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 1,009 records · Page 56Linked to original sources
PubMed1978

An intracellular study of dendrodendritic inhibitory synapses on mitral cells in the rabbit olfactory bulb.

1. In the rabbit olfactory bulb, intracellular potentials were recorded from mitral cells and from neurones in the granule cell layer (g.c.l.) following lateral olfactory tract (l.o.t.) stimulation. 2. Most recordings from mitral cells showed large (5-21 mV) and prolonged (60-650 msec) i.p.s.p.s subseuqent to the antidromic spikes. These i.p.s.p.s decreased in amplitude and then reversed in polarity by progressive increase in hyperpolarizing current applied intracellularly. They were accompanied by a prominent and long lasting (up to 100 msec) conductance increase of the mitral cell membrane. 3. Reversed i.p.s.p.s of mitral cells having quite different time courses from the original hyperpolarizing i.p.s.p.s suggest that the inhibitory synapses are widely distributed on the soma and dendrites. 4. E.p.s.p.s could be recorded from g.c.l. cells whose onset latency was approximately 0.6 msec shorter than that of mitral cell i.p.s.p.s. Comparison of the behaviour of e.p.s.p.s in g.c.l. cells and that of mitral cell i.p.s.p. under various conditions of l.o.t. stimulation suggests that these g.c.l. cells are the inhibitory interneurones mediating mitral cell inhibition. 5. The results support the hypothesis of dendrodentritic pathways for activation of granule cells and subsequent inhibition of mitral cells.

Animals↗
PubMed1991

Histologic abnormalities of large and small coronary arteries, neural structures, and the conduction system of the heart found in postmortem studies of individuals dying from the toxic oil syndrome.

Hundreds died and thousands were poisoned by rapeseed oil adulterated with aniline and sold illegally in Spain in 1981. The clinical manifestations, now known as the toxic oil syndrome, include pulmonary hypertension and right ventricular hypertrophy plus widespread vascular and neural lesions in other organs. Many of the late deaths ended with a scleroderma-like illness. Because scleroderma involves the heart, in this study we examined the small and large coronary arteries, neural structures, and conduction system from eight victims dying with the toxic oil syndrome. Dense fibrosis of the sinus node in two hearts resembled changes found in scleroderma. Atrionodal junctional hemorrhages and cystic degeneration of the sinus node present in the other six hearts resembled changes found in lupus erythematosus. Small and large coronary arteries exhibited focal fibromuscular dysplasia and a proliferative cystic myointimal degeneration. This latter abnormality was associated with sloughing of the inner wall and embolization of the detached fragment downstream in the same coronary artery. Every heart had many degenerative lesions within nerves, ganglia, and the coronary chemoreceptor. Both the arterial and neural abnormalities prominently involved the conduction system. Based upon observations by others with experimental feeding of rapeseed oil containing either high or low erucic acid, we suggest that this oil must remain a major suspected cause of the toxic oil syndrome, particularly in conjunction with some as yet unexplained facilitative influence by oleoanilids. If this is so, it is important to reconsider the widely recommended use of any rapeseed oil product as a suitable food for man or other animals.

Adolescent↗
PubMed2006

[Relationship between adverse neural tension and nerve conduction studies in patients with symptoms of the carpal tunnel syndrome].

The purpose of this study was to evaluate, through a series of cases, the relationship between the adverse neural tension of median nerve (ANTm) and the electrophysiological involvement in 38 patients with symptoms of the carpal tunnel syndrome (CTS), submitted to nerve conduction studies (NCS). The main measures had been ANTm (in degrees) obtained through the test of neural tension provocation (TNTP) and parameters of the NCS, divided into three groups: normal, without severe electrophysiological alteration and with severe electrophysiological alteration. Significant correlations were found between ANTm and parameters of the NCS (p<0.05), as well as between ANTm and the three groups defined by the electrophysiologic alteration (rs=+0.437, p=0.002). The TNAm values were significantly higher in the arms with electrophysiologic diagnoses (p=0.007). It is suggested that the ANTm does have a participation in the physiopathology of the CTS, and the use of therapeutical procedures that diminish the development of neural tension.

Arm↗
PubMed1986

Mechanisms of central conduction time prolongation in brain-stem auditory evoked potentials.

