[EXTRACRANIAL ELECTRIC STIMULATION. II. EFFECT OF ELECTRIC STIMULATION ON THE NUMBER OF CIRCULATING EOSINOPHILS].
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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)
Action potentials arising from retinal ganglion cells ultimately create visual percepts. In persons blind from retinitis pigmentosa and age-related macular degeneration, viable retinal ganglion cells remain, and the retina can be stimulated electrically to restore partial sight. However, it is unclear what neuronal elements in the retina are activated by epiretinal electrical stimulation. This study investigated the effects of cellular geometry, electrode to neuron distance, stimulus duration, and stimulus polarity on excitation of a retinal ganglion cell with an epiretinal electrode. Computer-based compartmental models representing simplified retinal ganglion cell morphology provided evidence that the threshold for excitation was lower when an electrode was located in proximity to the characteristic 90 degrees bend in the axon of the retinal ganglion cell than when it was located over a passing axon of the nerve fiber layer. This electrode-position-dependent difference in threshold occurred with both cathodic and anodic monophasic stimuli, with point source and disk electrodes, at multiple electrode-to-neuron distances, and was robust to changes in the electrical properties of the model. This finding reveals that the physical geometry of the retinal ganglion cells produces stimulation thresholds that depend strongly on electrode position. The low excitation thresholds near the bend in the axon will result in activation of cells local to the electrode at lower currents than required to excite passing axons. This pattern of activation provides a potential explanation of how epiretinal electrical stimulation results in the production of punctuate, rather than diffuse or streaky phosphenes.
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1. The hypophysiotrophic area of the rat hypothalamus was studied in vitro. The preparation remained viable for at least 3 hr and showed oxygen consumption varying between 68.9-120 mumole/g.hr. The tissue potassium ion content (per unit wet weight) fell to about 50% of the in vivo concentration during this time compared with 15% in the presence of ouabain (10(-4) M). Histological examination of tissue incubated for 3 hr showed variable perineuronal oedema but the nuclei were of normal appearance and none showed the pyknotic changes that would be associated with cell degeneration.2. Corticotrophin releasing hormone (CRH) in the medium pooled from five to twenty hypothalami was assayed in five to twelve rats which were median-eminence lesioned 48 hr earlier. In vitro corticosterone production of quartered adrenals was used as the end point of the assay. Regression lines of the dose-response curves for ACTH, crude CRH and different volumes of medium from electrically stimulated hypothalami were parallel. CRH output was maximal at 75 Hz and 100 muA when the square-wave pulses lasted for 1 msec. No CRH activity was found on stimulation of cerebral cortex or thalamic tissue pieces of equivalent size.3. Hypothalami taken from rats, adrenalectomized 7-14 days previously, released several-fold more CRH into the medium during electrical stimulation than the initial content of the tissue, showing that the tissue was capable of synthesizing CRH in vitro. The hypothalami taken from intact rats released considerably less CRH into the medium than tissue taken from 12 to 14 day adrenalectomized rats. The hyper-secretion of CRH observed in hypothalami taken from adrenalectomized rats was abolished by pre-treatment with 5 mg/100 g s.c. of corticosterone 24 hr before removal of the tissue. It is therefore proposed that the delayed negative feed-back action of corticosterone at the hypothalamic level is by the suppression of CRH synthesis and that the effect of secretion is secondary to the effect on synthesis.4. The presence of Ca(2+) in the medium was essential for the release of CRH.5. CRH secretion increases linearly with doses of acetylcholine from 5.5 x 10(-15)-5.5 x 10(-14) M. Cerebral cortex incubated with acetylcholine showed no CRH activity. The effect of acetylcholine was reduced by atropine (3.5 x 10(-13) M). Median eminence-pituitary stalk fragments (which contain mainly terminal axons of neurones) incubated with acetylcholine showed no CRH stimulation in the doses that activate the release of CRH using the hypophysiotrophic hypothalamus. Acetylcholine may act as a neurotransmitter at the dendritic level in the CRH neurone.
Twenty patients with intractable obsessive-compulsive neurosis were operated under local anesthesia. Each patient had a lesion produced in 1 of the 4 brain targets: anterior internal capsule, rostral cingulum, middle cingulum, and genu of the corpus callosum. Before destructive permanent lesions were produced, the target area was stimulated electrically. Stimulation gave subjective or objective reactions in 30% of the patients: diminished anxiety, 3 patients; increased anxiety, 1 patient, and motor responses, 2 patients. None experienced an obsessive reaction to stimulation. The clinical effect of surgery was usually good.
Electrodes were implanted into HL in cats. Influence of implantation on daily food intake and alimentary preferences was investigated. Then, the particular sites were stimulated electrically and the general behavior of cats and their attitude towards the food was observed. Implantation effected food intake in different manner in particular individuals. All animals changed their preferences in the direction of raw meat. Electrical stimulation of sites producing alimentary behavior (10 from the 35 investigated) caused the same preference. Alimentary behavior occuring during the stimulation of these sites seems not to be related to the increase of hunger drive.
