Spectral non-stationarities of slow wave field potentials in the rat brain related to the estrus cycle.
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AChE-positive cells suddenly amass in a superficial layer of the neuroepithelium; this layer finally covers, in a sheat-like manner, the entire surface of the embryonic chicken brain. This feature is functionally not understood; however, it appears shortly after the neurons become postmitotic, and the lateral extensions of this layer can easily be traced using histochemistry on serial brain sections. The layer can therefore be exploited to delineate spatially the waves of onset of biochemical tissue differentiation. We have studied whole brains between stages 11 and 30 and provide the first complete spatial schemes of brain differentiation based on computer-reconstructed, two- and three-dimensional maps. The brain does not differentiate in one smooth coherent wave, but instead five separate primary AChE-activation zones are detected: the first originating at stage 11 ("rhombencephalic wave"), the second at the same time ("midbrain wave"), the third at stage 15 ("tectal wave"). A fourth zone develops later, at stage 18, from the bottom part of the telencephalon to the top. Retinal development also starts at stage 18. In a given area, it appears that AChE-development shortly precedes that of the formation of major fiber tracts. AChE might therefore represent a prerequisite for fiber growth and pathfinding.
The generator sources of each wave of the laryngeal brain stem evoked response (LBR) have yet to be precisely demonstrated, although this has been studied in several animal species. This study was carried out to record the near-field brain stem activity as well as the far-field brain stem activity in the cat under the same experimental setup, and to search for the generator sources of the waves. Under general anesthesia, the LBR tracings were recorded adjacent to and within the brain stem following direct electrical stimulation of the internal branch of the superior laryngeal nerve. Reproducible positive and negative waves were detected by the far- and near-field techniques. Mean latencies, configurations, and reproducibility of each wave were demonstrated. From these results, we speculate on the generator sources of each wave.
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The only mesopontine neurons previously described as involved in the transfer of ponto-geniculo-occipital (PGO) waves from the brain stem to the thalamus were termed PGO-on bursting cells. We have studied, in chronically implanted cats, neuronal activities in brain-stem peribrachial (PB) and laterodorsal tegmental (LDT) cholinergic nuclei in relation to PGO waves recorded from the lateral geniculate (LG) thalamic nucleus during rapid-eye-movement (REM) sleep. We constructed peri-PGO histograms of PB/LDT cells' discharges and analyzed the interspike interval distribution during the period of increased neuronal activity related to PGO waves. Six categories of PGO-related PB/LDT neurons with identified thalamic projections were found: 4 classes of PGO-on cells: PGO-off but REM-on cells: and post-PGO cells. The physiological characteristics of a given cell class were stable even during prolonged recordings. One of these cell classes (1) represents the previously described PGO-on bursting neurons, while the other five (2-6) are newly discovered neuronal types. (1) Some neurons (16% of PGO-related cells) discharged stereotyped low-frequency (120-180 Hz) spike bursts preceding the negative peak of the LG-PGO waves by 20-40 msec. These neurons had low firing rates (0.5-3.5 Hz) during all states. (2) A distinct cell class (22% of PGO-related neurons) fired high-frequency spike bursts (greater than 500 Hz) about 20-40 msec prior to the thalamic PGO wave. These bursts were preceded by a period (150-200 msec) of discharge acceleration on a background of tonically increased activity during REM sleep. (3) PGO-on tonic neurons (20% of PGO-related neurons) discharged trains of repetitive single spikes preceding the thalamic PGO waves by 100-150 msec, but never fired high-frequency spike bursts. (4) Other PGO-on neurons (10% of PGO-related neurons) discharged single spikes preceding thalamic PGO waves by 15-30 msec. On the basis of parallel intracellular recordings in acutely prepared, reserpine-treated animals, we concluded that the PGO-on single spikes arise from conventional excitatory postsynaptic potentials and do not reflect tiny postinhibitory rebounds. (5) A peculiar cellular class, termed PGO-off elements (8% of PGO-related neurons), consisted of neurons with tonic, high discharge rates (greater than 30 Hz) during REM sleep. These neurons stopped firing 100-200 msec before and during the thalamic PGO waves. (6) Finally, other neurons discharged spike bursts or tonic spike trains 100-300 msec after the initially negative peak of the thalamic PGO field potential (post-PGO elements, 23% of PGO-related neurons).(ABSTRACT TRUNCATED AT 400 WORDS)
