[Effect of light on the electrogenesis process in pigmented neurons of the pond snail].
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Animals↗
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Correlation of spinal cord blood flow and function in experimental compression.
Focal spinal cord blood flow was measured in the left dorsal column of monkeys' spinal cords at T6 during slow balloon compression of the same segment. The physiological integrity of the spinal cord was monitored by the recording of the summated spinal evoked response (SER). In all cases, the evoked response did not disappear until the blood flow in the compressed segment was zero. In four animals, a definite phase of hyperemia occurred during compression, at which time the amplitude of the evoked response was reduced. A post-ischemic hyperemia occurred in seven animals. The evoke response returned in all animals to a varying degree within one-hour post-deflation. The results suggest that mechanical forces of compression, rather than ischemia, are mainly responsible for the loss of neural conduction in such a model. If ischemia plays a role at all in the loss of function in such a model, it appears that focal ischemia secondary to compression in the spinal cord must be profound for loss of physiologic function to occur.
Animals↗
Central somatosensory conduction in man: neural generators and interpeak latencies of the far-field components recorded from neck and right or left scalp and earlobes.
Early somatosensory evoked potential (SEP) components to median nerve or finger stimulation were recorded with non-cephalic references in normal young adults. Detailed topographic data over scalp and neck were related to anatomical observations on the actual conduction distances in dorsal column, medial lemniscus and thalamo-cortical parts of the somatosensory pathway. The extrapolation of afferent conduction velocity (CV) measured from sensory nerve potentials along the peripheral nerve to the C6-C7 spinal segments identified the spinal entry time with the onset of the neck N11 or scalp P11 (far field 2 or FF2). The first far field (FF1) is generated in the nerve proximal to axilla. The definite latency shift of the spinal negativity along the neck indicates a CV of 58 m/sec. Data about the maximal diameter of lemniscal axons in man were used to calculate a CV of 40.5 m/sec. Consideration of transit times from spinal entry to cortex and of synaptic delays clarified the arrival times of the afferent volley at various relay nuclei, and also suggested a thalamo-cortical CV of about 33 m/sec. Interpeak and onset-to-peak measures on scalp far fields suggest that FF3-FF4 are generated in medial lemniscus rather than above the thalamus. Consistent differences in amplitude, but not in wave form, were recorded at right and left earlobes for FF2 (larger ipsilaterally) and FF3-FF4 (larger contralaterally). The scalp topography of far fields was analysed in detail.
Adult↗
Heart conduction system: a neural crest derivative?
Using the anti-neurofilament monoclonal antibody iC8 we report here that muscle fibers of the conduction system of the adult and developing rabbit heart express a cytoskeletal protein antigenically and electrophoretically similar to the middle subunit of neurofilaments (NF-M). In the 11-day embryo a number of cardiac muscle cells also express a neural crest surface marker recognized by the monoclonal antibody HNK-1. Both markers are found in many cells of the 3rd and 4th branchial arches, which are populated by cells of neural crest origin. In the 11-day embryo cells of the 4th branchial arch are in close proximity to and intermingled with the atrial myocardium: cells co-expressing sarcomeric myosin heavy chain with iC8 and HNK-1 immunoreactivity are seen at these sites. The findings suggest that conduction tissue cells of the rabbit heart originate from a population of neural crest-derived cells migrating from the branchial arches into the developing heart.
Animals↗
Beat-by-beat modulation of AV conduction. II. Autonomic neural mechanisms.
We examined the mechanism by which autonomic neural activity associated with respiration and blood pressure modulates atrioventricular (AV) conduction in conscious dogs. Mongrel dogs were anesthetized and instrumented under sterile conditions to record atrial and ventricular electrograms and blood pressure. In the conscious state, electrocardiogram (ECG), respiration, blood pressure, and electrograms were recorded continuously, and heart rate and AV interval were plotted graphically as a function of time. To delineate the role(s) of sympathetic and parasympathetic activity, AV conduction was studied during abrupt and linear changes in heart rate after administration of atropine, propranolol, or both. In the basal state and after propranolol, AV interval oscillated with respiration both in the absence of atrial pacing and at pacing rates 10-100 beats/min above control. Following atropine, oscillations in AV interval associated with respiration were abolished; however, linear and abrupt heart rate increases resulted in AV conduction changes that were associated with fluctuations in blood pressure. In contrast, after both atropine and propranolol, alterations in blood pressure or respiration did not influence AV conduction and rate-dependent prolongation of AV conduction occurred. We conclude that in the basal state, AV conduction is influenced predominately by changes in parasympathetic activity which is the major determinant of respiratory-related AV interval oscillations; after atropine, sympathetic activity produces fluctuations in both AV conduction and blood pressure; and intrinsic rate-dependent properties of the AV node are modulated continually by both divisions of the autonomic nervous system.
