Low-amplitude Spikes Research Articles

Mitochondrial Dysregulation and Impaired Autophagy in iPSC-Derived Dopaminergic Neurons of Multiple System Atrophy.

SummaryMultiple system atrophy (MSA) is a progressive neurodegenerative disease that affects several areas of the CNS, whose pathogenesis is still widely unclear and for which an effective treatment is lacking. We have generated induced pluripotent stem cell-derived dopaminergic neurons from four MSA patients and four healthy controls and from two monozygotic twins discordant for the disease. In this model, we have demonstrated an aberrant autophagic flow and a mitochondrial dysregulation involving respiratory chain activity, mitochondrial content, and CoQ10 biosynthesis. These defective mechanisms may contribute to the onset of the disease, representing potential therapeutic targets.

Report of progressive myoclonus ataxia (PMA) in two Chinese pedigrees

Objective: To describe the clinical characteristics of patients diagnosed with progressive myoclonus ataxia (PMA) from two Chinese pedigrees.Methods: An analysis of clinical data is presented and inferences drawn. Results: The propositus from pedigree-I (9-year-old female) could not walk stably and had a history of frequent falls. The symptoms aggravated over time until she lost the ability to take care of herself. Her physical and mental development (including cognitive ability) was normal. She had an ataxic gait, ataxic dysarthria, bilateral horizontal nystagmus and visible limb myoclonus. She failed the bilateral finger-to-nose and heel-knee-tibia tests and could not walk in a straight line. Babinski signs were not observed. EEG tracing during sleep showed low-amplitude spikes and spike-and-slow waves in the bilateral frontal and mid-frontal areas. Her magnetic resonance imaging scan was normal. In pedigree-II, the propositus (a 54-year-old male) could not walk stably and had a history of occasional falls for the past 34 years. The symptoms aggravated gradually until he lost the ability to perform routine daily activities. There was no history of convulsions. His physical and mental faculties, as well as the neurological findings were similar to those of the pedigree-I. Both proposituses did not respond well to symptomatic treatment. A novel mutation has been identified in SGCE gene (NM_003919:exon3:c.360delT:p.A120fs) using exome sequencing.Conclusion: PMA patients from the two pedigrees had autosomal dominant mode of inheritance, with variability in the age of onset and disease severity. The cardinal symptoms were myoclonic seizures and ataxia without mental retardation.

Fractal dimension analysis for spike detection in low SNR extracellular signals

Objective. Many algorithms have been suggested for detection and sorting of spikes in extracellular recording. Nevertheless, it is still challenging to detect spikes in low signal-to-noise ratios (SNR). We propose a spike detection algorithm that is based on the fractal properties of extracellular signals and can detect spikes in low SNR regimes. Semi-intact spikes are low-amplitude spikes whose shapes are almost preserved. The detection of these spikes can significantly enhance the performance of multi-electrode recording systems. Approach. Semi-intact spikes are simulated by adding three noise components to a spike train: thermal noise, inter-spike noise, and spike-level noise. We show that simulated signals have fractal properties which make them proper candidates for fractal analysis. Then we use fractal dimension as the main core of our spike detection algorithm and call it fractal detector. The performance of the fractal detector is compared with three frequently used spike detectors. Main results. We demonstrate that in low SNR, the fractal detector has the best performance and results in the highest detection probability. It is shown that, in contrast to the other three detectors, the performance of the fractal detector is independent of inter-spike noise power and that variations in spike shape do not alter its performance. Finally, we use the fractal detector for spike detection in experimental data and similar to simulations, it is shown that the fractal detector has the best performance in low SNR regimes. Significance. The detection of low-amplitude spikes provides more information about the neural activity in the vicinity of the recording electrodes. Our results suggest using the fractal detector as a reliable and robust method for detecting semi-intact spikes in low SNR extracellular signals.

Focal automaticity manifesting as incessant right atrial tachycardia

A 75-year-old woman without structural heart disease presented with incessant regular monomorphic atrial tachycardia (AT). Spontaneous arrhythmia termination was repeatedly followed by a single sinus beat before reinitiation. Variations in tachycardia cycle length (CL) between 200 and 400 ms were frequently observed. The P-wave morphology was consistent with a focal origin from the crista terminalis; however, electroanatomic mapping (CARTO 3 system, Biosense Webster Inc., Diamond Bar, CA) demonstrated centrifugal activation of the right atrium originating from the atrial septal wall near the fossa ovalis. Further mapping at the site of the earliest atrial activation during AT revealed a rapid, regularly discharging focus (Figure 1, blue dot) at fixed 100-ms CL represented by the low-amplitude (0.17 mV) spike electrograms (↓) with an isoelectric interval between successive spikes. The accompanying local atrial potential (▼) during firing was clearly sharper, higher (0.75 mV), and well separated from the preceding spike at fixed 30-ms conduction delay but of lower amplitude (0.95 mV) than that during sinus beats (*). The recorded abnormal activity could not be detected when the catheter tip was moved a few millimeters. The initiation and termination of firing at the site of interest were recorded during catheter manipulation. The onset of AT on the surface electrocardiogram did not always coincide with the initiation of local, high-frequency activity but did terminate immediately with cessation of local firing. The first tachycardia P wave and subsequent discernible P waves were identical. Alterations in the degree of atrial capture by the focal activity (from 2:1 to