Using a multiple-site optical recording technique with a voltage-sensitive dye, we found that widely spreading depolarization waves were evoked by dorsal root stimulation in embryonic chick spinal cords. Spatiotemporal maps of the depolarization waves showed that the signals were mainly distributed in the ventral half of the slice, with the highest activity in the ventrolateral area. The propagation velocity of the waves was estimated to be in the order of mm/s. Depolarization waves were evoked in the ventral root-cut preparation, but not in the dorsal root-cut preparation, suggesting that the wave was triggered by synaptic inputs from the primary afferents, and that activation of the motoneurons was not essential for wave generation. In intact spinal cord-brain preparations, the depolarization wave propagated rostrally and caudally for a distance of several spinal segments in normal Ringer's solution. In a Mg(2+)-free solution, the amplitude and extent of the signals were markedly enhanced, and the depolarization wave triggered in the cervical spinal cord propagated to the brainstem and the cerebellum. The depolarization wave demonstrated here had many similarities with the vagus nerve-evoked depolarization wave reported previously. The results suggest that functional cell-to-cell communication systems mediated by the depolarization wave are widely generated in the embryonic central nervous system, and could play a role in large-scale coactivation of the neurons in the spinal cord and brain.
BACKGROUND AND PURPOSE: Cardiac arrhythmias mediated by the sympathetic nervous system have been implicated in sudden, unexplained deaths in patients with epilepsy. Cerebral blood flow velocities (CBFV) as measured by transcranial Doppler are characterized by slow spontaneous oscillations in part attributed to changes in sympathetic activity (M waves, 3 to 9 cycles per minute) and to discharges of monoaminergic neurons in the brain stem (B waves, 0.5 to 2 cycles per minute). This study was designed to compare spontaneous fluctuations of CBFV in patients with epilepsy with those in normal control subjects. METHODS: Simultaneous registrations of scalp electroencephalograms, with electrodes placed according to the 10-20 System, and transcranial Doppler recordings of both middle cerebral arteries were performed in 27 patients (9 with primary generalized epilepsy, 18 with focal epilepsy). Data analysis of CBFV was based on the envelope curves of the Doppler spectrum. A fast Fourier transformation over the 20-minute CBFV curve was performed, and the amplitudes of B and M waves were calculated and compared with those in 20 normal, age-matched control subjects. RESULTS: While the amplitudes of the B waves in both groups were similar, patients with epilepsy showed significantly increased M waves. Patients with focal epilepsy did not present asymmetries between the normal hemisphere and the side of the epileptic focus with respect to both M and B waves. CONCLUSIONS: Enhanced M waves in epileptic patients may reflect increased sympathetic activity even in the absence of seizures. This study provides further evidence for an autonomic dysfunction as a possible mechanism for sudden unexplained death in patients with epilepsy.
Slow-wave oscillations of the mean frequency of multi-unit activity (MUA) were studied in the cerebral subcortical structures of parkinsonic and epileptic patients treated with the aid of implanted electrodes, during sleep, drowsiness and awakening. During slow-wave sleep, the MUA slow-wave oscillations become augmented, the number of oscillatory components increases as well as the amount of oscillations with identical or similar periods in different structures. During paradoxical sleep, the total amount of oscillatory components decreases. The MUA rhythmic activity is quite obvious in awakening from sleep, the short-period components prevailing. The data obtained reveal high incidence of the rhythms with periods of about 20 sec which is considered from the standpoint of the hypothetical adaptogenic rhythm in the CNS developing at the moments of certain efforts and adaptive activity of the organism.