The wave I-wave V delay in the auditory brain-stem response is commonly used as a diagnostic tool in otoneurology. Normative values have been established for different populations and different types of stimuli. This I-V delay has been known for some time as "central conduction time" or "central transmission time." This implies that the measure reflects in normal and in pathologic cases delays due to nerve conduction, synaptic transmission, and neural integration and is not caused by cochlear processes. By virtue of the traveling wave delay in the cochlea, amounting to some 4 ms from the base to the "500-Hz place," it is conceivable that this delay contributes to the I-V delay. From a series of 69 pontine angle tumors in which the auditory brain-stem response was recorded, we selected cases with an apparent peripheral origin of a prolonged I-V delay by comparing the whole-click response to responses derived from high-pass noise masking. It seems that cases with an increased I-V delay in the whole-click response but (almost) normal I-V delays in the narrow-band response are indicative of small intracanalicular acoustic neuroma.

Brain Stem↗
PubMed1999

Temperature sensitivity of transduction and action potential conduction in a spider mechanoreceptor.

Previous work has suggested that the activation energy of mechanotransduction is higher than expected from the simple electrochemistry of ion channels, but the temperature sensitivity of mechanically activated receptor current has not been measured directly before. We used the single-electrode voltage-clamp technique to measure receptor currents in sensory neurons of the VS-3 slit-sense organ in the spider, Cupiennius salei. Receptor currents were generated by deforming the cuticular slits. Conduction velocity in afferent axons from the same organ was also measured by recording action potentials at two locations in the leg during mechanical stimulation of the slits. Activation energies of mechanotransduction and conduction velocity were estimated by making the measurements at a range of temperatures. The mean activation energy for receptor current was 23.1 kcal/mol (96.6 kJ/mol), corresponding to a Q10 value of 3.2. Conduction velocity in the afferent axons was approximately equal to 5 m/s at room temperature and it was much less temperature sensitive, with an activation energy of 6.3 kcal/mol (26.3 kJ/mol), corresponding to a Q10 value of 1.5. These results provide the first direct measurements of the activation energy of mechanically activated currents and support previous suggestions that a high thermal energy barrier is involved in mechanotransduction.

Action Potentials↗
PubMed1976

Responses of primate locus coeruleus and subcoeruleus neurons to stimulation at reinforcing brain sites and to natural reinforcers.

In alert rhesus monkeys the activity of 64-neurons was recorded in the locus coeruleus and subcoeruleus region, collectively referred to as coeruleus (C) neurons. C neurons were identified physiologically by antidromic activation from electrodes in the medial forebrain bundle (MFB) and medial septal nucleus which sustained intracranial self-stimulation (ICSS) behavior, and/or anatomically by their proximity to microlesions at unit recording sites. The following results were obtained: (1) the current intensity that supported the highest rate of MFB and septal ICSS was similar to the current intensity for evoking antidromic responses in C neurons; (2) stimulation in the vicinity of the dopaminergic neurons of nucleus A10 did not activate C neurons; (3) C neurons were antidromically activated by ipsilateral and contralateral MFB shocks; (4) the C axons had slow estimated conduction velocities (1-5 m/sec), and a mean neural refractory period of 0.8 msec; (5) the behaviorally determined refractory period for MFB ICSS was also approximately 0.8 msec; and (6) mean firing rates while the monkey sat quietly were 15 +/- 2 Hz (S.D.) for subcoeruleus cells and 5 +/- 3 Hz for locus coeruleus cells, and activity of most cells changed negligibly during operant responding for apple-sauce reinforcement. These results suggest that the reinforcing effects of ICSS may be mediated by activation of coeruleus cells, but that these cells do not appear to be strongly involved in operant responding for natural reinforcers.

Animals↗
PubMed1988

Tonic descending inhibition of the spinal cardio-sympathetic reflex in the cat.