Propofol-induced electroencephalographic seizures in neonatal rats: the role of corticosteroids and γ-aminobutyric acid type A receptor-mediated excitation.

An imbalance between excitation and inhibition in the developing central nervous system may result in a pathophysiological outcome. We investigated the mechanistic roles of endocrine activity and γ-aminobutyric acid type A receptor (GABAAR)-mediated excitation in electroencephalographic seizures caused by the GABAAR-selective anesthetic propofol in neonatal rats. Postnatal day 4-6 Sprague Dawley rats underwent a minor surgical procedure to implant electrodes to measure electroencephalographic activity for 1 hour before and 1 hour after intraperitoneal administration of propofol (40 mg·kg). Various treatments were administered 15 minutes before administration of propofol. Episodes of electroencephalographic seizures and persistent low-amplitude spikes occurred during propofol anesthesia. Multifold increases in serum levels of corticosterone (t(10) = -5.062; P = 0.0005) and aldosterone (t(10) = -5.069; P = 0.0005) were detected 1 hour after propofol administration in animals that underwent experimental manipulations identical to those used to study electroencephalographic activity. Pretreatment with bumetanide, the Na-K-2Cl cotransporter inhibitor, which diminishes GABAAR-mediated excitation, eliminated both seizure and spike electroencephalographic activities caused by propofol. Mineralocorticoid and glucocorticoid receptor antagonists, RU 28318 and RU486, depressed electroencephalographic seizures but did not affect the spike electroencephalographic effects of propofol. Etomidate, at a dose sufficient to induce loss of righting reflex, was weak at increasing serum corticosteroid levels and eliciting electroencephalographic seizures. Etomidate given to corticosterone-pretreated rat pups further increased the total duration of electroencephalographic seizures caused by administration of exogenous corticosterone (t(21) = -2.512, P = 0.0203). Propofol increases systemic corticosteroid levels in neonatal rats, which along with GABAAR-mediated excitation appear to be required for propofol-induced neonatal electroencephalographic seizures. Enhancement of GABAAR activity alone may not be sufficient to elicit neonatal electroencephalographic seizures.

Reduced availability of voltage-gated sodium channels by depolarization or blockade by tetrodotoxin boosts burst firing and catecholamine release in mouse chromaffin cells.

Mouse chromaffin cells (MCCs) of the adrenal medulla possess fast-inactivating Nav channels whose availability alters spontaneous action potential firing patterns and the Ca(2+)-dependent secretion of catecholamines. Here, we report MCCs expressing large densities of neuronal fast-inactivating Nav1.3 and Nav1.7 channels that carry little or no subthreshold pacemaker currents and can be slowly inactivated by 50% upon slight membrane depolarization. Reducing Nav1.3/Nav1.7 availability by tetrodotoxin or by sustained depolarization near rest leads to a switch from tonic to burst-firing patterns that give rise to elevated Ca(2+)-influx and increased catecholamine release. Spontaneous burst firing is also evident in a small percentage of control MCCs. Our results establish that burst firing comprises an intrinsic firing mode of MCCs that boosts their output. This occurs particularly when Nav channel availability is reduced by sustained splanchnic nerve stimulation or prolonged cell depolarizations induced by acidosis, hyperkalaemia and increased muscarine levels. Action potential (AP) firing in mouse chromaffin cells (MCCs) is mainly sustained by Cav1.3 L-type channels that drive BK and SK currents and regulate the pacemaking cycle. As secretory units, CCs optimally recruit Ca(2+) channels when stimulated, a process potentially dependent on the modulation of the AP waveform. Our previous work has shown that a critical determinant of AP shape is voltage-gated sodium channel (Nav) channel availability. Here, we studied the contribution of Nav channels to firing patterns and AP shapes at rest (-50 mV) and upon stimulation (-40 mV). Using quantitative RT-PCR and immunoblotting, we show that MCCs mainly express tetrodotoxin (TTX)-sensitive, fast-inactivating Nav1.3 and Nav1.7 channels that carry little or no Na(+) current during slow ramp depolarizations. Time constants and the percentage of recovery from fast inactivation and slow entry into closed-state inactivation are similar to that of brain Nav1.3 and Nav1.7 channels. The fraction of available Nav channels is reduced by half after 10 mV depolarization from -50 to -40 mV. This leads to low amplitude spikes and a reduction in repolarizing K(+) currents inverting the net current from outward to inward during the after-hyperpolarization. When Nav channel availability is reduced by up to 20% of total, either by TTX block or steady depolarization, a switch from tonic to burst firing is observed. The spontaneous occurrence of high frequency bursts is rare under control conditions (14% of cells) but leads to major Ca(2+)-entry and increased catecholamine release. Thus, Nav1.3/Nav1.7 channel availability sets the AP shape, burst-firing initiation and regulates catecholamine secretion in MCCs. Nav channel inactivation becomes important during periods of high activity, mimicking stress responses.

