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Results for “Brain waves”

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At least 811 records · Page 45Linked to original sources

PubMed1990

Paradoxical sleep-promoting effects of brain extract from paradoxical sleep-deprived rats.

Brain extract was obtained from whole brains of donor rats following four days of paradoxical sleep deprivation (PSD). Intraperitoneal injection of this brain extract in normal (i.e., not pretreated) recipient rats led to a significant increase of paradoxical sleep (PS) which was beginning at the third hour postinjection and still present on the day after treatment. Both PS episode number and PS episode duration were increased by the PSD extract, whereas slow-wave sleep was not influenced. Brain extract of nondeprived control rats, on the other hand, had no significant effects. In the present experiments, an extract volume obtained from two donor brains was transferred to one recipient. Compared to our earlier investigations (one donor brain/one recipient) this higher "dose" of PSD extract exerted a more pronounced and prolonged effect. These results support the idea that some PS-inducing factor(s) accumulating in the brain during PS deprivation may be involved in the regulation of paradoxical sleep.

Animals↗

PubMed2000

Intercellular Ca(2+) waves in rat hippocampal slice and dissociated glial-neuron cultures mediated by nitric oxide.

Nitric oxide (NO) may participate in cell-cell communication in the brain by generating intercellular Ca(2+) waves. In hippocampal organotypic and dissociated glial-neuron (>80% glia) cultures local applications of aqueous NO induced slowly propagating intercellular Ca(2+) waves. In glial cultures, Ca(2+) waves and Mn(2+) quench of cytosolic fura-2 fluorescence mediated by NO were inhibited by nicardipine, indicating that NO induces Ca(2+) influx in glia which is dihydropyridine-sensitive. As NO treatments also depolarised the plasma membrane potential of glia, the nicardipine-sensitive Ca(2+) influx might be due to the activation of dihydropyridine-sensitive L-type Ca(2+) channels. Both nicardipine-sensitive intercellular Ca(2+) waves and propagating cell depolarisation induced by mechanical stress of individual glia were inhibited by pretreating cultures with either an NO scavenger or N(G)-methyl-L-arginine. Results demonstrate that NO can induce Ca(2+) waves in hippocampal slice cultures, and that Ca(2+) influx coupled to NO-mediated membrane depolarisation might assist in fashioning their spatio-temporal dynamics.

Animals↗

PubMed1992

The I' potential of the brain-stem auditory-evoked potential.

We have consistently recorded a positive wave which precedes wave I, and is called I', within the human brain-stem auditory-evoked potential. It is postulated that I' represents initial neural activity of the auditory nerve, which presumably has as its origin auditory nerve dendrites. Thus, I' may represent a summed far-field dendritic potential from currents of excitatory postsynaptic potentials. We report latency and amplitude values of I'.

Acoustic Stimulation↗

PubMed1995

Genetic threshold hypothesis of neocortical spike-and-wave discharges in the rat: an animal model of petit mal epilepsy.

Neocortical high-voltage spike-and-wave discharges (HVS) in the rat are an animal model of petit mal epilepsy. Genetic analysis of total duration of HVS (s/12 hr) in reciprocal F1 and F2 hybrids of F344 and BN rats indicated that the phenotypic variability of HVS cannot be explained by a simple, monogenic Mendelian model. Biometrical analysis suggested the presence of additive, dominance, and sex-linked-epistatic effects, buffering maternal influence, and heterosis. High correlation was observed between average duration (s/episode) and frequency of occurrence of spike-and-wave episodes (n/12 hr) in parental and segregating generations, indicating that common genes affect both duration and frequency of the spike-and-wave pattern. We propose that both genetic and developmental-environmental factors control an underlying quantitative variable, which, above a certain threshold level, precipitates HVS discharges. These findings, together with the recent availability of rat DNA markers for total genome mapping, pave the way to the identification of genes that control the susceptibility of the brain to spike-and-wave discharges.

Action Potentials↗

PubMed1998

Focal brain injury and its effects on cerebral mantle, neurons, and fiber tracks.

Following a mild cortical impact injury delivered by a piston to the right sensorimotor cortex of the anesthetized rat, we evaluated mantle loss, neuronal changes, and fiber track degeneration by deOlmos silver stains up to 8 weeks after injury. Darkened neurons indicating damage (chromatolysis) occurred widely throughout both hemispheres and were seen from 1 h to 8 weeks after injury. This effect might have occurred from pressure wave damage from piston impact, brain displacement or deafferentation. Cerebral mantle loss was variable but fiber track degeneration related to projection and corticofugal descending tracks associated with the right sensorimotor system was rather constant. Unexpectedly, considerable fiber track degeneration occurred within the cerebellum, especially the inferior vermis. Cells directly under the piston face were surprisingly well-preserved but axon degeneration studies showed that these apparently intact neuronal cell bodies were surrounded by a dense network of degenerating fiber tracks. The intact cells, therefore, may have been functionally cut off from the rest of the brain owing to interruption of their efferents and afferents. The increased susceptibility of axons compared to cell bodies seen with this focal injury is similar to that observed with diffuse brain injury. The early appearing, severe and widespread axon damage we observed suggests that amelioration of focal traumatic brain injury will have to be directed promptly to the preservation of axons as well as cell bodies.

