretylium pretreatment, the deep breath evoked short‐lasting vasoconstrictions at all sites. In the cold state there was no change of vascular resistance in the bretylium‐pretreated area, whereas in the control areas an initial tendency towards vasoconstriction was followed by a significant transient vasodilatation. After rewarming, transient vasoconstrictions reappeared at the control sites, whereas only a transient vasodilatation occurred at the bretylium‐pretreated site.
In six healthy subjects we also monitored the effects of a deep breath on skin sympathetic nerve activity (recorded by microneurography in the peroneal nerve), and skin vascular resistance within the innervation zone of the impaled nerve fascicle in the foot. Data from thirty deep breaths per subject were averaged.
In the cold state, the deep breath induced a strong increase in neural discharge, followed by a transient reduction of nerve traffic lasting approximately 15 s and associated with a subsequent reduction of vascular resistance.
We conclude that the deep breath‐induced vasodilatation in the cold state is due to reduction of sympathetic vasoconstrictor nerve traffic. The vasodilatation after bretylium treatment in the warm state raises the possibility that a deep breath induces two simultaneous neural reactions, a vasoconstrictor and an active vasodilator component, the latter being weaker and normally masked by the strong vasoconstrictor component.
Localization of cAMP‐ and aldosterone‐induced K+ secretion in rat distal colon by conductance scanning
Authors: Grotjohann I. , Gitter A. H. , Köckerling A. , Bertog M. , Schulzke J. D. , Fromm M. 
Published: September 2004

Aldosterone‐ and adrenaline‐induced K+ secretion were investigated in rat late distal colon using conductance scanning and Ussing chamber techniques. K+ secretion was unmasked by the K+ channel blocker tetraethylammonium (TEA). Electrogenic Na+ absorption was inhibited by amiloride. Rb+ net fluxes consistently measured about 80 % of K+ secretion estimated using change in short‐circuit current (ΔISC) measurements.
Partial block of K+ absorption by mucosal ouabain did not change TEA‐sensitive K+ secretion. Thus, K+ absorption and K+ secretion are not coupled.
Additivity of Rb+ fluxes as well as ΔISC caused by 3 nM aldosterone (6 h in vitro incubation) and, subsequently, adrenaline suggested additivity of aldosterone‐induced and cAMP‐mediated K+ secretion in the presence of amiloride.
Conductance scanning under control conditions revealed a small TEA‐sensitive K+ conductivity in surface epithelium (0.3 ± 0.2 mS cm−2) but not in crypts, as well as a small basal K+ secretion in surface epithelium (ΔISC= 0.3 μmol h−1 cm−2), which increased during sham incubation.
Aldosterone (3 nM, 6 h in vitro incubation) resulted, after correction for the basal K+ secretion, in a K+ secretion of ΔISC= 0.9 μmol h−1 cm−2. Aldosterone induced a TEA‐sensitive conductivity of 1.1 ± 0.3 mS cm−2 in surface epithelium, but not in crypts.
Adrenaline (5 μm) caused, in fresh tissue, a K+ secretion of ΔISC= 1.2 μmol h−1 cm−2 and equal conductivity changes in crypts (0.7 ± 0.2 mS cm−2) and surface epithelium (0.7 ± 0.1 mS cm−2).
We conclude that K+ secretion induced by aldosterone in physiological concentration is restricted to surface epithelium, whereas cAMP‐mediated K+ secretion is located equally in crypts and surface epithelium.
Electrical characteristics and responses to jejunal distension of neurons in Remak's juxta‐jejunal ganglia of the domestic fowl
Authors: Smith Terence K. , Lunam Christine A. 
Published: September 2004