Transient epileptiform signaling during neuronal network development: regulation by external stimulation and bimodal GABAergic activity

A predominance of excitatory activity, with protracted appearance of inhibitory activity, accompanies cortical neuronal development. It is unclear whether or not inhibitory neuronal activity is solicited exclusively by excitatory neurons or whether the transient excitatory activity displayed by developing GABAergic neurons contributes to an excitatory threshold that fosters their conversion to inhibitory activity. We addressed this possibility by culturing murine embryonic neurons on multi-electrode arrays. A wave of individual 0.2–0.4mV signals (“spikes”) appeared between approx. 20–30 days in culture, then declined. A transient wave of high amplitude (>0.5mV) epileptiform activity coincided with the developmental decline in spikes. Bursts (clusters of ≥3 low-amplitude spikes within 0.7s prior to returning to baseline) persisted following this decline.Addition of the GABAergic antagonist bicuculline initially had no effect on signaling, consistent with delayed development of GABAergic synapses. This was followed by a period in which bicuculline inhibited overall signaling, confirming that GABAergic neurons initially display excitatory activity in ex vivo networks. Following the transient developmental wave of epileptiform signaling, bicuculline induced a resurgence of epileptiform signaling, indicating that GABAergic neurons at this point displayed inhibitory activity. The appearance of transition after the developmental and decline of epileptiform activity, rather than immediately after the developmental decline in lower-amplitude spikes, suggests that the initial excitatory activity of GABAergic neurons contributes to their transition into inhibitory neurons, and that inhibitory GABAergic activity is essential for network development.Prior studies indicate that a minority (25%) of neurons in these cultures were GABAergic, suggesting that inhibitory neurons regulate multiple excitatory neurons. A similar robust increase in signaling following cessation of inhibitory activity in an artificial neural network containing 20% inhibitory neurons supported this conclusion. Even a minor perturbation in GABAergic function may therefore foster initiation and/or amplification of seizure activity, as well as perturbations in long-term potentiation.

Rhythmic heart beat artefacts mimicking an ictal EEG pattern with abundant interictal epileptiform activity in both mother and child

We present the EEG findings in a two-year-old girl with cryptogenic localisation-related epilepsy. The electroencephalogram showed fronto-temporal spike-wave discharges. In addition, the EEG repeatedly showed activity at different electrodes consisting of spikes with varying amplitude, rhythmicity and frequency, mimicking polyspikes. Both low- and high-amplitude spikes were generated from the same electrodes, however, only the low-amplitude spikes coincided with features of the child's electrocardiogram. Video monitoring showed the child's head resting on her mother's chest. This spike pattern was shown to be a heart beat artefact originating from the mother, as implied by the rhythmicity and the shift to other electrodes by moving the child's head, causing electrocardiogram artefacts on the posterior electrodes. This case study underscores the importance of routine use of simultaneous electroencephalogram and video monitoring. [Published with video sequences].

Rippling is not always electrically silent in rippling muscle disease

Rippling muscle disease (RMD) is a myopathy with hyperirritability, the pathophysiology for which is uncertain.We report electromyographic findings in a 30-year-old man with RMD. Clinical features included muscle rippling and percussion-induced rapid muscle contractions. Both were associated with bursts of short-duration, low-amplitude spikes, which resembled single muscle fiber discharges. Our case stands in contrast to previously reported cases, which showed either electrical silence or motor unit potential discharges associated with rippling, and may represent muscle fiber hyperexcitability.