Animals↗
Surface modification of neural probes with conducting polymer poly(hydroxymethylated-3,4- ethylenedioxythiophene) and its biocompatibility.
A novel conducting polymer, poly(hydroxymethylated-3,4-ethylenedioxythiophene) (PEDOT-MeOH), was electrochemically deposited onto the electrodes of micromachined neural probes. Uniformly distributed film was obtained from aqueous solution when doped with polystyrenesulfonate. The surface morphology was rough and had good cellular adhesion. Impedance spectroscopy showed that the magnitude of coated electrode was lower than that of the bare gold over a range of frequencies from 10(0)to 10(5) Hz. Since the biocompatibility of the interface between the neural probes and brain tissue plays an important role when the probes are implanted in the central nervous system for long-term application, biomolecules were incorporated into the coating. Nonapeptide CDPGYIGSR was codeposited as the counterion in the conducting films. The surface morphology of the coating was fuzzy, providing many bioactive sites for interaction with neural cells. The magnitude of impedance was as low as 53 kOmega at the biologically relevant frequency of 1 kHz. An in vitro experiment demonstrated that the neuroblastoma cells grew preferentially on the PEDOT-MeOH/CDPGYIGSR-coated electrode sites and spread beyond the electrode area.
Bridged Bicyclo Compounds, Heterocyclic↗
Effects of temperature on interictal discharge at penicillin epileptogenic foci.
The effects of local brain temperature on acute focal penicillin epilepsy in the exposed hippocampus of cat were studied. Results from anesthetized and from immobilized, unanesthetized animals were compared. Over the temperature range 26 to 43 degrees C (at the alveus), the interictal spike interval and duration of the spike discharge varied inversely with temperature. The former showed a Q10 of 2.4 and the latter a Q10 of 1.5, with no difference due to type of preparation. A significant trans-hippocampal thermal gradient may imply that these values are underestimates by 20% or more. The low Q10 of duration of the paroxysmal discharge was consistent with the known temperature dependence of impulse conduction velocity of intracortical neural networks. The high Q10 of the interictal interval, on the other hand, was consistent with the view that some slow endogenous, perhaps metabolic factor such as a NA,K-ATPase modulated excitability at the focus of penicillin spikes.
Action Potentials↗
Modulation of impulse conduction along the axonal tree.
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Action Potentials↗
[Transcranial magnetic stimulation].
Transcranial magnetic stimulation (TMS) allows non-invasive study and modulation of cortical excitability in humans. Changes in cortical excitability in physiological and pathological conditions can be tracked by measurements such as motor threshold, motor evoked potentials, recruitment curves, intracortical facilitation and inhibition. The central motor conduction time can estimate neural transmission in central motor pathways. Changes in areas of representation in sensorimotor cortex can be studied with cortical mapping. Modulation of cortical processing can be used to evaluate different brain functions. Therapeutic use in depression, Parkinson's disease and epilepsy has raised great interest over the past decade. Non-invasive cortical mapping may be achieved by combining TMS to other neurophysiological/ neuroimaging techniques. TMS has great potential both as an investigational and as a therapeutical tool in Neurology and Psychiatry.
Brain Diseases↗
Surface modification of neural recording electrodes with conducting polymer/biomolecule blends.
The interface between micromachined neural microelectrodes and neural tissue plays an important role in chronic in vivo recording. Electrochemical polymerization was used to optimize the surface of the metal electrode sites. Electrically conductive polymers (polypyrrole) combined with biomolecules having cell adhesion functionality were deposited with great precision onto microelectrode sites of neural probes. The biomolecules used were a silk-like polymer having fibronectin fragments (SLPF) and nonapeptide CDPGYIGSR. The existence of protein polymers and peptides in the coatings was confirmed by reflective microfocusing Fourier transform infrared spectroscopy (FTIR). The morphology of the coating was rough and fuzzy, providing a high density of bioactive sites for interaction with neural cells. This high interfacial area also helped to lower the impedance of the electrode site and, consequently, to improve the signal transport. Impedance spectroscopy showed a lowered magnitude and phase of impedance around the biologically relevant frequency of 1 kHz. Cyclic voltammetry demonstrated the intrinsic redox reaction of the doped polypyrrole and the increased charge capacity of the coated electrodes. Rat glial cells and human neuroblastoma cells were seeded and cultured on neural probes with coated and uncoated electrodes. Glial cells appeared to attach better to polypyrrole/SLPF-coated electrodes than to uncoated gold electrodes. Neuroblastoma cells grew preferentially on and around the polypyrrole/CDPGYIGSR-coated electrode sites while the polypyrrole/CH(3)COO(-)-coated sites on the same probe did not show a preferential attraction to the cells. These results indicate that we can adjust the chemical composition, morphology, electronic transport, and bioactivity of polymer coatings on electrode surfaces on a multichannel micromachined neural probe by controlling electrochemical deposition conditions.
