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PubMed1998

Fos expression in the ferret trigeminal nuclear complex following tooth pulp stimulation.

The aim of this study was to establish which regions of the trigeminal nucleus are activated by tooth pulp stimulation in the normal ferret. The distribution of Fos-like immunoreactivity was examined following electrical stimulation of the tooth pulp in the awake and anaesthetized ferret. Stimulus-specific labelling was found in subnuclei caudalis and oralis of the trigeminal spinal nucleus. Three groups of chronically prepared animals; conscious, anaesthetized (alphaxolone/alphadolone) and anaesthetized-paralysed (alphaxolone/alphadolone with gallamine triethiodide), received electrical stimuli to both the upper and lower left canine teeth (1 Hz train of 3 x 0.5 ms at 200 Hz) at an amplitude of 10 times the threshold of the jaw opening reflex. Three control groups were treated identically except no stimulus was given. In stimulated anaesthetized and anaesthetized-paralysed animals, Fos-positive profiles were seen in laminae I and II of subnucleus caudalis and in the medial part of subnucleus oralis. There was no labelling evident in subnucleus interpolaris or the main sensory nucleus, or contralaterally in any of the subnuclei. In all conscious stimulated animals there was additional bilateral Fos-positive labelling, mainly in the deeper laminae of subnucleus caudalis. This bilateral labelling was not stimulus-specific as it was also seen in conscious non-stimulated animals. After correction for this bilateral labelling no significant difference was found between conscious, anaesthetized and anaesthetized-paralysed groups of stimulated animals or between the different groups of control animals. These results support the concept that the rostral parts of the trigeminal spinal nucleus are involved in processing of nociceptive input. They also demonstrate that light alphaxolone/alphadolone anaesthesia has no effect on stimulus-specific Fos expression following tooth pulp stimulation. The second aim of this study was to develop a clearly defined model for future studies in which Fos expression is no different to that seen in the conscious state. As in the conscious animal, labelling not associated with the stimulus is difficult to distinguish from stimulus specific labelling, further studies using this model of trigeminal nociceptive pathways would be best carried out in lightly anaesthetized animals.

Anesthesia, General↗
PubMed2001

Determination of iodide with 1,3-dibromo-5,5-dimethylhydantoin (DBH) in comparison with the ICl-method. Analytical methods of pharmacopeias with DBH in respect to environmental and economical concern. Part 3.

USP 1995 (The United States Pharmacopeia, 23rd Edit., (1995), potassium iodide p. 1265, sodium iodide p. 1424), PH. EUR. 1997 (European Pharmacopoeia, third ed., Council of Europe, Strasbourg, (1997), potassium iodide p. 1367, sodium iodide p. 1493) and JAP 1996 (The Japanes Pharmacopoeia, 13th ed. (1996), potassium iodide p. 578, sodium iodide p. 630) determine iodide with the ICl-method (J. Am. Chem. Soc. 25 (1903) 756-761; Z. Anorg. Chem. 36 (1903) 76-83; Fresenius Z. Anal. Chem. 106 (1936) 12-23; Arzneibuch-Kommentar, Wissenschaftliche Erläuterungen zum Europäischen Arzneibuch, Wissenschaftliche Verlagsgesellschaft mbH, Stuttgart, Govi-Verlag - Pharmazeutischer Verlag GmbH, Eschborn, 12th suppl. (1999), K10 p. 2), using chloroform, which is toxic and hazardous to environment. Without the application of chlorinated hydrocarbons USP 2000 (The United State Pharmacopeia, 24th ed. (2000), potassium iodide p. 1368, sodium iodide p. 1535) and Brit 1999 (British Pharmacopoeia London, (1999), Appendix VIII C, p. A162) titrate iodide with the redox indicator amaranth. A titration with potentiometric indication giving two end-points at the step of I(2) and [ICl(2)](-) is described. Due to the high concentration of hydrochloric acid required for the ICl-method, the determination with DBH (1,3-dibromo-5,5-dimethylhydantoin; 1,3-dibromo-5,5-dimethyl-2,4-imidazolidinedione) can be recommended and is performed easily. Similarly, the iodide content of gallamine triethiodide may be analyzed with DBH by application of a visual two-phase titration in water and ethyl acetate or with potentiometric indication in a mixture of 2-propanol and water. During the removal of the excess of DBH 4-bromo-triethylgallamine (2,2',2"-[1-bromo-benzene-2,3,4-triyltris(oxy)]N,N,N-triethylethanium) is formed.