In the present study, the relationship between the pattern of electrical stimulation and glucose uptake was investigated in slow-twitch muscles (soleus) and fast-twitch muscles (epitrochlearis) from Wistar rats. Muscles were stimulated electrically for 30 min in vitro with either single pulses (frequencies varied between 0.8 and 15 Hz) or with 200-ms trains (0.1-2 Hz). Glucose uptake (measured with tracer amount of 2-[(3)H]deoxyglucose) increased with increasing number of impulses whether delivered as single pulses or as short trains. The highest glucose uptake achieved with short tetanic contractions was similar in soleus and epitrochlearis (10.9 +/- 0.7 and 12.0 +/- 0.8 mmol x kg dry wt(-1) x 30 min(-1), respectively). Single pulses, on the other hand, increased contraction-stimulated glucose uptake less in soleus than in epitrochlearis (7.5 +/- 1.1 and 11.7 +/- 0.5 mmol x kg dry wt(-1) x 30 min(-1), respectively; P < 0.02). Glucose uptake correlated with glycogen breakdown in soleus (r = 0.84, P < 0.0001) and (epitrochlearis: r = 0.91, P < 0.0001). Contraction-stimulated glucose uptake also correlated with breakdown of ATP and PCr and with reduction in force. Our data suggest that metabolic stress mediates contraction-stimulated glucose uptake.
The purpose of this study is to investigate the induced eye movements by the cerebellar nuclei stimulation in the rabbits. Forty-five pigmented rabbits were used in this experiments. The cerebellar nuclei, especially medial nucleus, were stimulated electrically and the induced eye movements were observed. The results were as follows. 1. The horizontal nystagmus was produced by the electrical stimulation of the medial, anterior interposed, or posterior interposed nuclei. 2. The horizontal nystagmus towards the ipsilateral to the stimulated side was observed when the caudal portion of the medial nucleus was stimulated. On the other hand, the horizontal nystagmus towards the contralateral to the stimulated side was observed when the rostral portion of the medial nucleus was stimulated. 3. The latency of the field potential in the vestibular nucleus by stimulating the medial cerebellar nucleus, and that in the reverse situation, were 0.7 to 1.1 msec. 4. After the destruction of the lateral vestibular nucleus, no nystagmus was elicited by the stimulation of the medial cerebellar nucleus. From these results, it can be concluded that there is the monosynaptic connection between the medial cerebellar nucleus and the lateral vestibular nucleus. This indicates that the stimulation of the medial cerebellar nucleus produces the excitation of the vestibular nucleus via the cerebello-vestibular fibers and produces the nystagmus in the pigmented rabbits.
This study was performed in order to investigate whether activation of sensory fibres within the sciatic and vagal nerves might influence the release of oxytocin. In anaesthetized rats the sciatic and vagal nerves were stimulated electrically in an afferent direction with a variety of stimuli. Rats were also stroked on their backs or nociception was inflicted by pinching a foot. Plasma oxytocin levels were measured with a highly sensitive radioimmunoassay in samples drawn from the carotid artery. Afferent electrical stimulations of both sciatic and vagal nerves at 5 V, 0.2-2 ms and 3-10 Hz caused immediate significant elevations of oxytocin levels. Thus, basal levels increased by 30-184%. Furthermore, in response to touch and nociceptive stimuli, oxytocin levels rose by 181% and 206%, respectively. These data indicate that oxytocin can be released by stimulation of peripheral nerves originating in the skin and/or muscle and in the gastrointestinal tract and thus these organs may be involved in the control of oxytocin secretion.
Sarcoplasmic reticulum fragments (S.R.F.) were isolated from skeletal and heart muscles. These fragments were found to take up Ca(++) very actively from media. When monophasic square waves were passed through the S.R.F. suspension, the Ca(++) uptake by S.R.F. was decreased. When the suspension was stimulated electrically after the Ca(++) was taken up by S.R.F., the initiation and the cessation of the stimulation were followed by the release and re-uptake of Ca(++) by S.R.F., respectively. The degree of inhibition of the Ca(++) uptake as well as of the Ca(++) release by electrical stimulation was dependent on the voltage and the frequency of stimulation. The presence of inorganic phosphate or oxalate modified the influence of electrical stimulation on the release and the uptake of Ca(++) by S.R.F. Attempts were made to observe the release of Ca(++) by electrical stimulation from unfractionated sarcoplasmic reticulum remaining in myofibers, and the interaction of the released Ca(++) with myofibrils in vitro. For this purpose, the glycerol-extracted fiber was selected as a muscle model, since it contains both sarcoplasmic reticulum and myofibrils. It was found that electrical stimulation of skeletal and heart glycerol-extracted fibers resulted in the contraction of fibers. It appeared that the contraction of glycerol fibers by electrical stimulation was caused by the Ca(++) release from sarcoplasmic reticulum by stimulation.