Animals↗
Integration of heart rate and sympathetic neural effects on AV conduction.
Sympathetic activation increases heart rate (HR) and reduces atrioventricular interval (AVI), whereas atrial pacing alone increases AVI. We sought to differentiate the direct effects of sympathetic activation on atrioventricular (AV) conduction time from the indirect changes associated with concurrent alterations in HR. We recorded electrocardiograms, blood pressure (BP), and intracardiac electrograms from chloralose-anesthetized autonomically decentralized dogs. Beat-by-beat HR and AVI data were collected continuously. Sympathetic stimulation (0.25-2.5 Hz; mean 0.81 Hz) resulted in a HR change of +60 beats/min after 60 s. This tachycardia was associated with a mean decrease in AVI of 22 ms. Computer-driven atrial pacing to reproduce the HR associated with control sympathetic stimulation caused a mean AVI increase of 10 ms. Propranolol (200 micrograms) was then administered via the sinoatrial node artery and sympathetic stimulation repeated. Although HR remained constant, AVI decreased by 14.8 ms. The AVIs associated with an identical HR achieved by two different mechanisms (sympathetic stimulation and atrial pacing) were significantly different. Although removal of the contribution of sympathetically induced HR changes on AV conduction might be expected to result in potentiation of neural effects at the AV node, none was evident. Thus sympathetic activity restricted to the AV node is less effective in influencing AV conduction than the response that occurs when HR changes occur concurrently. Therefore, the opposing actions of HR and sympathetic tone on AV conduction may not be predicted by a simple linear relationship.
Animals↗
Sympathetic neural inhibition of conducted vasodilatation along hamster feed arteries: complementary effects of alpha1- and alpha2-adrenoreceptor activation.
Vasodilatation initiated on arterioles of skeletal muscle ascends into the proximal feed arteries through cell-to-cell conduction along the endothelium and into smooth muscle. Whereas perivascular sympathetic nerve activity (SNA) can inhibit conducted vasodilatation and restrict muscle blood flow, the signalling events mediating this interaction are poorly defined. Therefore, using isolated pressurized (75 mmHg) feed arteries (diameter (microm) at rest = 53 +/- 3; maximum = 99 +/- 2; n = 86) of the hamster retractor muscle, we tested the hypothesis that distinct yet complementary signalling pathways underlie the ability of SNA to inhibit conduction. Conducted vasodilatation was initiated using ACh microiontophoresis (1 microA; 250, 500 and 1000 ms) and SNA was initiated using local field stimulation (30-50 V; 1 ms at 2, 8 and 16 Hz). With vasodilatations of 5-20 microM, conduction increased with ACh pulse duration and was inhibited progressively as the frequency of SNA increased. During SNA, conduction was partially restored with inhibition of alpha1- (0.1 microM prazosin) or alpha2- (0.1 microM RX821002) adrenoreceptors and fully restored with both antagonists present. Activating alpha1- (50 nM phenylephrine) or alpha2- (1 microM UK 14,304) adrenoreceptors inhibited conduction partially and their simultaneous activation inhibited conduction cumulatively (P < 0.05). Elevated [K+]o (30 or 40 mM) or phorbol esters (0.5 microM) also inhibited conduction yet similar constriction with l-NNA (50 microM) or Bay K 8644 (10 nM) did not. Thus, the activation of alpha1- and alpha2-adrenoreceptors inhibits conducted vasodilatation through complementary signalling events. With robust coupling along the endothelium, our modelling predicts that the inhibition of conduction by SNA can be explained by reduced electrical coupling through myoendothelial gap junctions or greater current leak across smooth muscle cell membranes.
Adrenergic Agonists↗
Modulation of neural cell membrane conductance by the herbal anxiolytic and antiepileptic drug aswal.
To evaluate the effects of aswal on ionic fluxes and neuronal excitation, we performed extracellular and whole cell patch clamp recordings on CA1 pyramidal neurons of guinea pigs and Long-Evans rats. Aswal (100- 250 mg/l) was administered systemically, and its effects on the rate of synchronized extracellular field potentials (EFP), membrane parameters, action potentials and postsynaptic potentials were recorded. The extracellular results obtained are consistent with calcium antagonistic properties. Intracellular recordings suggest that a direct sodium antagonistic effect as seen in many antiepileptic drugs plays no significant role. Further effects on ligand gated ion channels are discussed controversially. In summary, the cellular action of aswal appears heterogeneous with calcium antagonism playing a prominent role in counteracting excitation which may be a common feature in epilepsy and different psychiatric conditions as mood and anxiety disorder.
