Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neural Conduction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,603 records · Page 89Linked to original sources

Electrophysiological evaluation of the patient with acute spinal cord injury.

This article reviews basic principles, equipment and techniques, and clinical applications of electrophysiologic monitoring in patients with spinal cord injuries. Four groups of electrophysiologic measurements are considered: Somatosensory evoked potentials (SEPs); motor evoked potentials (MEPs); electromyography (EMG) and nerve conduction studies; and late responses, including H reflex, M response, and F wave. Reports of SEP recordings in spinal cord injury, as drawn from the literature, are tabulated in detail.

Electromyography↗

Neurochemistry of the central vestibular pathways.

This review focuses on the neurochemistry of the central vestibular pathways. The main emphasis will be on the analysis of the central vestibular nuclei neurons, since several papers published in the past 5 years have provided important information on the role that neurotransmitter-dependent conductances play in the central processing of vestibular inputs. Indeed, increasing evidence suggests that both the non-linear intrinsic membrane properties of the neurons and the nature of the different neurotransmitters and neuromodulators involved in the vestibular network contribute to the various operations required for stabilising gaze and posture. It has also been demonstrated that the neurotransmitter-dependent conductances together with the ionic voltage-dependent conductances may determine the firing patterns of the medial vestibular neurons and interfere with their integrative properties. We hope that this review will show that by combining in vitro and in vivo electrophysiological approaches and the new powerful neuropharmacological techniques developed from the recent advances of molecular biology, the vestibular system can be used as a good model to elucidate some of the basic properties of the brain including learning, neural computation, network reconfiguration and post-lesional plasticity.

Acetylcholine↗

Depressor responses to stimulation of sympathetic afferents in monkeys and dogs.

In dogs and monkeys anesthetized with pentobarbital sodium, stimulation of the cut central ends of the stellate cardiac nerve, the left and right anterior ansae subclavia, and the stellate ganglia resulted in a depressor response when stimulating fibers with conduction velocities in the range of 2.5-10 m/s. These afferents are in the A delta-fiber-type range. Pressor responses could be elicited by stimulating afferent fibers with conduction velocities in the range of 0.5-3.0 m/s. These fibers are in the C-fiber-type range. Stimulation of the abdominal sympathetic afferents always resulted in a depressor response regardless of the conduction velocities of the fibers. No changes in heart rate were observed. Bilateral cervical vagotomy did not alter the pressor or depressor responses.

Adrenergic Fibers↗

A new aspect of the collision test principle: cell body distance from recording site.

A theoretical method is described for estimating the distance between a spike recording-site, possibly axonal, and the corresponding cell body of unknown location. The method requires that an orthodromic spike be recorded following an antidromic spike, with estimation of a collision interval analogous to that used for establishing antidromicity. To calculate the distance between recording-site and cell body, values are needed for the collision interval between antidromic and succeeding orthodromic spikes, the refractory period of the spike, and the antidromic conduction speed. Problems may arise in determining the last value. The method is illustrated with antidromic spikes recorded in the medial thalamus of the cat upon stimulating the caudate nucleus.

Animals↗

An electrophysiological demonstration of the axonal projections of single spinal interneurones in the cat.

1. Single interneurones excited from group Ia afferents and located in the ventral horn of the spinal cord in the cat were activated antidromically by stimulation of their axons with one micro-electrode while recording extracellularly close to their somas with a second micro-electrode. The interneurones studied were those which, according to previous indirect evidence, should mediate the reciprocal Ia inhibition of motoneurones.2. Two subgroups of these interneurones were studied: those excited from group Ia afferents in the quadriceps (Q) and posterior bicepssemitendinosus (PBSt) nerves. Most of them could be activated from a number of separate loci in the PBSt and Q motor nuclei respectively and from the ventral or lateral funiculi.3. The location of the axonal branches and the extent of their branching in the motor nuclei were reconstructed by comparing the latencies of the responses and the thresholds (0.1-5 muA) for antidromic activation of single interneurones from different electrode positions in a number of tracks, having previously established the relation between the threshold and the distance from the stimulated fibres. For the main branches in the white matter the conduction velocity was found to be about 70 m/sec.4. The axonal projections of the investigated interneurones were found to be fully consistent with the hypothesis that they mediate reciprocal inhibition of motoneurones.