Hydantoins↗
PubMed1979

Equilibrium binding of [3H]tubocurarine and [3H]acetylcholine by Torpedo postsynaptic membranes: stoichiometry and ligand interactions.

Studies are presented of the equilibrium binding of [3H]-d-tubocurarine (dTC) and [3H]acetylcholine (AcCh) to Torpedo postsynaptic membranes. The saturable binding of [3H]dTC is characterized by two affinities: Kd1 = 33 +/- 6 nM and Kd2 = 7.7 +/- 4.6 microM, with equal numbers of binding sites. Both components are completely inhibited by pretreatment with excess alpha-bungarotoxin or 100 microM nonradioactive dTC and competitively inhibited by carbamylcholine with a KI = 100 nM, but not affected by the local anesthetics dimethisoquin, proadifen, and meproadifen. The biphasic nature of [3H]dTC binding was unaltered in solutions of low ionic strength and by preparation of Torpedo membranes in the presence of N-ethylmaleimide, a treatment which yields dimeric AcCJ receptors. dTC competitively inhibits the binding of [3H]AcCH and decreases the fluorescence of 1-(5-dimethylaminonaphthalene-1-sulfonamido)ethane-2-trimethylammonium (Dns-Chol) in a manner quantitatively consistent with its directly measured binding properties. It decreases the initial rate of 3H-labeled Naja nigricollis alpha-toxin binding by 50% at 60 nM with an apparent Hill coefficient of 0.58. The stoichiometry of total dTC, AcCh, and alpha-neurotoxin binding sites in Torpedo membranes was determined by radiochemical techniques and by a novel fluorescence assay utilizing Dns-Chol as an indicator, yielding ratios of 0.9 +/- 0.1:0.9 +/- 0.2:1, respectively. The biphasic equilibrium binding function is not unique to dTC since other ligands inhibited [3h]acCh binding in a biphasic manner with apparent inhibition constants as follows: gallamine triethiodide (K11 = 2 microM, K12 = 1 mM); Me2dTC (K11 = 500 nM, K12 = 10 microM); decamethonium (K11 = 100 nM, K12 = 1.6 microM). Carbamylcholine, however, inhibited [3H]AcCh binding with a single KI = 100 nM. The observed competition between those ligands and [3H] AcCh cannot be completely accounted for by competitive interaction with two different affinities, and the deviations are discussed in terms of the positive cooperativity of the [3H] AcCh binding function itself. It is concluded that dTC binds only to the AcCh sites in Torpedo membranes and that those sites display two affinities for dTC but only one for AcCh.

Acetylcholine↗
PubMed1975

Effects of anesthetics on ponto-geniculo-occipital waves from the oculomotor nucleus of the cat.

Effects of anesthetics and doxapram on pontogeniculo-occipital (PGO) waves from the oculomotor nucleus were studied in acute experiments in cats paralyzed by gallamine triethiodide. The anesthetic agents studied in the present experiment (thiopental, ketamine, Innovar, nitrous oxide, and halothane) decreased, while doxapram increased, the total number of PGO waves. As the doses of anesthetics increased, PGO waves were abolished, but they returned to control levels or below control levels when the concentrations of anesthetics were decreased. The results indicate that the anesthetics studied inhibit the activity of the central mechanism associated with the oculomotor system. PGO waves may prove a useful index of the level of anesthesia.

Anesthesia, Inhalation↗
PubMed1994

Spatial correlation of suppressive and excitatory receptive fields with direction selectivity of complex cells in cat striate cortex.

