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At least 55 records · Page 3Linked to original sources
PubMed2002

The effect of electrical stimulation of the corticospinal tract on motor units of the human biceps brachii.

In healthy human subjects, descending motor pathways including the corticospinal tract were stimulated electrically at the level of the cervicomedullary junction to determine the effects on the discharge of motoneurones innervating the biceps brachii. Post-stimulus time histograms (PSTHs) were constructed for 15 single motor units following electrical stimulation of the corticospinal tract and for 11 units following electrical stimulation of large diameter afferents at the brachial plexus. Responses were assessed during weak voluntary contraction. Both types of stimulation produced a single peak at short latency in the PSTH (mean 8.5 and 8.7 ms, respectively) and of short duration (< 1.4 ms). In separate studies, we compared the latency of the responses to electrical stimulation of the corticospinal tract in the relaxed muscle with that in the contracting muscle. The latency was the same in the two conditions when the intensity of the stimulation was adjusted so that responses of the same size could be compared. Estimates of the descending conduction velocity and measurements of presumed peripheral conduction time suggest that there is less than 0.5 ms for spinal events (including synaptic delays). We propose that in response to electrical stimulation of the descending tract fibres, biceps motoneurones receive a large excitatory input with minimal dispersion and it presumably contains a dominant monosynaptic component.

Arm↗
PubMed2006

Wide-pulse-width, high-frequency neuromuscular stimulation: implications for functional electrical stimulation.

Electrical stimulation (1-ms pulses, 100 Hz) produces more torque than expected from motor axon activation (extra contractions). This experiment investigates the most effective method of delivering this stimulation for neuromuscular electrical stimulation. Surface stimulation (1-ms pulses; 20 Hz for 2 s, 100 Hz for 2 s, 20 Hz for 3 s) was delivered to triceps surae and wrist flexors (muscle stimulation) and to median and tibial nerves (nerve stimulation) at two intensities. Contractions were evaluated for amplitude, consistency, and stability. Surface electromyograph was collected to assess how H-reflexes and M-waves contribute. In the triceps surae, muscle stimulation produced the largest absolute contractions (23% maximal voluntary contraction), evoked the largest extra contractions as torque increased by 412% after the 100-Hz stimulation, and was more consistent and stable compared with tibial nerve stimulation. Absolute and extra contraction amplitude, consistency, and stability of evoked wrist flexor torques were similar between stimulation types: torques reached 11% maximal voluntary contraction, and extra contractions increased torque by 161%. Extra contractions were 10 times larger in plantar flexors compared with wrist flexors with muscle stimulation but were similar with nerve stimulation. For triceps surae, H reflexes were 3.4 times larger than M waves during nerve stimulation, yet M waves were 15 times larger than H reflexes during muscle stimulation. M waves in the wrist flexors were larger than H reflexes during nerve (8.5 times) and muscle (18.5 times) stimulation. This is an initial step toward utilizing extra contractions for neuromuscular electrical stimulation and the first to demonstrate their presence in the wrist flexors.

Adult↗
PubMed1995

Release of cerebral 5-hydroxytryptamine evoked by electrical stimulation of the dorsal and median raphe nuclei: effect of a neurotoxic amphetamine.