1. These studies were initiated to understand the neural sites and mechanisms controlling head movements during gaze shifts. Gaze shifts are made by saccadic eye movements with and without head movements. Sites were stimulated electrically within the brain stem of awake, trained monkeys relatively free to make head movements to study the head-movement components of gaze shifts. 2. Electrical stimulation in and around the gigantocellular reticular nucleus evoked head movements in the ipsilateral direction. Gaze shifts were never evoked from these sites, presumably because the vestibulo-ocular reflex compensated. The rough topography of this region included large head movements laterally, small movements medially, downward movements from dorsal sites, and upward movements more ventrally. 3. The initial position of the head influenced the magnitude of the elicited movement with larger movements produced when the head was directed to the contralateral side. Attentive fixation was associated with larger and faster head movements when compared with those evoked during spontaneous behavior. 4. The superior colliculus makes a significant contribution to gaze shifts and has been shown to contribute to head movements. Because the colliculus is a major source of afferents to the gigantocellular reticular nucleus, comparable stimulation studies of the superior colliculus were conducted. When the colliculus was excited, shifts of gaze in the contralateral direction were predominant. These were most often accomplished by saccadic eye movements, however, we frequently elicited head movements that had an average latency 10 ms longer than those elicited from the reticular head movement region. Sites evoking head movements tended to be deeper and more caudal than loci eliciting eye movements. Neither the onset latencies, amplitudes, nor peak velocities of head movements and eye movements were correlated. Gaze shifts evoked from the caudal colliculus with the head free were larger than those elicited from the same site with the head fixed. 5. These studies demonstrate that both the superior colliculus and gigantocellular reticular nucleus mediate head movements. The colliculus plays a role in orienting to external events, and so collicular head movements predominantly were associated with gaze shifts, with the eye and head movements uncoupled. The medullary reticular system may play a role in the integration of a wider range of movements. Head movements from the medullary reticular sites probably participate in several forms of head movements, such as those that are related to postural reflexes, started volitionally, and/or oriented to external events.
1. The effect of E. coli lipopolysaccharide (LPS) on sympathetic neuro-effector transmission was studied in the rabbit mesenteric artery. The experiments were performed on artery rings isolated 5 or 20 h after intravenous treatment with LPS or saline as well as on artery rings isolated from non-treated rabbits (for assessment of the effect of in vitro preincubation with LPS). In most experiments, neural elements in the arteries were stimulated electrically (10 V, 2 ms, 1-32 Hz). 2. Preincubation with LPS (10 micrograms ml-1) for 5 or 20 h had no effect on the contraction responses of endothelium-intact artery rings to electrical stimulation. In contrast, in vivo intravenous pretreatment with LPS (10 micrograms) led to an inhibition of the contraction; LPS elicited this effect when injected 20 h, but not 5 h, before the experiment. The effect of LPS was eliminated in artery rings isolated from animals receiving an inhibitor of protein synthesis (actinomycin D or cycloheximide) before treatment with LPS. LPS (injected 20 h before the experiment) had no effect on the concentration-response curves for exogenous noradrenaline and tyramine in endothelium-intact artery rings. 3. The inhibition of electrically induced contractions produced by LPS treatment in endothelium-intact artery rings was attenuated by atropine and yohimbine, but not by phentolamine. Yohimbine plus atropine restored the depressed contraction to the normal level. Clonidine and acetylcholine mimicked the effect of LPS in endothelium-intact artery rings isolated from saline-treated animals. 4. When steady-state contractions were induced by 5 min of stimulation at 16 Hz, acetylcholine or clonidine reduced the contraction in endothelium-denuded artery rings from both saline-treated rabbits and animals receiving LPS 20 h before the experiment. The reduction produced by acetylcholine or clonidine of the contraction in artery rings from LPS-treated rabbits was significantly greater than in artery rings from saline-treated animals.5. These results suggest that treatment of rabbits with LPS inhibits noradrenaline release from sympathetic nerve endings via increased sensitivity of both prejunctional inhibitory muscarinic receptors and x2-adrenoceptors in mesenteric arteries. They also suggest that the effect of LPS is independent of endothelial cells but linked to protein synthesis.