Electrical stimulation of the left inferior cardiac nerve elicited a two-component reflex potential (spinal and supraspinal reflexes) in the ipsilateral white ramus T3 from which recordings were made in chloralose-anaesthetised cats. Reversible interruption of all spinal pathways achieved by cooling the spinal cord at C2/C3 produced an enhancement of the spinal reflex and abolished the supraspinal reflex, the latter usually being the more prominent reflex potential prior to spinal cord block. The spinal cord block-induced increase in the amplitude of the spinal reflex was, however, less than the increase observed during stimulation of the somatic intercostal nerve T4. Recordings of the afferent volley following cardiac nerve stimulation and analysis of the stimulus-reflex response relationship in neuraxis-blocked cats indicated that the spinal reflex as determined here was activated by A delta afferent fibres. However, if stimulus strength was raised above C-fibre threshold, spinal cord block revealed in addition a late spinal reflex response. In some cases, the appearance of this late potential was accompanied by a secondary decline of the earlier spinal reflex potential, possibly indicating C-fibre-mediated afferent inhibition. Neither baroreceptor activation nor denervation had any effect on spinal reflex amplitudes. Pharmacologically, clonidine given i.v. to cats with a blocked neuraxis reduced the spinal reflex amplitudes to pre-block values, an action which could be antagonised by the subsequent administration of the alpha 2-adrenoceptor antagonist rauwolscine. When given to non-pretreated cats with intact neuraxis, however, neither rauwolscine nor its analog yohimbine were capable of inducing a persistent release from tonic inhibition. The results suggest that both purely visceral and somato-visceral reflexes are subject to tonic descending inhibition, but they do not support the hypothesis that a catecholamine is the responsible transmitter mediating this inhibition.

Adrenergic alpha-Antagonists↗
PubMed2004

Restitution dynamics during pacing and arrhythmias in isolated pig hearts.

INTRODUCTION: The dependence of action potential duration (APD) on the preceding diastolic interval (DI), i.e., restitution, has been purported to predict the development of alternans and reentrant arrhythmias. However, restitution depends on the history of activation (i.e., memory), and its relevance to arrhythmia induction and maintenance is unknown. METHODS AND RESULTS: Using a dual-camera video imaging system, we recorded action potentials from thousands of sites on the surface of the isolated pig heart. A steady-state pacing (SSP) protocol was performed to generate the SSP APD restitution curve. During SSP, the minimum DI and APD were 57 +/- 6 ms and 107 +/- 6 ms, respectively. The restitution slope was >1 for DIs <85 +/- 5 ms; however, alternans were not observed. Abrupt decreases in cycle length (CL) resulted in a rapid (<5 beats) decrease in APD followed by a slower decrease to "steady state." DI, APD pairs for the initial beats following these rate changes were significantly above the SSP restitution curve. DI, APD pairs measured during sustained ventricular fibrillation clustered significantly below the SSP restitution curve, at significantly shorter APDs (57 +/- 4 ms) and DIs (49 +/- 6 ms) than could be achieved during SSP. In addition, abrupt increases in CL following SSP resulted in APDs significantly shorter than those predicted from the SSP restitution curve. CONCLUSION: Our results indicate that the responses of APD and DI to sudden rate changes and during arrhythmias are not predicted by the SSP restitution relationship. Acute dynamics act to damp out the proarrhythmic oscillations predicted from the SSP restitution curve.

Action Potentials↗
PubMed1988

Selective depression of conduction of premature action potentials in canine Purkinje fibres by class Ib antiarrhythmic drugs: comparison with Ia and Ic drugs.

Microelectrodes were used to record action potentials and to estimate their conduction velocity in canine Purkinje fibres 8-15 mm long mounted in a tissue bath. The effects of varying stimulation rates and protocols were studied in the presence of nine different class I antiarrhythmic drugs at each of two concentrations (high and low therapeutic range). In all cases, as stimulation rate increased (range of cycle lengths 1000 ms to 200 ms), conduction velocity in the presence of a drug fell progressively below that in control solution at the same rate. No major differences in rate dependent behaviour at steady state were observed between the subclasses Ia, Ib, and Ic. Differences were apparent, however, in the rate at which conduction velocity fell after a sudden decrease in cycle length. This was studied using two protocols. In the first of these, the conduction velocity was recorded of each action potential of a 20 beat train induced after a long rest period. In the presence of class Ib drugs (lignocaine, tocainide, and mexiletine) there was a rapid decline within 2-3 beats to a new equilibrium level of conduction velocity. Class Ia drugs (quinidine, disopyramide, and procainamide) required 12-16 beats to achieve equilibrium, and class Ic agents (flecainide, encainide, and lorcainide) produced slow falls in conduction velocity that did not reach equilibrium within the 20 beat trains. The second protocol involved interpolation of increasingly premature extrastimuli. Class Ib drugs progressively slowed conduction of premature beats as the diastolic interval was reduced below 300-400 ms.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