Recent neuroanatomical data suggest that the axons and terminals of serotonergic neurons of the dorsal and median raphe nuclei are morphologically and pharmacologically distinct. Here we attempted to establish a functional in vivo model of serotonergic terminals derived from these nuclei, and then carry out a preliminary comparison of their physiological and pharmacological properties. Brain microdialysis was used to monitor extracellular 5-hydroxytryptamine in the hippocampus (dorsal and median raphe innervation) and frontal cortex (preferential dorsal raphe innervation) of the anaesthetized rat. To distinguish 5-hydroxytryptamine released by terminals of dorsal raphe neurons from that released by median raphe neurons, one or other of these nuclei was stimulated electrically. Electrical stimulation of either the dorsal or median raphe nucleus evoked a release of 5-hydroxytryptamine in the hippocampus. Whereas stimulation of the dorsal raphe nucleus also released 5-hydroxytryptamine in the frontal cortex, stimulation of the median raphe nucleus did not. No release of 5-hydroxytryptamine was evoked when electrodes were located in regions bordering the dorsal raphe nucleus and the median raphe nucleus. The amounts of hippocampal 5-HT released by stimulation of the dorsal or median raphe nucleus were found to be similarly altered by a 5-hydroxytryptamine uptake inhibitor (citalopram) and calcium-free perfusion medium, and also by increasing stimulation frequency (2-10 Hz). Furthermore, the amount of 5-hydroxytryptamine released by electrical stimulation of either the dorsal raphe nucleus or median raphe nucleus was markedly reduced in rats pretreated with p-chloroamphetamine. In summary, our data show that electrical stimulation of the dorsal or median raphe nucleus releases 5-hydroxytryptamine in a regionally specific manner (hippocampus versus frontal cortex), suggesting that serotonergic nerve terminals of the dorsal and median raphe pathways were being activated selectively. Using this model, we found no differences in the responsiveness of dorsal and median raphe pathways to a specific set of physiological and pharmacological manipulations. In particular, our data suggest that the neurotoxic action of p-chloroamphetamine may not be targeted solely on serotonergic axons and terminals of the dorsal raphe nucleus but includes those of the median raphe nucleus.

Animals↗
PubMed1991

Seminal emission by electrical stimulation of the spermatic nerve and epididymis.

The spermatic nerve and epididymis were stimulated electrically in dogs to elucidate the possibility of artificial seminal emission after bilateral transection of the hypogastric nerves and sympathetic trunks. Before transection, electrical stimulation of a distal end of the severed spermatic nerve caused a trace amount of emission in two dogs and no emission in the remaining four. In contrast, 1 month after the transection, stimulation of a distal end of the severed spermatic nerve caused seminal emission in all six dogs examined, with full seminal volume in four dogs and partial volume in the remaining two. Anatomically, sympathetic nerves originating from the upper portion of the lumbar sympathetic ganglia descended along the spermatic arteries to the testes as spermatic nerves. The present results indicate that spermatic nerves have the potential to generate seminal emission as a compensatory pathway after bilateral transection of the hypogastric nerves. Both direct and percutaneous electrical stimulation of epididymal tails resulted in a full volume of seminal emission in all dogs with transection of both hypogastric nerves and lumbosacral sympathetic trunks as well as in unoperated controls, while high voltage (8 V vs 40-80 V) was required to cause seminal emission by electrical stimulation on the skin surface. Direct stimulation of epididymal tails in men undergoing orchidectomy as treatment for prostatic carcinoma or during biopsy of the contralateral testis in a patient with a testicular tumour, resulted in seminal emission in all five epididymides examined either from the end of the severed vas deferens or in the posterior urethra if the vas deferens was not severed.

Animals↗
PubMed1988

Tetrodotoxin-resistant contractions induced by electrical stimulation of bladder muscle from man, rabbit and rat.

Isolated detrusor preparations from man, rabbit and rat were suspended in an organ bath and isometric tension was recorded. The preparations were stimulated electrically in the presence of Bay K8644 and nifedipine before and after neuronal blockade with tetrodotoxin. Transmural electrical stimulation produced frequency-dependent contractions in all preparations. Bay K8644 significantly increased and nifedipine decreased these contractions. TTX effectively suppressed the response to electrical field stimulation in all species. When Bay K8644 was added to TTX blocked preparations, the responses to electrical stimulation were partly restored in bladder strips from man and rat. No increase in response was seen in the rabbit preparations. However, if the extracellular K+-concentration was increased to 10 mM (which per se did not affect the response) Bay K8644 significantly increased the contractions. All responses elicited by electrical stimulation in the presence of TTX were abolished by nifedipine. It is concluded that if the bladder smooth muscle is exposed to factors that can increase its sensitivity to contractile agents, this may result in uncontrolled (unstable) bladder contractions. Such contractions may use the 'normal' transmitter substances, but may be triggered at a lower stimulus intensity than normal. As a non-specific increase in membrane excitability seems to be associated with an influx of calcium through voltage-sensitive calcium channels, calcium antagonists, together with agents specifically blocking relevant transmitter substances, would offer an effective therapy against the unstable bladder.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2001

Optical measurement of cell-to-cell coupling in intact heart using subthreshold electrical stimulation.