Animals↗

PubMed1991

Subcortical and cortical components of the MLR generating system.

The contributions of the auditory thalamo-cortical pathway, mesencephalic reticular formation, and inferior colliculus to the surface recorded auditory middle latency response (MLR) were assessed by selective inactivation of these areas with lidocaine. Evoked responses were recorded simultaneously from these areas and from the cortical surface. Lidocaine-induced changes were compared across recording sites. In the guinea pig, surface components measured from over the temporal lobe (waves A, B and C) and the midline (waves M- and M+) have been previously shown to reflect the activity of two distinct generating mechanisms. Effects of lidocaine injections corresponded to selective changes in components from these two systems. Injections in the medial geniculate body (MGB) were associated with total disruption of surface potentials measured over the temporal lobe, auditory cortex (AC) responses, and local activity in MGB. Thus the thalamo-cortical pathway appears to be important for the generation of MLRs recorded from the surface of the temporal lobe. These injections generally did not alter the surface midline responses or activity obtained from either the mesencephalic reticular formation (mRF) or the inferior colliculus (IC). Lidocaine injections within AC did not alter the basic response morphology of surface potentials, nor were significant changes measured within AC. Lidocaine injections into the mRF produced changes in all surface temporal potentials, the M+ midline surface potential, and in local potentials recorded from MGB and mRF. Injections into the IC changed surface and subcortical responses at all sites. This was the only injection to affect activity at the latency of surface midline wave, M-1. This wave may be the animal analogue for human wave Na. Control experiments indicated that the effects observed were specific to the neural inactivation of target areas. The MLR generating system appears to consist of contributions and interactions from multiple areas including the auditory thalamo-cortical pathway, mRF and IC. The animal model and experimental strategy described appear promising for linking the contributions from specific brain areas to surface MLR waves.

Animals↗

PubMed1998

Oxidized glutathione promotes sleep in rabbits.

Glutatione is implicated in sleep regulation. There are circadian changes in brain glutathione levels, and nocturnal intracerebroventricular (i.c.v.) slow infusion of oxidized glutathione (GSSG) or reduced glutathione (GSH) promotes rapid-eye-movement sleep (REMS) and non-REMS (NREMS) in rats. In the present experiments, we tested the effects of GSSG on duration of sleep, NREMS intensity, and brain temperature in another species, rabbits. Male New Zealand rabbits were injected with isotonic NaCl on a baseline day and one dose of GSSG on the test day [0.15, 1.5, 15, and 150 microg/rabbit, i.c.v., or 1.5 or 15 mg/kg intravenously (i.v.)]. Electroencephalogram (EEG), motor activity, and brain temperature were recorded for 6 h. Injection of 15 microg GSSG i.c.v. significantly increased the time spent in NREMS in the first 3 h after the injection. Injection of 0.15, 1.5, and 150 microg i.s.v. GSSG, as well as systemic injections of GSSG did not affect NREMS. Intensity of NREMS as measured by EEG slow-wave activity during NREMS, and brain temperature were not affected by any of the treatments. These results are consistent with the hypothesis that glutathione may be a sleep-inducing factor in the brain.

Animals↗

PubMedDate not supplied

ECoG spectral analysis of apamin effects on the rat brain with pretrigeminal or high spinal transection of the central nervous system.

Rats were injected into one lateral ventricle (icv) with apamin (50 and 100 ng per animal). The resulting desynchronization pattern in the electro-corticogram (ECoG) and the symptoms of apaminism (uncoordinated hypermotility and jerks) were monitored. The results of presented experiments contributed additional data concerning the topography of apamin effects. When injected into the ventricle of intact rats, generalized apaminism and massive desynchronization (reduction of total power and increase in beta waves band) of the cortical ECoG emerged. Transection of the spinal cord at the C1-C2 level (encéphalé isolé preparation) displayed apaminism of the head together with significant decrease in the total and relative power connected with a significant decrease in both beta and theta waves. Pretrigeminal transsection of the brain stem abolished the desynchronization in ECoG, whereas the generalized apaminism persisted, however it occurred after a longer latency than in intact animals. Morphine (10 mg/kg, sc) reversed the ECoG effects of apamin in intact rats but remained without effect on the motility changes. Our data indicate that apamin acts primarily on the brain stem and spinal cord, i.e. the structures possessing a sensory input, and by that way indirectly on the higher integrating systems.

