[Changes in hemodynamics upon nociceptive stimulation, electrical stimulation of the septum of the brain and a combination of both].
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Animals↗
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Human jaw-opening muscle responses elicited by multiple-site electrical stimulation.
Electrical stimuli were applied to subjects' upper and/or lower gingivae around the right canines; (i) during maintained relaxation of masticatory muscles; (ii) at an active opening position; (iii) while clenching in an incisal edge-to-edge contact (IEC) position; and (iv) at the wide-open position. Reflex responses of the suprahyoid and jaw-closing muscles were obtained using surface electrodes. The electrical stimulation produced segmented reflex excitation(s) in the suprahyoid muscle and conventional reflex excitation and/or inhibition in the jaw-closing muscles when some background activity was maintained in the muscle(s). The excitatory reflex in the suprahyoid muscle responded to multiple site electrical stimulation which was delivered on both the upper and lower jaw simultaneously rather than to single site stimulation. Also, the responses depended on the intensity of the electrical stimulation. In particular, stronger intensities resulted in longer latencies. The results support the suggestions in our previous studies with mechanical stimuli, i.e. that the human jaw-opening reflex can be obtained only when some background activity is maintained in the jaw openers, perhaps due to low threshold afferent input, and that spatial summation may be effective for the reflex.
Adult↗
Intracellular Ca2+ response of rabbit oocytes to electrical stimulation.
Electrical stimulation is known to cause activation in mammalian oocytes, possibly by eliciting an elevation in intracellular calcium (Ca2+). This study reports intracellular Ca2+ concentrations in mature rabbit oocytes using the Ca2+ indicator fura-2. Calcium levels were determined prior to, during, and after the administration of an electrical pulse (3.6 kV/cm for 60 microseconds). Baseline Ca2+ levels ranged from 30 to 90 nM. The intracellular Ca2+ transient evoked by a pulse, peaked at 11 sec, was highly variable in amplitude (40-300 nM) and returned to prepulse levels within 300 sec. Electrically stimulated oocytes did not exhibit repetitive Ca2+ transients. The size of the cytoplasmic Ca2+ rise was influenced by the duration of the pulse, the field strength and the concentrations of external Ca2+ rise was influenced by the duration of the pulse, the field strength and the concentrations of external Ca2+ (P less than 0.05). Oocytes electrically stimulated in the presence of 100 microM CaCl2, which evoked Ca2+ transients with a mean magnitude of 120 nM, activated at a higher rate (P less than 0.05) than oocytes stimulated in the presence of either higher or lower levels of external Ca2+. Although oocytes electrically shocked at 16-18 hr after administration of human chorionic gonadotropin (hphCG) activated at a lower rate than oocytes stimulated at 22-24 hphCG (P less than 0.05), their intracellular Ca2+ response to the pulse was similar (P less than 0.05). These results indicate that electrical pulse parameters and extracellular Ca2+ concentrations can be used to modulate intracellular Ca2+ levels and optimize oocyte activation rates.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Mechanisms controlling choline transport and acetylcholine synthesis in motor nerve terminals during electrical stimulation.
Electrical stimulation of the chick ciliary nerve leads to a frequency-dependent increase in the Na+-dependent high affinity uptake of [3H]choline (SDHACU) and its conversion to acetylcholine (ACh) in the nerve terminals innervating the iris muscle. The forces that drive this choline (Ch) uptake across the presynaptic membrane were evaluated. Depolarization with increased [K+] out or veratridine decreases Ch accumulation. In addition to the electrical driving force, energy is provided by the Na+ gradient. Inhibition of the Na,K-ATPase decreased the Ch taken up. Thus, changes in the rate of Ch transport are dependent on the electrochemical gradients for both Ch and Na+. Ch uptake and ACh synthesis were increased after a conditioning preincubation with high [K+] out or veratridine. As is the case for electrical stimulation, this acceleration of Ch uptake and ACh synthesis was strongly dependent on the presence of Ca++ in the incubation medium. Na+ influx through a TTX-sensitive channel also contributed to this acceleration. Inasmuch as membrane depolarization reduces the initial velocity of Ch uptake and ACh synthesis, their increases during electrical stimulation therefore cannot be the direct effect of the depolarization phase of the action potential. Instead they are the result of the ionic fluxes accompanying the presynaptic spike. It is concluded that stimulation of Ch uptake and ACh synthesis by nerve activity depends first, on the ACh release elicited by Ca++ influx after depolarization and second, on the activation of the Na,K-ATPase due to Na+ entry. Furthermore, it is suggested that the release of ACh after stimulation drives translocation of cytoplasmic ACh into a protected compartment (probably vesicular). This recompartmentation of intraterminal ACh stimulates ACh synthesis by mass action, allowing further accumulation of Ch.
Acetylcholine↗
Activation of Ca2+/Mg2+ ATPase in heart sarcolemma upon electrical stimulation.
Electrical stimulation of the rat heart sarcolemmal membranes with a square wave current was found to increase Ca2+-ATPase activity. This activation of the enzyme was dependent upon the voltage of the electric current, frequency of stimulation and duration of stimulation of the sarcolemmal membranes. The increase in Ca2+-ATPase was reversible upon terminating the electrical stimulation. The activation of sarcolemmal Ca2+-ATPase due to electrical stimulation was markedly depressed when the reaction was carried out at high pH (7.8 to 8.2), low pH (6.6 to 7.0), high temperatures (45 to 50 degrees C) and low temperatures (17 to 25 degrees C) of the incubation medium. Ca2+-antagonists, verapamil and D-600, unlike other types of inhibitors such as propranolol and ouabain, were found to reduce the activation of sarcolemmal Ca2+-ATPase by electrical stimulation. These results support the view that Ca2+/Mg2+ ATPase may be involved in the gating mechanism for opening Ca2+-channels in the sarcolemmal membrane upon excitation of the cardiac muscle.