Electrical coupling between myocytes plays a critical role in propagation, repolarization, and arrhythmias. On the basis of predictions from cable theory, we hypothesized that the cardiac space constant (lambda) measured from the decay of subthreshold transmembrane potential (ST-Vm) in space would provide an index of regional cell-to-cell coupling in the intact heart. With the use of voltage-sensitive dyes, the distribution of ST-Vm was measured from hundreds of sites in close proximity to the site of subthreshold stimulation. lambda was calculated from the exponential decay of ST-Vm in space. Consistent with known directional differences in axial resistance, the spatial distribution of ST-Vm was strongly dependent on fiber orientation, because lambda was significantly (P < 0.001) longer along (1.5 +/- 0.1 mm) compared with across (0.8 +/- 0.1 mm) fibers. There was a close linear relationship (P < 0.001) between conduction velocity (CV) and lambda along all fiber angles tested. Reducing gap junctional conductance by heptanol reversibly decreased CV and lambda in parallel by approximately 50%. In contrast, sodium channel blockade by flecainide slowed CV by 40% but had no effect on lambda, reaffirming that lambda was an index of passive but not active membrane properties. These data establish the feasibility of measuring lambda as an index of cell-to-cell coupling in the intact heart, and indicate strong dependency of lambda on fiber orientation and pharmacological alterations of gap junction conductance.

Animals↗
PubMed1993

Perception of olfactory and intranasal trigeminal stimuli following cutaneous electrical stimulation.

Based on previous research it may be hypothesized that the perception of odorants is modified by an axon reflex emanating from trigeminal afferents activated via the skin and/or the intranasal respiratory epithelium. The present experiment investigated the effects of trigeminal cutaneous stimulation on intensity estimates of intranasal chemical stimuli. While the left nostril was stimulated chemically with olfactory and trigeminal stimulants, four regions of the face were stimulated electrically. Intensity estimates of the chemical stimuli tended to increase after cutaneous electrical stimulation which may be interpreted in terms of response priming. The effect of electrical stimulation did not differ at the 4 stimulation sites. The results argue against the hypothesis that the processing of intranasal chemical stimuli is modified peripherally by cutaneous trigeminal excitation.

Adolescent↗
PubMed1995

Two types of vasodilatation in cat choroid elicited by electrical stimulation of the short ciliary nerve.

Choroidal blood vessels are innervated by three types of vasoactive nerve fibers: sympathetic, parasympathetic and sensory fibers in the short ciliary nerve. We investigated whether or not stimulation of the short ciliary nerve elicits vasodilatation. In 30 cats (2-4 kg) anesthetized with pentobarbital sodium (30 mg kg-1, i.v.) and artificially ventilated (pancuronium bromide; 0.2 mg kg-1 hr-1, i.v.), choroidal blood flow was continuously measured trans-sclerally with a laser Doppler flowmeter. The lateral short ciliary nerve was stimulated electrically (0-50 V, 2 msec, 20 Hz, for 10 sec) at two sites, one close to the eyeball (site P) and the other between the main and accessory ciliary ganglia (site Q). Choroidal vasodilatation occurred with a high incidence (80%) in response to electrical stimulation of the short ciliary nerve at site P or Q, when cats had been treated with the alpha-adrenergic blocking agent phentolamine (3 mg kg-1) to eliminate sympathetic vasoconstrictor effects. A long-lasting vasodilatation was observed during 1% capsaicin application to the nerve bundle at site P, but not at site Q and capsaicin nearly abolished the vasodilatation evoked by stimulation at site P, but not that evoked from site Q. Vasodilatation elicited by electrical stimulation at site P or Q was not sensitive to the ganglion-blocking agent hexamethonium (3 mg kg-1, i.v.).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1977

Temporal patterns of vasopressin release following electrical stimulation of the amygdala and the neuroendocrine pathway in the monkey.