The aim of the study was to account for direction selectivity of visual cortical neurons through systematic positional mismatch between excitatory and suppressive influences on each neuron. Direction-selective complex neurons were therefore recorded from striate cortex of cats lightly anaesthetized with halothane in nitrous oxide-oxygen. All but small residual eye movements were eradicated with intravenous gallamine triethiodide. Excitatory receptive field (ERF) dimensions and centring were quantified with optimal sine-wave grating stimuli, appropriately windowed to limit them to variable locations along and across the receptive field (RF) centre. Related suppressive receptive fields (SRFS) were similarly mapped during binocular conditioning, induced by an optimal grating applied to the other eye and drifting continuously in each neuron's preferred direction. Its purpose was to elevate ongoing levels of discharge to reveal often concealed null suppression. ERF and SRF profiles were systematically offset, especially along the line of preferred direction such that, for stimuli moving in the non-preferred direction, the SRF lay ahead of the ERF. Derivations of ERFS and SRFS during conditioning, within a single batch of trials, excluded eye movements as a source of positional mismatch. It is concluded that this mismatch may provide the basis for direction selectivity and the emergence of null suppression.

Animals↗
PubMed1977

Physiological studies on facial reflexes in the rat.

Experiments were performed on 36 male albino rats anaesthetized with pentobarbitone sodium and paralyzed with gallamine triethiodide. Recordings were made with single and multibarrel glass microelectrodes in the facial nucleus and monopolar silver wire electrodes on the lingual, facial, glossopharyngeal and hypoglossal nerves. The absolute refractory period for facial motoneurones is 2-3 ms, the relative refractory period has a duration of 26-34 ms and the range in axonal conduction velocities is from 15 to 45 m.sec-1. No evidence for afferent fibres in the muscle branches of the facial and hypoglassal nerves could be found. The lingual and glossopharyngeal nerves show reflex connexions with both the facial and hypoglassal nerves. The time courses of the potentiations and depressions of test facial antidromic field potentials following lingual and glossopharyngeal conditioning stimuli are given. Evoked synaptic activity and the distribution of field potentials in the facial mucleus following lingual and glossopharyngeal nerve stimulation are also described. The observed lingual and glossopharyngeal-facial reflexes are discussed with respect to blink reflexes.

Action Potentials↗
PubMed1966

The effects of cyclopropane, halothane and ether on central baroreceptor pathways.

1. The reductions in arterial pressure and preganglionic sympathetic activity evoked by aortic nerve stimulation in the rabbit were studied before and during administration of constant inspired concentrations of the inhalation anaesthetics cyclopropane, halothane, and ether. The background anaesthetic was pentobarbitone, gallamine triethiodide was given, and pulmonary ventilation was with 100% oxygen.2. During light pentobarbitone anaesthesia, aortic nerve stimulation usually induced similar reductions in arterial pressure and preganglionic discharge, expressed as the maximum percentage reduction from prestimulation levels. There were two components in the sympathetic responses, attributable to A and C fibre excitation in the aortic nerve, which was also shown to contain a third fibre group with properties similar to those of B fibres.3. The arterial pressure, heart rate, and preganglionic sympathetic responses to aortic nerve stimulation were rapidly and profoundly inhibited by 50% cyclopropane, which also produced arterial hypertension.4. Halothane (3%) significantly inhibited the depressor responses, but even in the presence of severe hypotension the arterial pressure could usually be further reduced by aortic nerve stimulation. The inhibitory effects of 2% halothane were slow in onset and not pronounced. In the concentrations used, these actions of halothane were significantly less than those of cyclopropane.5. The inhibitory effects of ether on the depressor responses were roughly intermediate between those of cyclopropane and halothane; complete suppression of the responses occurred with high ether concentrations, which were also liable to cause circulatory collapse.6. It is concluded that the three anaesthetics significantly inhibit impulse transmission through central baroreceptor pathways; the implications of the findings are discussed in relation to the different circulatory actions of these anaesthetics.

Action Potentials↗
PubMed1970

The role of the cervical sympathetic nerve in the regulation of oxygen consumption of the carotid body of the cat.