Nonresorbable, nonporous, particulate hydroxyapatite (HA) was implanted on the mandible in rabbits and stimulated electrically, 4 hours per day, during the first postoperative week. Stimulated and control implant sites were recovered 8 weeks postoperatively and examined histologically. The HA migrated into the mandible in the electrically treated specimens, and was routinely found in intimate association with preexisting mandibular bone. In the controls, the HA remained superior to the mandibular surface. In further studies (without electrical stimulation) in which the implant site was recovered 26 weeks postoperatively, HA was observed in the mandible; some HA particles migrated completely through the mandible and were found in the adjacent soft tissue. It was concluded that, under the conditions studied, electrical stimulation does not promote bone growth into HA, but rather produces the opposite result--it promotes more rapid movement of HA particles into the mandibular bone. The HA particle migration into the mandible observed (longer postoperative times) in the absence of electrical stimulation suggests that migration is a general property of HA particles when placed over bone under muscle.
The reproducibility of focussed ultrasound-induced intra-articular pain was compared with that of electrically induced cutaneous pain over a period of time by measuring both the evoked potential (EP) amplitude and visual analogue scale (VAS) score. The responses to ultrasound were more variable than those to electrical stimulation. A greater degree of accommodation occurred during electrical stimulation compared with ultrasound stimulation. A statistically significant correlation between the EP amplitude and the VAS score was found for each form of stimulation. Changes in EP amplitude correlated with changes in the perception of pain as measured by the VAS score, rather than stimulus intensity, which remained constant for each subject throughout the duration of the experiment. A single oral dose of pethidine produced a statistically significant decrease in the EP amplitude and the VAS score in each case.
In the alert monkey we have compared the properties of saccades elicited by a visual stimulus (V-saccades) with those generated by electrical stimulation in the superior colliculus (E-saccades). We found that whereas there exists a graded relation between E-saccade amplitude and current strength, E-saccade direction is remarkably independent of electrical stimulation parameters. At sufficiently high current strengths (about 20 microA), E-saccades are consistently directed toward the center of the movement field of nearby cells, except when stimulation is performed at sites near the collicular borders. Further interesting differences between the amplitude and direction behaviour were observed when the variability in E-saccade vectors, obtained with fixed stimulation parameters, was analyzed. In all cases, E-saccade amplitude scatter exceeds direction scatter, suggesting the possibility of a polar coordinate organization for the coding of saccade metrics. These data are compared with V-saccade scatter data, recently obtained in the human (Van Opstal and Van Gisbergen 1989c). Finally, an analysis of saccade dynamics shows that E-saccades can reach V-saccadic velocities at higher current strengths. However, at near-threshold current strengths, where E-saccade amplitude decreases, we found at most stimulation sites (22/37) that E-saccades are consistently slower than V-saccades of the same amplitude. Possible mechanisms underlying the collicular role in saccade generation are discussed.
Evoked motor potentials can be elicited by magnetic cortical or electric spinal stimulations. The central conduction time (CCT) corresponds to the difference in latencies between the total conduction time (from cortex to muscle) and the peripheral conduction time (from spinal cord to muscle). CCT is the sum of the conduction time in the cortico-spinal fibers, of the spinal synaptic delay, and of the conduction time in the proximal part of the motor roots. CCT values (mean + standard deviation) were determined in 20 healthy subjects ranging from 21 to 56 years of age (mean 31.2). Results of magnetic cortical stimulation were compared to the results of electrical stimulation of the cortex. CCTs after magnetic cortical stimulation were longer than CCTs after electric cortical stimulation. This could be explained by the fact that electrical stimulation elicits a direct response in the cortico-spinal tract whereas magnetic cortical stimulation has indirect effects on the pyramidal cells of the motor cortex through excitatory interneurons. Compared with electrical stimulation, the magnetic stimulation has the great advantage of being painless and allows a safe evaluation of the central motor pathways in man.
The aim was to measure the effect of gastric electrical stimulation on the frequency of canine antral pacesetter potentials (PPs), the strength of antral contractions, and the rate of gastric emptying while fasting, after feeding and with pentagastrin stimulation. Four conscious dogs with a stimulating electrode placed 10 cm proximal to the pylorus and recording electrodes and strain gauges placed 7, 5 and 3 cm proximal to the pylorus underwent myoelectric and strain gauge recordings while fasting, after feeding (250 ml 5% dextrose labelled with polyethylene glycol), and during pentagastrin infusion (0.5 micrograms kg-1 min-1) on four separate days. On each day, electrical stimulation was done using one of four stimulation frequencies (0, 6, 30 and 1200 stimuli per minute [s.p.m.]). Stimulation at 6 and 30 s.p.m. increased the fasting and fed PP frequency, whereas 1200 s.p.m. stimulation did not. Feeding decreased the maximum driven frequency, and pentagastrin increased it. Neither the motility index nor the gastric emptying rate were consistently changed by stimulation at any frequency. In conclusion, canine proximal antral stimulation at 6 and 30 s.p.m. sped PP frequency during fasting and after feeding, but stimulation over a wide range of frequencies had little effect on gastric contractions and emptying.