To evaluate a possible role of the amygdala (Amyg) in the neural control of arginine vasopressin (AVP) release, adult female monkeys (Macaca mulatta) with electrodes chronically implanted in the Amyg, hypothalamus and pituitary gland were given 5% dextrose and water infusions and were stimulated electrically at these sites. Immediately before and after, and at 5, 10, 15 and 30 min intervals following electrical stimulation, blood samples were withdrawn from unanesthetized monkeys, through implanted cardiac cannulae, for radioimmunoassay (RIA) of plasma AVP and for plasma osmolality determination. In the Amyg-stimulated monkeys, plasma AVP rose rapidly to peak values at the end of stimulation followed by an abrupt post-stimulation fall to control levels in 30 min. A small yet significant rise in plasma osmolality was also observed. Electrical stimulation of the hypothalamus and the pituitary gland yielded a temporal pattern of plasma AVP rise and fall identical to that seen following Amyg stimulation. Blood sampling, precisely timed to the onset and end of the stimulus train, was important in capturing the rise and fall in plasma AVP. Stimulus intensity determined the magnitude of plasma AVP elevation at each of these sites, with the highest current densities yielding the highest levels of plasma AVP. It is suggested that the Amyg may be involved in the neural triggering of AVP release from the neurohypophysis.

Amygdala↗
PubMed1975

Phosphatidic acid metabolism, calcium ions and transmitter release from electrically stimulated synaptosomes.

Synaptosomes isolated from guinea pig brain cortex were stimulated electrically in a medium containing [32P]-orthophosphate. The electrical stimulation caused increased labelling of phosphatidic acid in a synaptic vesicle fraction prepared by osmotic shock of the incubated synaptosomes. Electrical stimulation also provokes transmitter release from the synaptosomes. Both increased phosphatidate labelling and transmitter release required calcium ions in the medium. The effects are discussed in relation to earlier work with acetylcholine and the possible involvement of membrane phosphatidic acid in transmitter release by exocytosis.

Animals↗
PubMed1974

The release of labelled acetylcholine and choline from cerebral cortical slices stimulated electrically.

1 In order to establish the origin of the increased efflux of radioactivity caused by electrical stimulation of cerebral cortical slices which had been incubated with [(3)H]-choline, labelled choline and acetylcholine (ACh) collected by superfusion were separated by gold precipitation.2 In the presence of physostigmine electrical stimulation (1 Hz, 10 min) increased the release of only [(3)H]-ACh which was greatly enhanced by the addition of atropine.3 Continuous stimulation in the presence of physostigmine resulted in an evoked release of [(3)H]-ACh which declined asymptotically. This evoked release appeared to follow first-order kinetics with a rate constant which remained stable over the course of prolonged stimulation.4 The rate constant for the evoked release of [(3)H]-ACh with 1 Hz stimulation was three times greater in the presence of physostigmine and atropine than in the presence of physostigmine alone, while the size of the store from which [(3)H]-ACh was released was nearly identical under these two conditions.5 In the absence of physostigmine and atropine, stimulation caused the appearance of only [(3)H]-choline in the samples.6 Reduction of [(3)H]-ACh stores before the application of physostigmine resulted in a reduced evoked release of total radioactivity, both in the absence or presence of physostigmine and atropine, and decreased the evoked release of [(3)H]-ACh without affecting the release of [(3)H]-choline.7 Results suggest that electrical stimulation of cortical slices which had been incubated with [(3)H]-choline causes the release of only [(3)H]-ACh, both in the presence or absence of an anticholinesterase. The evoked increase in the efflux of total radioactivity is therefore a good measure of the release of [(3)H]-ACh.