1. Carotid body blood flow (c.b.f.) and carotid arterial-carotid body venous oxygen (A-V O(2)) difference were measured and carotid body oxygen consumption calculated in twenty-six cats anaesthetized with pentobarbitone sodium, paralysed with gallamine triethiodide and ventilated mechanically.2. With the sinus nerves intact and with blood gas tensions and carotid sinus pressure within physiological limits, section of either the pre- or post-ganglionic cervical sympathetic nerve on the same side caused an average rise in c.b.f. of 9.2 mul./min, in A-V O(2) difference of 0.09 ml./100 ml. and in carotid body oxygen consumption of 0.075 mul./min.3. When the pre- or post-ganglionic cervical sympathetic nerves were stimulated, c.b.f. and A-V O(2) difference fell. The fall in c.b.f. was enhanced at high P(a, CO2); the fall in A-V O(2) difference and in calculated oxygen consumption was enhanced at low mean arterial pressure (M.A.P.) or P(a, O2).4. Following sympathectomy, a reduction of M.A.P. at constant P(a, O2) and P(a, CO2) caused a fall in c.b.f. and a commensurate rise in A-V O(2) difference so that carotid body oxygen consumption remained approximately constant.5. When P(a, O2) was altered over the range 35 to > 400 mm Hg, or P(a, CO2) over the range 27-70 mm Hg at constant M.A.P., c.b.f. changed by amounts which were similar to those observed when the sympathetic nerves were intact and A-V O(2) difference changed in the opposite direction so that carotid body oxygen consumption similarly remained constant.6. Comparison of these results with those observed when the sympathetic nerves were intact indicates that the sympathetic nerves exert a vasoconstrictor effect upon carotid body blood vessels over a wide range of blood gas tensions and arterial pressure and that they also tend to diminish the rate of carotid body oxygen consumption. The mechanisms which may be involved in this regulation are discussed.

Animals↗
PubMed1971

Effects of mecamylamine on responses of carotid body chemoreceptors in vivo to physiological and pharmacological stimuli.

1. Effects of mecamylamine on the spontaneous discharge rate of afferent fibres of carotid body chemoreceptors in vivo and their responses to ACh, NaCN, HCl and hypoxia were studied in sixteen cats.2. Cats were anaesthetized with sodium pentobarbitone, paralysed with gallamine triethiodide and artificially ventilated. Chemoreceptor excitants were injected into the common carotid artery; mecamylamine was given intravenously.3. Mecamylamine, 230 mug/kg or greater, failed to diminish either the rate of spontaneous discharge of carotid body chemoreceptors at high arterial oxygen tensions (greater than 130 mm Hg), or the responses of these receptors to NaCN (0.5-25 mug), HCl or hypoxic blood.4. Responses of chemoreceptor afferent fibres to ACh (1.0-50 mug) in the same preparations were either completely abolished or considerably reduced by mecamylamine.5. These data do not support the hypothesis of a cholinergic mechanism for the initiation of chemosensory discharges in the carotid body, either at rest or in response to stimuli such as NaCN, acid or hypoxia.

Acetylcholine↗
PubMed1980

Projections from Pacinian corpuscles and rapidly adapting mechanoreceptors of glabrous skin to the cat's spinal cord.

1. Single axons innervating Pacinian corpuscles and rapidly adapting mechanoreceptors of the foot and toe pads were injected with horseradish peroxidase near their entrance to the lumbosacral spinal cord in cats anaesthetized with chloralose and paralysed with gallamine triethiodide. Subsequent histochemistry revealed the morphology of the intra-spinal parts of the axons. 2. All Pacinian corpuscle axons that could be traced into the dorsal root bifurcated upon entering the cord into ascending and descending branches. All Pacinian corpuscle axons gave rise to collaterals that entered the dorsal horn. 3. The collaterals of Pacinian corpuscle afferent fibres had a distinctive morphology. They provided two regions of termination, a larger dorsal region in laminae III and IV and a smaller ventral region in laminae V and VI. Within the dorsal region the terminal axons ran mainly in the longitudinal axis of the cord and carried many boutons en passant. Within the ventral region the axons ran dorso-ventrally in the transverse plane of the cord and although carrying some boutons en passant also gave rise to clusters of boutons. 4. The collaterals of rapidly adapting afferent fibres had a distinctive morphology different from that of the Pacinian corpuscle afferent fibre collaterals. The termination region of rapidly adapting afferents was limited almost exclusively to lamina III, with only slight extension into lamina IV. Boutons were mainly of the en passant type and terminal axons were generally orientated within the longitudinal axis of the cord. 5. The morphology of the afferent fibre collaterals is discussed in relation to the physiology of the dorsal horn.