Animals↗
Abnormalities of the coronary arteries, neural structures and conduction system of the heart observed postmortem in the eosinophilia-myalgia syndrome, with a discussion of comparative findings from the toxic oil syndrome.
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Aged↗
Conduction properties of identified neural pathways in the central nervous system of mice in vivo.
Various lines of transgenic or knockout mice are now available that have abnormalities in neuron, glial cells or neuron-glial interaction. However, the techniques for quantitative analysis of their pathophysiological functions are still limited. We established an experimental model system to measure the properties of nerve conduction of identified neural pathways in the CNS using anesthetized and immobilized mice. Dorsal column (DC), vestibulospinal/reticulospinal tracts (VRST) and pyramidal tract (PT) were stimulated by inserting stimulating electrodes into the dorsal column nuclei, medial longitudinal fasciculus, and the medullary pyramid, respectively. Volleys were recorded at various segments in the cervical spinal cord with surface electrodes, and their conduction velocities (CVs) and relative refractory periods (RRPs) were measured. The CVs of the DC, VRST and PT were 26.25 +/- 4.96 m/s (n = 7), 51.55 +/- 4.65 m/s (n = 7), 8.89 +/- 1.81 m/s (n = 7), respectively. Data from paired stimulation indicated that the median values of RRPs of the DC, VRST and PT were 10, 2 and 4 ms, respectively, which suggested marked difference among individual tracts. This is the first attempt to measure the conduction properties of the central tracts in mice in vivo. This experimental procedure will give us a physiological measure of CNS functions in normal and genetically manipulated mice and contribute to clarifying the molecular mechanisms and pathophysiology of neurodegenerative diseases such as multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS).
Animals↗
[Simultaneous measurement of conduction velocity in the neural sensory and motor fibers during segmental stimulation].
The study concerned the method of investigation of upper extremity nerves which makes possible a simultaneous measurement of the conduction velocity in the motor and sensory fibres over the whole length of the nerve. Recording of responses was based on the use of surface electrodes which are safe, less painful for the patient, and provide sufficiently great responses without the necessity of using the averaging technique. Owing to simultaneous responses from the motor and sensory fibre from several stimulation sites along the nerve the localization of injury and its type are easier to establish. The method is less time-consuming than the conventional one and may be used by technicians.
Adult↗
Propofol anticonvulsant activity in experimental epileptic status.
We have examined the anticonvulsant properties of propofol in high doses in two experimental models of status epilepticus: generalized pentylenetetrazol (PTZ)-induced seizures and partial, cortically applied penicillin G-induced seizures. Propofol was administered either as a single bolus injection or as a bolus injection followed by an infusion for 1 h. When administered as a single bolus injection, propofol 12 mg kg-1 suppressed electrical and clinical seizures in PTZ generalized epileptic status, and an infusion of 50 mg kg-1 h-1 prevented the reappearance of electrical and clinical signs. In focal epileptic status, the single dose stopped paroxysmal activity and the associated clonic jerks for a few seconds. When the bolus dose was followed by an infusion, the firing bursts were replaced by isolated spikes, and contralateral jerks became sporadic and feeble. The greater efficacy of propofol against PTZ convulsions may be a reflection of the opposite action of the two drugs on neural membrane conductance: PTZ induces paroxysmal neural discharge by enhancing membrane conductance while propofol appears to decrease membrane conductance, thus suppressing paroxysmal discharge. There was no close relationship between blood concentration of the anaesthetic and its clinical effects, at least after a short-term infusion, as used in the present experiments. We suggest that propofol may be a potentially useful drug in status epilepticus in patients in whom benzodiazepines, barbiturates and phenytoin have failed.
Action Potentials↗
Auditory brainstem evoked potentials in evaluating the central effects of middle ear effusion.
Auditory brainstem evoked potentials (ABEP) were recorded to determine whether children who suffered in the past, or suffered at time of examination from Secretory otitis media (S.O.M.), exhibited slowed conduction along their auditory brainstem. Five groups of subjects were examined: children with active S.O.M. during the examination, children with S.O.M. in the past who were treated non-surgically and recovered, children with S.O.M. in the past who were treated surgically and recovered, children who were treated by insertion of ventilating tubes (V.T.), and had S.O.M. during the examination (recurrent S.O.M.), and a control group of neurologically and audiologically normal, age-matched children with no history of S.O.M. 205 ears were tested in all. Each of the groups was subdivided according to the severity of hearing loss, duration and type of treatment. These parameters were evaluated within and between groups, and in relation to the control group. Significant increases of interpeak latency differences (IPLD) between peaks V and III as well as V to I were found in the S.O.M. groups compared to the control group. The duration of the disease was found to be the dominant factor slowing central conduction. These findings confirm the suggestion that attenuation in auditory stimulation at an early age affects central conduction.
Audiometry, Evoked Response↗