Anesthesia↗

PubMedDate not supplied

Rotating spiral waves in fertilized ascidian eggs.

Excitable systems modelled by reaction-diffusion equation may be expected to produce quite complex spatial patterns. Winfree [1974] demonstrated experimentally, in the Belousov-Zhabotinskii reaction, the existence of particular waves called rotating spiral waves. Later Keener and Tyson [1986] presented a thorough analysis of these waves in excitable systems. Spiral waves can also be observed in brain tissue (Shibata and Bures [1974]), while it seems that the precursor to cardiac fibrillation is the appearance of rotating waves of electrical impulses (Winfree [1983]). In this work we suppose the appearance of Ca++ spiral waves in the vegetal pole of ascidian egg cells after the first ooplasmic segregation. Previously we observed that (Ballarò and Reas [2000a]), when the myoplasm is completely localized in the vegetal region (excitable stage) and the ascidian egg cell is perturbed by an increase of Ca++ concentration in the culture medium, the cell reacts by showing persistent mechanical waves of contraction which exist as long as the cell is perturbed. Experimentally we observed the production of a polar lobe located in the vegetal region and the change of the inclination of mitotic furrow, after the appearance of a myoplasmic spiral wave in the vegetal pole. So we suppose that the myoplasmic spiral wave is due to a Ca++ spiral wave, and the myoplasmic spiral wave then causes the changes in the shape of the cell (polar lobe, inclination of mitotic furrow, etc.). Moreover we give a simple geometrical description of a spiral wave.

Animals↗

PubMed1990

Alterations in synaptosomal neurotransmitter amino acids in "petit-mal" rats at a daytime and a nighttime.

The synaptosomal fractions of 6 brain areas-olfactory tubercles (OT), frontal cortex (FC), striatum (Sr), amygdala (A), thalamus (Th), hypothalamus (Hy) - have been analyzed for their neurotransmitter amino acids (AA) content in Wistar rats exhibiting "petit-mal" epilepsy (PM-E) and in controls (C). The analysis was carried out at 11 p.m. (nighttime corresponding to the acrophase for the hourly number of spike-wave complexes) and at 11 a.m. (daytime). A day versus night rhythmicity is recorded for synaptosomal inhibitory AA in control and in PM-E rats. However, day versus night variations are more frequent and more prominent in C rats than in PM-E rats. Two day versus night variations exist only in PM-E rats: increases of GABA level in Sr and of Asp in Hy. Differences between PME-and C in synaptosomal AA content are more likely to be present during the nighttime. During this period lower AA values for PM-E rats are found for one or several inhibitory AA in OT, Th, and FC. It seems that the differences between PM-E and C concerning the inhibitory AA correlate with the number of spike-wave discharges. Only in one brain area is there a similar difference for PM-E and C during daytime and nighttime: a decreased GABA content for PM-E rats in OT. The decrease is larger in nighttime than in daytime. This difference may serve as a marker for this epileptic disorder. Moreover, it is in OT that the greatest number of PM-E versus C differences in synaptosomal neurotransmitter AA are observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

PubMed1998

New laser techniques for diagnosis and treatment of deep-seated brain lesions.

The five years survival rate of deep-seated malignant brain tumors after surgery/radiotherapy is virtually 100% mortality. Special problems include: (1) lesions often present late; (2) position: lesions overlies vital structures, so complete surgical/radiotherapy lesion destruction can damage vital brain-stem functions; and (3) difficulty in differentiating normal brain from malignant lesions. This study aimed to use the unique properties of the laser: (a) to minimize damage during surgical removal of deep-seated brain lesions by operating via fine optic fibers; and (b) to employ the propensity of certain lasers for absorption of (nontoxic) dyes and absorption and induction of fluorescence in some brain substances, to differentiate borders of malignant and normal brain, for more complete tumor removal. A fine laser endoscopic technique was devised for removal of brain lesions, which minimized thermal damage and shock waves. A compatible endoscopic fluoroscopic laser technique was developed to differentiate brain tumor from normal brain.

Brain↗

PubMed1984

Spreading depression and the blood-brain barrier.

The propagation of spreading cortical depression was studied in rabbits during the reversible opening of the blood-brain barrier induced by hypertonic aqueous solutions of sodium chloride and sodium diatrizoate. The rupture of the blood-brain barrier was monitored by the leakage of Evans blue-albumin from pial vessels. Spreading depression was monitored by recording its characteristic slow voltage variations. Test substances were injected into the carotid artery or topically applied to the pia-arachnoid surface. Intracarotid injection of hypertonic solutions that open the blood-brain barrier do not block the propagation of spreading depression. Topical application of NaCl solutions can block the spread of the cortical depression reaction without opening the blood-brain barrier. Recurrent spreading depression waves at a mean frequency of one every 5 min, for 4 h do not cause the release of Evans blue-albumin complex from pial vessels.