BAEP records were obtained from 30 brain-dead patients. Three BAEP patterns were observed: (1) no identifiable waves (73.34%), (2) an isolated bilateral wave I (16.66%), and (3) an isolated unilateral wave I (10%). When wave I was present, it was always significantly delayed. Significant augmentation of wave I amplitude was present bilaterally in one case and unilaterally in another. On the other hand, in serial records from 3 cases wave I latency tended to increase progressively until this component disappeared. During the same period, wave I amplitude fluctuations were observed. A significant negative correlation was found for wave I latency with heart rate and body temperature in 1 case. Two facts might explain the progressive delay and disappearance of wave I in brain-dead patients: a progressive hypoxic-ischaemic dysfunction of the cochlea and the eighth nerve plus hypothermia, often present in brain-dead patients. Then the incidence of wave I preservation reported by different authors in single BAEP records from brain-dead patients might depend on the moment at which the evoked potential study was done in relation to the onset of the clinical state. It is suggested that, although BAEPs provide an objective electrophysiological assessment of brain-stem function, essential for BD diagnosis, this technique could be of no value for this purpose when used in isolation.
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This study was carried out to clarify the changes of pulse pressure of the intracranial pressure pulse wave in ischaemic brain oedema. Intracranial pressure and PP were measured in two groups of anaesthetized dogs; 1) increased volume of cerebrospinal fluid by cisternal saline injection (control group), 2) brain oedema caused by focal ischaemia (oedema group). Ischaemia was induced by 2 hours of occlusion of the anterior, middle cerebral and internal carotid arteries. The canine focal ischaemic model showed consistent ischaemic damage in the caudate nucleus and produced brain oedema successfully. PP increased linearly with rising ICP to 35 mm Hg, and PP in the oedema group was significantly smaller than that in the control group at the same ICP value. The slopes of the regression equation of ICP and PP were significantly different between the oedema and control group (oedema: 0.057 +/- 0.029, control: 0.106 +/- 0.009), mean +/- SD, P less than 0.005). These results suggest that PP is easily affected by ischaemic brain oedema, which indicates increase of the brain tissue in the cranium. We conclude that PP is affected even at the same ICP value when intracranial components have altered.
Following inoculation of herpes simplex virus type 1 (HSV-1) into the anterior chamber of one eye of a Balb/c mouse, a pattern of ocular retinal disease occurs which is characterized by retinal necrosis, disruption of the retinal architecture of the uninoculated contralateral eye, and sparing of the retina of the virus-inoculated eye. Our direct virus culture studies have revealed that, after uniocular anterior chamber inoculation, virus reaches the uninoculated eye in two temporally separate waves. The first wave of virus is detected in the uninoculated eye as early as one day postinoculation (pi), long before virus is found in either of the optic nerves or the brain. The second wave of virus arrives in this eye between 7 and 10 days pi. Sequentially, the path of the second wave of virus appears to move from the injected eye to (1) the ipsilateral optic nerve, (2) the brain, (3) the contralateral optic nerve, and (4) the posterior segment of the uninoculated contralateral eye, suggesting that interocular spread of the second wave of virus after anterior chamber inoculation occurs via neural pathways. Results of histopathologic examinations and virus culture studies suggest that the early wave of virus contributes to the inflammation observed at the angle structures of the contralateral eye 7-8 days pi and that the second wave of virus accounts for the peak virus titer observed on day 10 pi, a peak which coincides with the destruction of the retina of this eye. It is proposed that the first wave is causally related to the development of retinitis, which occurs as the second wave reaches the retina.
Neurofeedback is being utilized more commonly today in treating individuals who have attention deficit hyperactivity disorder (ADHD). Neurofeedback, which is based on theories that recognize the organic basis of ADHD, utilizes biofeedback to guide individuals to regulate their brain activity. Neurofeedback relies on research that has demonstrated that most individuals who have ADHD, as compared to matched peers, have excess slow wave activity and reduced fast wave activity. It provides immediate feedback to the individual about his or her brain wave activity in the form of a video game, whose action is influenced by the individual's meeting predetermined thresholds of brain activity. Over several sessions of using the video and auditory feedback, individuals reduce their slow wave activity and/or increase their fast wave activity. Individuals who complete a course of training sessions often show reduced primary ADHD symptoms. Research has shown that neurofeedback outcomes compare favorably to those of stimulant medication.