Remak's nerve is a ganglionated nerve trunk found only in birds that runs parallel to the gut from the duodenal‐jejunal junction to the cloaca. We report the first electrophysiological characterization of these neurons and their responses to gut distension.
A segment of chicken jejunum with attached Remak's nerve was pinned in an electrophysiological chamber. Neurons in Remak's ganglia were impaled with microelectrodes. The adjacent segment of gut was distended with fluid.
One hundred and thirty neurons were characterized into three electrophysiological classes: (i) tonic neurons (74 %) fired action potentials spontaneously (frequency 3.5 Hz) and continuously (up to 40 Hz) throughout a depolarizing current pulse; (ii) AD neurons (22 %) fired a brief burst of action potentials (1‐10), which were followed by a prolonged after‐depolarization (AD) of duration 2.8 ± 0.3 s; and (iii) phasic neurons (4 %) fired an initial burst of action potentials followed by an after‐hyperpolarization (duration, 520.0 ± 32.0 ms). Tetrodotoxin (1 μM) abolished action potentials in tonic and AD neurons as well as the after‐depolarization.
Spontaneous fast excitatory postsynaptic potentials (FEPSPs) occurred in all classes of neurons; they were not observed, however, in ganglia isolated from the jejunum.
Intracellular injection of biocytin revealed that neurons could be characterized into four morphological classes. Tonic neurons, which had long and extensive dendritic trees, were Remak's Type I, II and IV neurons. AD neurons also comprised Remak's type II neurons. Phasic neurons were Remak's Type III neurons. Most neurons had axons that projected orally along Remak's nerve.
Distension of the jejunum evoked FEPSPs and action potentials in tonic neurons, and repetitive bursts of action potentials (1‐4) followed by an after‐depolarization in AD neurons. All responses to distension were blocked by hexamethonium (300 μM) and tetrodotoxin (1 μM).
In conclusion, neurons in Remak's juxta‐jejunal nerve appear to regulate gut motility. Three distinct electrophysiological classes of neurons were observed, all of which appear to be activated by distension sensitive cholinergic intestinofugal neurons in the jejunum.
Effect of hydrogen peroxide and dithiothreitol on contractile function of single skeletal muscle fibres from the mouse
Authors: Andrade Francisco H. , Reid Michael B. , Allen David G. , Westerblad Håkan 
Published: September 2004

We used intact single fibres from a mouse foot muscle to study the role of oxidation‐reduction in the modulation of contractile function.
The oxidant hydrogen peroxide (H2O2, 100‐300 μM) for brief periods did not change myoplasmic Ca2+ concentrations ([Ca2+]i) during submaximal tetani. However, force increased by 27 % during the same contractions.
The effects of H2O2 were time dependent. Prolonged exposures resulted in increased resting and tetanic [Ca2+]i, while force was significantly diminished. The force decline was mainly due to reduced myofibrillar Ca2+ sensitivity. There was also evidence of altered sarcoplasmic reticulum (SR) function: passive Ca2+ leak was increased and Ca2+ uptake was decreased.
The reductant dithiothreitol (DTT, 0.5‐1 mM) did not change tetanic [Ca2+]i, but decreased force by over 40 %. This was completely reversed by subsequent incubations with H2O2. The force decline induced by prolonged exposure to H2O2 was reversed by subsequent exposure to DTT.
These results show that the elements of the contractile machinery are differentially responsive to changes in the oxidation‐reduction balance of the muscle fibres. Myofibrillar Ca2+ sensitivity appears to be especially susceptible, while the SR functions (Ca2+ leak and uptake) are less so.
The influence of nerves on the secretion of immunoglobulin A into submandibular saliva in rats
Authors: Carpenter G. H. , Garrett J. R. , Hartley R. H. , Proctor G. B. 
Published: September 2004

The influence of sympathetic and parasympathetic nerve stimulations on salivary secretion of immunoglobulin A (IgA) was studied in the submandibular glands of anaesthetized rats by stimulating the nerve supplies with bipolar electrodes.
Although the flow of saliva from sympathetically stimulated glands was only 23 % of that from parasympathetically stimulated glands the output of IgA was over 2‐fold greater. This difference was attributable to influences of the nerves on IgA secretion through the epithelial cell polymeric immunoglobulin receptor‐mediated pathway, as Western blotting with specific antibodies to IgA and secretory component revealed that secretory IgA (SIgA) dominated in all saliva samples.
Study of saliva secreted in sequential periods of nerve stimulation or following rest pauses suggested that SIgA secretion occurred in the absence of stimulation but this was upregulated 2.6‐ and 6‐fold by parasympathetic and sympathetic nerve stimulations, respectively, compared with the calculated unstimulated rate.
The IgA content of extensively stimulated glands was 77 % of levels in unstimulated contralateral control glands despite a secretion into saliva equivalent to almost 90 % of the glandular IgA content. The IgA may be synthesized and secreted by glandular plasma cells at a rate which exceeds demand and/or such synthesis may be upregulated by nerve impulses.
The results indicate that salivary secretion of SIgA is upregulated by nerve impulses and that sympathetic nerves induce a greater effect than parasympathetic nerves.
Regulation of intracellular pH during H+‐coupled oligopeptide absorption in enterocytes from guinea‐pig ileum
Authors: Hayashi Hisayoshi , Suzuki Yuichi 
Published: September 2004