Administration, Topical↗

PubMed1991

Synchronous hippocampal bursting reveals network excitability defects in an epilepsy gene mutation.

A mutation at the tottering locus (tg, recessive, on chromosome 8) stimulates noradrenergic locus coeruleus axon terminal outgrowth and predisposes the brain to generalized spike-wave epilepsy in the young mouse. In an isolated synaptic circuit studied in vitro, the hyperinnervated mutant hippocampal pyramidal neurons respond normally when individually activated; however, latent neuronal signaling defects emerge during synchronous network bursting, revealing two conditional excitability phenotypes: a voltage-dependent prolongation of a complex synaptic response, the paroxysmal depolarizing shift, and a beta-adrenoreceptor-linked attenuation of the afterhyperpolarization. In this target brain region, the tg locus transforms neuronal excitability without altering measured intrinsic membrane properties, indicating that gene control of inherited epileptic traits may be mediated in part by activity-dependent modulation of network behavior favoring synchronous neuronal firing.

Animals↗

PubMed1991

[Experience with using extremely high frequency radiotherapy of the millimeter wave range in cerebrovascular disorders].

Vascular diseases of the brain (functional transient and ischemic apoplexy, circulatory encephalopathy) in 79 patients were treated by UHF electromagnetic field of millimetric wave range. 14 patients entered the control group. The treatment results are indicative of clear-cut trend to a decrease of arterial pressure, normalization of blood glucose level, arrest of DIC syndrome development.

Aged↗

PubMed1988

Spreading depression is not associated with neuronal injury in the normal brain.

This study was performed in order to evaluate whether waves of spreading depression (SD) induces irreversible neuronal injury. SD was elicited by topical application of 3 M KCl to the exposed cortex for 4-5 h and the resulting change of the cortical electrical potential showing the occurrence of SD, was recorded by glass microelectrodes. Histological examination of cerebral cortex revealed no signs of neuronal injury outside the area of KCl application as examine after 4 days recovery. The results indicate that recurrent waves of SD do not induce irreversible neuronal injury in the otherwise normal rat brain.

Animals↗

PubMed1990

A possible Japanese male case of Pelizaeus-Merzbacher disease.

A boy with an abnormal auditory brain stem response showing only a wave I-II pattern, congenital nystagmus, psycho-motor retardation, pyramidal tract signs and muscular hypotonia was reported. The auditory brain stem response, short latency somatosensory-evoked potential, somatosensory-evoked potential and visual-evoked potential indicated an intramedullary disorder of conduction. Magnetic resonance imaging revealed marked high signal intensity of the cerebral white matter in T2-weighted images, suggesting hypomyelination. A muscle biopsy specimen showed neurogenic changes with mild myogenic changes.

Brain↗

PubMed1992

Central conduction time in childhood autism.

To investigate the integrity of the brain-stem in 20 mentally handicapped children who met the Rutter criteria for autism, brain-stem auditory evoked potentials were obtained for a range of stimulus intensities. Central conduction times (CCTs) were calculated for the Wave I-Wave V interval of the brain-stem potentials. In children under 14 years of age CCTs were normal. In children 14 years of age and over, three of four girls and eight of nine boys had CCTs exceeding normal limits when compared with a group of controls of normal intelligence, matched for age and sex. CCTs recorded from a group of non-autistic mentally handicapped children were within normal limits. The age distribution are consistent with a maturational defect in myelination within the brain-stem in autism, a defect which may have a much wider anatomical distribution throughout cortical and subcortical structures.

Adolescent↗

PubMed1987

Physiology of the CSF flow-void sign: modification by cardiac gating.

Low-intensity signal seen within areas of narrowing within the ventricular system has been termed the CSF flow-void sign. This decreased signal is related to CSF flow and turbulence. Seven normal volunteers were examined, and the changes that occurred in the appearance of the CFVS were noted when data acquisition was modified by cardiac gating. Flow-void patterns within the internal cerebral veins and basilar artery were also examined. The results of this study confirm that CSF flow is related to cardiac systole and diastole. An increase in hypointensity is seen in the areas of the aqueduct of Sylvius and the foramen of Magendie during the time at which the systemic arterial pulse wave is transmitted into the brain. The physiology of this observation is related either to a direct hydraulic effect of the venous system on the CSF or to filling and expansion of the thin-walled cerebral venous system. Hypointensity or an increase in the width of the basilar artery and internal cerebral veins during systolic data acquisition was also noted. The mechanism of this phenomenon is related to propagation of the systemic arterial pulse wave.

Cerebral Ventricles↗