Action Potentials↗

The contribution of membrane hyperpolarization to adaptation and conduction block in sensory neurones of the leech.

The factors underlying sensory adaptation and conduction block have been studied in cutaneous mechanoreceptor neurones of the leech. A touch-sensitive cell was activated by applying mechanical or electrical stimuli to its receptive field on the skin. Impulses were recorded extracellularly from its axons and intracellularly from its cell body, which is situated within the C.N.S.1. Activation of the touch cell by mechanical stimuli revealed two distinct types of adaptation with characteristically different time courses. Sustained pressure on the skin caused a brief burst of impulses at the onset of the stimulus. This rapid adaptation to pressure was restricted to the part of the receptive field that had been stimulated mechanically. A second type of adaptation developed more slowly during the course of repetitive mechanical stimulation. It persisted for many seconds after the end of a train of impulses and appeared as an increase in the threshold to mechanical stimuli not only in the region of skin that had been rubbed but throughout the receptive field of the cell.2. Impulses initiated in the cell body propagated antidromically towards the skin and also raised the threshold to touch, indicating that after-effects of impulse activity were responsible for the long-lasting threshold increase.3. Repetitive mechanical stimulation could also produce a reversible conduction block in branches of the touch cell. The block occurred in discrete regions of low safety factor such as axonal branch points both within the ganglion and in the periphery. In some experiments impulses intermittently failed to reach one axonal branch yet continued to invade a separate branch of the same cell.4. Several lines of evidence indicate that both conduction block and the slow component of adaptation are linked to a prolonged hyperpolarization that follows repetitive stimulation of the touch cell. Strophanthidin, which blocks the after-hyperpolarization in touch cells, reduced the adaptation following trains of impulses and also relieved a conduction block previously established by repetitive stimulation. Furthermore, a comparison of the effects of hyperpolarizations produced by current injection and by repetitive firing showed that most of the threshold increase in the cell body after a train of impulses could be attributed directly to the membrane hyperpolarization.5. These experiments suggest several ways in which repetitive activity can have pronounced and long-lasting effects on the performance of a highly branched sensory cell. Thus a relatively small number of impulses in a touch cell can markedly decrease its sensitivity to touch. The functional role of the conduction block observed during vigorous stimulation is not as clear because activity for many seconds or minutes is usually needed to establish a block in the larger branches of the cell.

Action Potentials↗

Background synaptic conductance and precision of EPSP-spike coupling at pyramidal cells.

The temporal precision of converting excitatory postsynaptic potentials (EPSPs) into spikes at pyramidal cells is critical for the coding of information in the cortex. Several in vitro studies have shown that voltage-dependent conductances in pyramidal cells can prolong the EPSP time course resulting in an imprecise EPSP-spike coupling. We have used dynamic-clamp techniques to mimic the in vivo background synaptic conductance in cortical slices and investigated how the ongoing synaptic activity may affect the EPSP time course near threshold and the EPSP spike coupling. We report here that background synaptic conductance dramatically diminished the depolarization related prolongation of the EPSPs in pyramidal cells and improved the precision of spike timing. Furthermore, we found that background synaptic conductance can affect the interaction among action potentials in a spike train. Thus the level of ongoing synaptic activity in the cortex may regulate the capacity of pyramidal cells to process temporal information.

Animals↗

Vasogenic edema following acute and chronic spinal cord compression in the dog.

The T-13 spinal cord segment of dogs was compressed both acutely and chronically by means of a balloon catheter. The vascular permeability to protein was assessed using Evans blue albumin (EBA), and the dorsal column evoked potential recorded to monitor conduction failure. With acute compression sufficient to cause conduction failure there was a marked leakage of EBA from the intermediate gray matter, which spread into the dorsolateral white matter. The degree of edema was similar whether the compression was maintained or released. Chronic compression maintained over 4 to 5 hours did not increase vascular permeability, but following release of compression leakage of EBA occurred in the same cord locations observed with leakage from acute compressions. This increased permeability following release of chronic compression may result from reactive hyperemia. Dorsal column conduction returned after the release of both acute and chronic compression. The extravasated EBA was present both in the extracellular space and within cells. The results and their clinical application are discussed.

Acute Disease↗