Acetylcholine↗
PubMed1993

Chronic electrical stimulation of the facial nerve causes signs of facial nucleus hyperactivity.

The proximal segment of the facial nerve in rats was stimulated electrically daily for a duration of 2-10 min. After 4-8 weeks of such stimulation, 12 of 18 rats developed abnormal muscle responses that could be demonstrated by recording the electromyographic response from lower face muscles (the mentalis muscle) while the temporal branch of the facial nerve was being stimulated electrically. This abnormal electromyographic response consists of activity that appears in the latency range 6.5-15 ms. In addition, these chronically stimulated rats developed signs of facial synkinesis on the side that had been chronically stimulated. This could be demonstrated by recording electromyographic activity when the blink reflex was being elicited by electrical stimulation of the ophthalmic nerve. Rats in which electrodes had been implanted but which had not been stimulated did not develop any abnormal electromyographic activity. The abnormal electromyographic activity that could be recorded in rats that had been stimulated chronically could not be recorded 4-8 weeks after the stimulation had been terminated. We interpret these results to indicate that chronic electrical stimulation of the facial nerve can render the facial motonucleus hyperactive, and that the signs of this hyperactivity (abnormal muscle response and synkinesis) are similar to those typically seen in patients with hemifacial spasm. We thus presume that these results support the hypothesis that it is the irritation of the facial nerve from a compressing blood vessel that causes the facial nucleus to become hyperactive in patients with hemifacial spasm.

Animals↗
PubMed1987

Normal trunk muscle strength and endurance in women and the effect of exercises and electrical stimulation. Part 2: Comparative analysis of electrical stimulation and exercises to increase trunk muscle strength and endurance.

Several studies have shown positive correlations between muscle strength, flexibility, and the frequency of low-back pain. Weak trunk musculature and decreased endurance have thereby come to be identified as significant risk factors in the development of occupational back problems. Because it is widely accepted that exercise plays an important role in the conservative treatment and prevention of low-back pain, the goals of most rehabilitative programs involves improving the strength and endurance of the low-back pain patient. Whereas electrical stimulation has been shown to increase the muscle strength of the lower extremities, this effect has not been demonstrated for the trunk muscles. Part 2 is a prospective controlled study designed to document and to compare objectively the effects of electrical stimulation and exercise on trunk muscle strength. A total of 117 healthy women were divided randomly into four groups. Two groups received electrical stimulation with different electrical parameters, one group received exercises, and one group acted as a control group. The results showed that low-frequency electrical stimulation and exercises significantly (P less than .05) increased isokinetic back-muscle strength compared to the control and medium-high-frequency electrical stimulation groups. Both types of electrical stimulation, however, significantly increased (P less than .05) the endurance in the back muscles compared with the control and the exercise groups. This study showed that electrical stimulation may be a valuable treatment in the early care of low-back pain patients in maintaining and increasing strength and endurance of back muscles when a more active exercise program is too painful to perform.

Adolescent↗
PubMed1991

A study of the hypothalamic pulse-generating mechanism responsible for LH release: electrical stimulation of the medial basal hypothalamus in the ovariectomized guinea pig.

In order to examine the neurophysiological properties of the hypothalamus responsible for the pulsatile release of luteinizing hormone (LH) the medial basal hypothalamus (MBH) of the ovariectomized adult female guinea pig was stimulated electrically through an implanted electrode and LH release was monitored as an indication of luteinizing hormone-releasing hormone (LHRH) release. Electrical stimulation (ES) consisting of monophasic square wave pulses with 0.5 ms pulse duration was applied for 2 min at 60, 40, 20, or 10 min intervals. Current intensity (80, 200, 500 microA) and frequency (8, 50, 100 Hz) were varied to determine the parameters of ES which resulted in an LH pulse with amplitude similar to that of a pulse induced by the endogenous pulse-generating mechanism. Blood samples were collected at 5 or 10 min intervals through an indwelling catheter, and LH was measured by RIA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