Animals↗
PubMed1981

Direct observations on the contacts made between Ia afferent fibres and alpha-motoneurones in the cat's lumbosacral spinal cord.

1. The enzyme horseradish peroxidase was injected into identified lumbosacral alpha-motoneurones and Group Ia afferent fibres in cats anaesthetized with chloralose and paralysed with gallamine triethiodide. Subsequent histological examination allowed the determination of (a) the extent of the motoneuronal dendritic trees, (b) the number and location of Ia synapses upon the motoneurones. 2. alpha-motoneurones had seven to eighteen primary dendrites and each produced daughter branches up to the fourth to the sixth order. At dendritic bifurcations Rall's 3/2 Power Law was obeyed. There was little or no dendritic tapering up to about 800 micrometers from the soma. Beyond this distance, however, there was considerable tapering. 3. Horseradish peroxidase injections revealed that motoneuronal dendrites are much longer than previously thought. Individual dendrites could be traced for up to 1600 micrometers from the soma and dendritic trees were usually 2-3 mm from tip to tip. Nearly all the motoneurones had dendrites that entered the white matter of the cord. Dendrites could also reach as far dorsally as laminae V and VI. 4. Ia synapses upon motoneuronal somata were examined in cords counterstained with cresyl violet or methylene green. About 10% of Ia boutons in lamina IX were on somata and each Ia collateral terminated on 3.66 motoneuronal somata or the most proximal (30 micrometer) dendrites, with on average about two contacts per motoneurone. 5. Ten Ia afferent fibre-motoneurone pairs were injected with horseradish peroxidase. The following conclusions were drawn: (i) only one collateral of any given Ia axon makes contact with a motoneurone even though other collaterals from the same axon might pass through the dendritic tree, (ii) usually all contacts made between a Ia fibre and a motoneurone are at about the same geometrical distance from the soma, even when on different dendrites, (iii) between two and five contacts are made upon the dendritic tree (average 3.4) at distances of between 20 and 820 micrometers from the soma. 6. The results are discussed in relation to previous anatomical and electrophysiological work.

Animals↗
PubMed1981

Form and function of dorsal horn neurones with axons ascending the dorsal columns in cat.

1. Extracellular and intracellular recordings were made from dorsal horn neurones sending their axons through the dorsal columns in cats anaesthetized with chloralose and paralysed with gallamine triethiodide. 2. Seventeen neurones were injected with horseradish peroxidase through the intracellular micro-electrode, recovered from the histological material and shown to send their axons into the dorsal columns. 3. The cells had axonal conduction velocities of 30--47 ms-1; excitatory receptive fields that usually showed multireceptive characteristics, often including input from sensitive mechanoreceptors in glabrous skin; a third of the sample had a marked subliminal fringe to the excitatory field; inhibitory fields were usually situated proximal to the excitatory field and contiguous with it. 4. The cells were located in laminae III, IV and medial V. Dorsal cells had restricted dendritic trees that ascended in an essentially cylindrical volume of tissue through lamina II and often into I; cells intermediate in depth had more primary dendrites than the others, usually dorsally directed into lamina II, and a more extensive rostro-caudal development; deep, medial cells had dendritic trees that radiated extensively from the cell body but were restricted to the transverse plane. Two cells had axons that ascended the dorsolateral funiculus for a few mm before re-entering the dorsal horn, crossing it and reaching the dorsal columns. Collaterals were given off the axons in the grey matter, in the dorsolateral funiculus and the dorsal columns. 5. The form and function of the neurones are discussed.