Animals↗
Restoration of limb regeneration ability in frog tadpoles by electrical stimulation.
Electrical stimulation of advanced tadpoles of Rana breviceps for 24 hr with 3 microA current after hindlimb amputation through shank and ankle slightly increased the number of perfect regenerates as compared to controls. When amputation was made through thigh in tadpoles of the same stage regeneration failed in all cases of the controls but 24 hr stimulation of these tadpoles after similar operation with 3 and 10 microA currents induced fair degree of regeneration in 9 and 40% cases, respectively.
Animals↗
Electrical responses of the smooth muscle of the guinea-pig cerebral artery to brief electrical stimulation.
Electrical responses to brief electrical stimulation were investigated in the cerebral artery of a guinea-pig using a microelectrode. A single brief stimulus (0.05 ms) induced a spike potential followed by a depolarizing slow-potential, and these events were associated with muscle contraction. An outward current injected into the smooth muscle cell induced spike potential but failed to induce depolarizing slow-potential. These activities persisted in the presence of TTX (10(-6) M), guanethidine (5 X 10(-6) M), or atropin (10(-5) M). TEA (5 mM) enhanced the amplitude of the spike potential, but not that of the depolarizing slow-potential. When the external Na was reduced, the membrane transiently hyperpolarized. During this period, the depolarizing slow-potential could be evoked. In a Cl-deficient solution, the membrane depolarized and the amplitude of the depolarizing slow-potential decreased. From these observations it is believed that the contribution of K, Na, or Cl is minor. In a 20 mM-Ca solution, a brief stimulation induced neither spike potential nor depolarizing slow-potential, but did induce a hyperpolarizing slow-potential. The hyperpolarizing slow-potential was also induced in a Na-deficient solution, but only after completion of Na re-distribution across the membrane. These observations suggest that a substance released by brief stimulation produces a prolonged change in ionic conductances of the smooth muscle membrane, allowing the muscle to contract for a certain period.
Animals↗
Two theories of muscle strength augmentation using percutaneous electrical stimulation.
Electrical stimulation of muscle is a commonly used, well-substantiated strategy that physical therapists use to augment strength in patients with muscle weakness. Two distinctly different theories of strength augmentation using percutaneous muscle stimulation are presented. The first theory proposes that augmentation of muscle strength with electrically elicited muscle contractions occurs in a similar manner to augmentation of muscle strength with voluntary exercise. Electrically elicited muscle contractions of relatively high intensity with low numbers of repetitions strengthen muscle proportionally to the external load on the muscle in a manner that is equivalent to voluntary contraction. The second theory proposes that augmentation of muscle strength using percutaneous stimulation is fundamentally different from augmentation of strength with voluntary exercise. This theory uses the physiological differences between electrically elicited and voluntary contractions, such as the reversal of motor unit recruitment order, as a basis for argument. Both theories are partially substantiated using published literature. Strategies for testing both theories are also presented.
Electric Stimulation Therapy↗
Theoretical determination of the current density distributions in human vertebral bodies during electrical stimulation.
Electrical stimulation with a 60 kHz sinewave input signal, supplied via external plate electrodes on the skin surface, is presently being studied as a treatment for human systemic osteoporosis. In this paper, Maxwell's equations were solved for voltage and current density values at nodal points in a three-dimensional, anatomically-based, finite element grid model of the human trunk constructed from T5 to L5. Based on the dose response results from Luessenhop's castrated Sprague Dawley breeder rat experiment and our theoretical determination, the magnitude of the input current to the electrodes necessary to induce a response in the human vertebral body was determined. Four different electrode systems in current clinical use were evaluated, and the optimal input current determined. In addition, the effect of subcutaneous fat was studied.
Adipose Tissue↗
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↗
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↗
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↗
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↗
[A portable stimulator for electric stimulation of brain structures in freely moving animals].
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Brain↗
[Change in intestinal lymph flow during interoceptive stimulation and electric stimulation of visceral nerves].
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Animals↗
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↗
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↗
[Magneto-electrical stimulation (MES)--compared with percutaneous electrical stimulation (PES)].
The central motor conduction was studied in 30 normal volunteers using a recently developed magneto-electrical stimulation technique (MES). The results were compared with those obtained by percutaneous electrical stimulation technique (PES) described previously. We made a magnetic stimulator similar to that of Barker et al. To stimulate the motor cortex, the magnetic coil was placed over the head. It was placed over the seventh cervical spinous process (C7) for cervical stimulation, and the first lumbar spinous process (L1) for lumbar stimulation. Cortical stimulation was performed when the subjects were at rest, and also at during weak voluntary contraction in some of them. Recordings were made from the deltoid (Del), biceps brachii (Bi), extensor carpi radialis (ECR), thenar, quadriceps femoris (Quad), tibialis anterior (TA) and flexor hallucis brevis (FHB) muscles with a pair of surface electrodes. The cortical and spinal latent periods (Lcor and Lsp, respectively) were measured. The central conduction time (CCT) was obtained by subtracting Lsp from Lcor for each muscle. In all subjects, responses were readily obtained by cortical, cervical and lumbar stimulations without discomfort in all the muscles examined. The cortical responses with amplitudes of more than 1mV could be recorded even in the lower limb muscles. There were no significant differences in Lsp and CCT between MES and PES, in all the upper limb muscles examined. The Lcors of the lower limb muscles obtained by MES were not different from those obtained by PES. However, the Lsps obtained by MES were significantly shorter than those by PES in the Quad and TA muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