The mechanisms for regulating the intracellular pH (pHi) level during oligopeptide absorption were investigated in the enterocytes from guinea‐pig ileum by identifying the acid‐base transporters responsible for extruding H+ that enters the cell through the H+‐oligopeptide cotransporter.
The pHi level was measured by microfluorometry in an isolated villus tip loaded with the pH‐sensitive fluoroprobe 2′7’‐bis(2‐carboxyethyl)‐5(6)‐carboxyfluorescein (BCECF). The oligopeptide‐induced increment in the short‐circuit current (Isc) was determined in a mucosal sheet in Ussing chambers. A CO2/HCO3−‐buffered solution was used.
The superfusion of glycylglycine (Gly‐Gly, l0 mM) caused a decrease in pHi level, which returned to the basal level after removing Gly‐Gly. This pHi recovery was strongly dependent on extracellular Na+. Amiloride partially inhibited the pHi recovery rate with an IC50 value of 41 μM, the maximum inhibition being approximately 70 %. In the presence of amiloride at its maximum concentration (0.3 mM), the addition of 0.6 mM DIDS caused a further decrease, but did not abolish the pHi recovery rate. In the absence of CO2 and HCO3−, the pHi recovery was almost completely abolished by 0.3 mM amiloride.
The intracellular H+ accumulation induced by 0.3 mM amiloride or by 0.6 mM DIDS, as estimated from the pHi decrease and buffer capacity, was significantly greater during Gly‐Gly superfusion than under resting conditions.
The increase in Isc induced by luminal glycylproline was attenuated by either removing serosal Na+ or by adding 0.5 mM amiloride or 0.6 mM DIDS to the serosal side.
We conclude that both Na+‐dependent, amiloride‐sensitive acid extrusion, probably by the Na+‐H+ exchanger, and Na+‐ and HCO3−‐dependent, DIDS‐sensitive acid extrusion, possibly by the Na+‐HCO3− cotransporter, are involved in extruding H+ that enters cells by the H+‐oligopeptide cotransport. It is proposed that these acid extrusion (or base loading) mechanisms are present in the basolateral membrane and are important for maintaining oligopeptide absorption, as well as the acid extrusion mechanism in the apical membrane.
Effect of nitric oxide on single skeletal muscle fibres from the mouse
Authors: Andrade Francisco H. , Reid Michael B. , Allen David G. , Westerblad Håkan 
Published: September 2004

Single skeletal muscle fibres from a mouse foot muscle were used to investigate the effects of nitric oxide on contractile function.
We measured force production and myoplasmic free Ca2+ concentration ([Ca2+]i) in single fibres exposed to the nitric oxide donors S‐nitroso‐N‐acetylcysteine (SNAC) and nitroprusside.
The nitric oxide donors reduced myofibrillar Ca2+ sensitivity, whereas [Ca2+]i transients were increased during submaximal tetani. Force was largely unchanged. SNAC did not change maximum shortening velocity, the rate of force redevelopment, or force production at saturating [Ca2+]i.
The guanylyl cyclase inhibitor LY83583 increased tetanic [Ca2+]i but had no effect on Ca2+ sensitivity. LY83583 did not prevent the decrease in myofibrillar Ca2+ sensitivity in response to SNAC. The oxidizer sodium nitrite increased tetanic [Ca2+]i and decreased myofibrillar Ca2+ sensitivity.
We conclude that under our experimental conditions nitric oxide impairs Ca2+ activation of the actin filaments which results in decreased myofibrillar Ca2+ sensitivity.
Vestibulocollic reflexes evoked by short‐duration galvanic stimulation in man
Authors: Watson S. R. D. , Colebatch J. G. 
Published: September 2004

Vestibular‐dependent responses in leg muscles following transmastoid galvanic stimulation have been well characterized. Here we describe the properties of vestibulocollic responses evoked by transmastoid galvanic stimulation.
In twelve healthy human subjects we examined the averaged responses in unrectified sternocleidomastoid (SCM) EMG evoked by transmastoid stimulation using current pulses of 4 mA intensity and 2 ms duration. In ten subjects we also examined the effects of unilateral vestibular stimulation with the indifferent electrode at the vertex. In further experiments we studied the effects of different levels of background muscle activation, head position, current intensity and current duration. We compared these responses with click‐evoked vestibulocollic responses in SCM.
A clearly defined biphasic response, beginning with a surface positivity, was recorded in the SCM ipsilateral to the side of cathode placement in all subjects. We refer to this as the p13/n23 [g] (galvanic) response, given the close similarity, in terms of waveform and latencies, to the previously described click‐evoked p13/n23 vestibulocollic response. The amplitude of this response was linearly related to background muscle activation, current intensity and current duration, but independent of head position. Unilateral galvanic stimulation revealed the p13/n23 [g] response to be solely generated by the cathode.
A biphasic response beginning with a surface negativity (n12/p20 [g]) contralateral to the cathode was seen in all subjects and was generated by both the cathode contralaterally and the anode ipsilaterally.
Both the p13/n23 [g] and n12/p20 [g] potentials were abolished by selective vestibular nerve section and unaffected by severe sensorineural deafness.
We conclude that galvanic stimulation evokes short‐latency vestibulocollic reflexes. These vestibulocollic reflexes have properties that are distinct from those described for galvanic‐evoked vestibular reflexes in leg muscles, and which may be related to their differing physiological roles.