Animals↗
PubMed1982

The role of spinal cord transmission in the ventilatory response to electrically induced exercise in the anaesthetized dog.

1. The ventilatory response to electrically induced ;exercise' was studied in six chloralose-anaesthetized dogs. The on-transient and steady-state responses to ;exercise' were compared in the same dogs before and after spinal cord transection at T8/9 (dermatome level T6/7) on fifteen occasions.2. Phasic hind limb ;exercise' was induced for periods of 4 min by passing current (2 Hz modulated 50 Hz sine wave) between two needles inserted through the hamstring muscles. The maximum current used was 30 mA. This was below the level previously found to produce an artifactual stimulation of breathing with the cord intact.3. Cord transection produced no significant change in either the resting values of ventilation ( V(I)) and CO(2) production ( V(CO) (2)) or the ventilatory equivalent for CO(2) during ;exercise' ( big up tri, open V(I)/ big up tri, open V(CO) (2)).4. During the steady state of exercise P(a, CO) (2) was on average significantly lower than at rest with the cord intact (mean big up tri, openP(a, CO) (2), - 2.1 mmHg; range - 5.7 to + 1), and higher, though not significantly, with the cord cut (mean P(a, CO) (2), + 1.2 mmHg; range - 1.5 to + 4.3). However, even in the absence of spinal cord transmission, the ventilatory response to exercise could not be accounted for on the basis of CO(2) sensitivity; the big up tri, open V(I)/ big up tri, openP(a,CO) (2) obtained with exercise (apparent sensitivity) was significantly greater than that obtained with CO(2) inhalation (true sensitivity) both before and after cord section.5. V(I) and V(CO) (2) increased more slowly with the cord cut than with the cord intact. This was thought to be due to a slower increase in venous return in the absence of sympathetic innervation of the lower half of the body following cord transection.6. Similar experiments were performed during muscle paralysis (following gallamine triethiodide). Ventilation was maintained with a respirator controlled by phrenic nerve activity. These experiments showed an increase in ventilation, independent of muscle contraction, which was only present when the cord was intact and which was confined to the on-transient. Only in the absence of spinal cord transmission could there be certainty that the dynamics of the ventilatory response to electrically induced ;exercise' was free of artifact.7. It was concluded that spinal cord transmission is not necessary for the steady-state ventilatory response to electrically induced exercise of the hind limbs.8. The dog with spinal cord transection provides a suitable model for the study of the chemical control of breathing during electrically induced exercise.

Anesthesia, General↗
PubMed1983

Effects of combined carotid chemoreceptor and atrial receptor stimulation on renal blood flow in anaesthetized dogs.

In dogs anaesthetized with chloralose and artificially ventilated, carotid chemoreceptors were stimulated by changing the perfusate of the vascularly isolated carotid bifurcations from arterial to venous blood. Left atrial receptors were stimulated by distending balloons in two pulmonary vein-left atrial junctions and in this left atrial appendage. The left renal blood flow was measured by an electromagnetic flow meter at a constant systemic (renal) arterial pressure in preparations in which heart rate changes were prevented by administration of propranolol hydrochloride (0.5 mg kg-1) and atropine sulphate (0.4 mg kg-1). Muscular movement was prevented by gallamine triethiodide (0.2 mg kg-1). Stimulation of left atrial receptors resulted in a significant increase (P less than 0.001) in renal blood flow of 5.6 +/- 0.88 ml min-1 100 g-1 renal mass from a control of 223 ml min-1 100 g-1 renal mass. The responses were abolished by cooling the cervical vagus nerves to 6-8 degrees C. Stimulation of carotid chemoreceptors, by perfusion of the carotid bifurcations by venous blood, caused a decrease in renal blood flow of 20 +/- 6.9 ml min-1 100 g-1 renal mass from 224 ml min-1 100 g-1 renal mass. Stimulation of left atrial receptors during venous perfusion of carotid chemoreceptors resulted in an increase in renal blood flow of 10.9 +/- 1.82 ml min-1 100 g-1 renal mass from 208 ml min-1 100 g-1 renal mass. These results show that atrial receptors and chemoreceptors can interact in their effects on renal blood flow.

Animals↗
PubMed1983

Receptive field organization and response properties of spinal neurones with axons ascending the dorsal columns in the cat.

Micro-electrode recordings were made from single post-synaptic axons in the dorsal columns of cats anaesthetized with chloralose and paralysed with gallamine triethiodide. The recordings were made from the L5 segment and the axons were shown to project to the upper cervical level. Forty-eight units were recorded and the axons had conduction velocities of 22-61 ms-1, averaging 38.3 ms-1. Excitatory receptive fields were complex in many units, being made up of clearly defined, separate, low and high threshold areas. The receptive fields were often discontinuous. Only a few units behaved as if they received excitatory input from a single class of mechanoreceptors. A minority (13%) of units had labile, excitatory receptive fields that expanded in size during the recording period. About 40% of the units had inhibitory receptive fields. These were of two main types: either small and within or adjacent to the excitatory field, or large and separated from or adjacent to the excitatory field. The great majority of units had resting discharges upon isolation and these consisted of single impulses or bursts of impulses at short intervals separated by longer, irregular periods. The time course of inhibition produced by electrical stimulation of cutaneous nerves suggested presynaptic inhibitory components to the inhibition. Some inhibitory curves were very prolonged with maxima at about 100 ms and total durations of up to 400 ms. The complexity of the receptive field organization in these dorsal horn neurones is discussed, as is their possible significance as input neurones to the dorsal column nuclei.

Action Potentials↗
PubMed1984

On re-excitation of feline motoneurones: its mechanism and consequences.

Conditions required for re-excitation of lumbosacral motoneurones, i.e. for double impulses in the motor axons associated with a single soma-dendritic action potential, were examined in cats anaesthetized with pentobarbitone and paralysed with gallamine triethiodide. Simultaneous recording from a motoneurone (intracellular, and in some experiments also extracellular), and from its axon in a ventral root, was used to assess the relations between the soma and the double axonal action potentials. Action potentials (greater than 70 mV) evoked by brief depolarizing current pulses applied intracellularly were never observed to cause re-excitation. Re-excitation could, however, be regularly induced by procedures which increased the delay between the initial segment and soma-dendritic components of these potentials. Re-excitation could be evoked (i) when brief hyperpolarizing pulses were applied before the onset of the soma-dendritic spikes, (ii) when the depolarizing pulses were applied on a background of long hyperpolarizing pulses or (iii) when two action potentials were evoked in a quick succession (by two brief depolarizing pulses). No relationship was found between the presence of re-excitation of motor axons and the presence of the delayed depolarization which follows the soma-dendritic spikes. Neither re-excitation nor delayed depolarization were found to be dependent upon re-excitation of the initial segment. These observations are thus at variance with previous suggestions that the initial segment spikes induce the re-excitation of motor axons and that the initial segment spikes cause the delayed depolarization following soma-dendritic spikes. Since re-excitation of a motor axon occurred without any signs of a second initial segment spike, it is concluded that it is initiated at the level of the axon, most likely at the first node of Ranvier. Re-excitation of motor axons was also observed during repetitive firing induced by intracellular current injection. However, it occurred then only occasionally, and only under strong depolarizing drive. It is thus not expected to be a common phenomenon under natural conditions of repetitive firing.

Action Potentials↗
PubMed1987

An intracellular study of spinocervical tract cell responses to natural stimuli and single hair afferent fibres in cats.

1. Intracellular recordings were made from spinocervical tract (s.c.t.) neurones in cats anaesthetized with chloralose and paralysed with gallamine triethiodide. 2. In one series of experiments the cells' receptive fields were examined with the use of natural stimuli. Hair movement within the impulse firing zone of the cell evoked excitatory post-synaptic potentials (e.p.s.p.s) from which impulses were generated; in addition, in the majority of s.c.t. cells tested, areas were found within the impulse firing zone where hair movement elicited both e.p.s.p.s and inhibitory post-synaptic potentials (i.p.s.p.s). Outside the firing zones, both regions evoking e.p.s.p.s and regions evoking i.p.s.p.s were observed in all neurones examined in detail (ten cells). The responses of these neurones to a variety of natural stimuli showed the receptive fields of s.c.t. cells to be more complex than previously thought. 3. In a second series of experiments, intracellular recordings from s.c.t. cells were combined with intracellular recording and stimulation of single dorsal root ganglion cells belonging to group II hair follicle afferent fibres. When the afferent fibres innervated skin within the impulse firing zone of the s.c.t. cell, single afferent impulses evoked e.p.s.p. complexes consisting of both mono- and polysynaptic components; no i.p.s.p.s were observed in response to single hair follicle afferent impulses or to trains. Although the monosynaptic e.p.s.p. component was often large and had a fast rise time, s.c.t. cell impulses usually arose from the later components. Afferent fibres innervating the central region of the s.c.t. cell firing zones tended to evoke relatively large e.p.s.p.s with fast rise times. The rise times and amplitudes of the e.p.s.p.s evoked by afferent fibres from the periphery, however, varied between afferent fibres but included the slowest and smallest in the total sample of synaptically coupled pairs. Afferent fibres from outside the s.c.t. cell's firing zone were usually ineffective in setting up post-synaptic potentials, but one group III hair follicle afferent fibre, from an inhibitory receptive field component, gave rise to i.p.s.p.s. 4. The effects of pairs and trains of afferent impulses at intervals of 10, 25, 50, 100 and 200 ms were examined. At 25 ms the response to the second afferent impulse was profoundly less than that evoked by the first and was still substantially reduced at 200 ms interval. In all synaptically coupled pairs studied, the e.p.s.p. complex evoked by the second afferent impulse was smaller in amplitude than that evoked by the first.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1987

The effects of stimulating carotid chemoreceptors on renal haemodynamics and function in dogs.

1. Dogs were anaesthetized with chloralose and artificially ventilated. The carotid chemoreceptors were stimulated by changing the perfusion of vascularly isolated carotid sinus regions from arterial to venous blood. The mean carotid sinus pressure and the mean arterial blood pressure were held constant at 124 +/- 3 and 122 +/- 3 mmHg, respectively. Both vagosympathetic trunks were sectioned in the neck and propranolol (17 micrograms kg-1 min-1 I.V.) and gallamine triethiodide (0.2-2.0 mg kg-1 30 min-1 I.V.) were infused. Renal blood flow was measured by an electromagnetic flow probe, glomerular filtration rate by creatinine clearance, sodium excretion by flame photometry and solute excretion by osmometry. 2. In sixteen tests in thirteen dogs perfusion of the carotid sinus regions with venous blood resulted in significant decreases in renal blood flow from 271 +/- 24 to 198 +/- 21 ml min-1 100 g-1 renal mass; glomerular filtration rate from 41.0 +/- 4.8 to 22.1 +/- 3.1 ml min-1 100 g-1; filtration fraction from 0.25 +/- 0.02 to 0.19 +/- 0.02; urine flow from 0.48 +/- 1.0 to 0.21 +/- 0.03 ml min-1 100 g-1; sodium excretion from 18.1 +/- 4.1 to 12.9 +/- 4.2 mumol min-1 100 g-1; and osmolar excretion 327 +/- 42 to 171 +/- 26 mu osmol min-1 100 g-1. The right atrial pressure did not change significantly from 4.6 +/- 1.2 cmH2O. 3. In seven dogs, tying renal sympathetic nerves abolished all the responses except that of sodium excretion which was now reversed; sodium excretion increased from 68 +/- 19 to 116 +/- 38 mumol min-1 100 g-1 without significant change in right atrial pressure from 7.4 +/- 1.9 cmH2O. Crushing the carotid bodies, however, abolished all the responses. 4. The results show that carotid chemoreceptor stimulation can cause significant reflex effects on renal haemodynamics and function which are mediated via renal sympathetic nerves. They also show that the chemoreceptor stimulation can cause natriuresis in the absence of haemodynamic changes, in the denervated kidney, presumably via a humoral factor.

Animals↗