Regulation of intracellular Ca2+ by P2Y1 receptors may depend on the developmental stage of cultured rat striatal neurons

Mixed striatal cell cultures containing neurons and glial cells were grown either in neurobasal medium (NBM) or Dulbecco's modified Eagle's medium (DMEM). Whole-cell patch-clamp recordings indicated that, if at all, only a single, low amplitude spike was evoked shortly after starting the injection of a depolarizing current pulse into NBM neurons. In contrast, DMEM neurons fired series of high amplitude action potentials, without apparent spike frequency adaptation. The possible reason for the observed action potential failure in NBM neurons was a low density of Na+ channels per unit of membrane surface area. However, both in NBM and DMEM neurons, ATP did not induce inward current responses via P2X receptor-channels, although GABAA and N-methyl-D-aspartate (NMDA) receptor-channels could be activated by muscimol and NMDA, respectively. Ca2+ imaging experiments by means of the Fura-2 method were utilized to measure intracellular Ca2+ ([Ca2+]i) in neurons and glial cells. NBM, but not DMEM neurons responded to ATP with [Ca2+]i transients; glial cells grown in either culture medium were equally sensitive to ATP. ATP caused an increase of [Ca2+]i by a mechanism only partly dependent on external Ca2+; the residual ATP effect was blocked by cyclopiazonic acid (CPA) and was therefore due to the release of Ca2+ from its intracellular pools. The receptor involved was characterized by P2 receptor antagonists (PPADS, MRS 2179, AR-C69931MX) and was found to belong to the P2Y1 subtype. CPA caused an early [Ca2+]i response due to release from intracellular storage sites, followed by a late [Ca2+]i response due to the influx of this cation from the extracellular space, probably triggered by the opening of store-operated channels (SOCs) in the plasma membrane. It is concluded that in partial analogy with the effect of CPA, ATP releases [Ca2+]i via the Gq/phospholipase C/inositoltrisphosphate (IP3) pathway, thereby opening SOCs. It is hypothesized that this effect of ATP may have an important role for the proliferation and migration of striatal neuronal progenitors.

Impulse conduction in the jellyfish Aglantha digitale

In the jellyfish Aglantha digitale two forms of swimming arise from two separate propagating axonal impulses: a fast, overshooting action potential that depends on TTX-resistant Na+ channels, and a low-amplitude spike that depends on T-type Ca2+ channels. While the Na+ action potential is propagated simply and without distortion, the shape of the Ca2+ spike depends on the past history of the axon; it is processed as well as propagated. Patch- and voltage-clamp experiments show how three classes of K+ channels contribute to this apparently unique system. A dual Na+/Ca2+ impulse mechanism may increase the bandwidth of an axonal line of communication but it also places restrictions on the form of the synaptic input needed for spike initiation.

Limbic Paroxysmal Magnetoencephalographic Activity in 12 Obsessive-Compulsive Disorder Patients

We describe frontotemporal paroxysmal rhythmic activity recorded by magnetoencephalography (MEG) in patients with obsessive-compulsive disorder (OCD). Twelve patients with OCD (per ICD-10 and DSM-IV criteria), aged 18 to 65 years, were assessed using MEG. Patients' classification according to the Yale Brown OCD Scale was as follows: severe = 8, moderate = 3, and mild = 1. MEG findings were compared with those of 12 age- and sex-matched healthy subjects (control group) with no previous history of psychiatric or neurologic disorders. All study participants underwent neurologic and basic medical examinations, including magnetic resonance imaging, electrocardiograms (EEGs), and electrooculograms. The study was conducted between January 2001 and January 2002. Two types of MEG activity were observed in patients with OCD: (1) frontotemporal paroxysmal rhythmic activity with low-amplitude spikes (< 1 picoTesla) in 92% (11/12) of patients and (2) intermittent isolated spikes and sharp waves in all patients (12/12). The OCD group had paroxysmal rhythmic MEG activity in the cingulate cortex (12/12), insula (10/12), hippocampus (9/12), temporal superior gyrus and angular and supramarginal gyri (9/12), precentral and post-central gyri (8/12), orbitofrontal cortex (5/12), and parietal lobes (5/12). MEG recordings were normal in the control group, and EEG findings were normal in both the OCD and control groups. Frontotemporal paroxysmal rhythmic activity with a preferential limbic distribution is a sensitive MEG finding in patients with OCD. Although the pathophysiology of this abnormality remains unknown, a corticostriatal network dysfunction was hypothesized.

Organization of neural networks in the neocortex.

Implanted semimicroelectrodes were used in conscious cats to record spike discharges from groups of close-lying neurons, i.e., multineuron activity, in the deep layers of the frontal and motor areas of the cortex at different levels of food motivation. Spike activity was extracted from 4-7 neurons and interneuronal interactions were studied by cross-correlation analysis between neighboring neurons in each zone (local networks) and between neurons in two zones (distributed networks) with analysis epochs of 0-100 msec. The results showed that neurons in local networks can be divided into two subgroups: neurons with high-amplitude spikes and a predominance of output (divergent) connections and neurons with low-amplitude spikes and a predominance of input (convergent) connections. Local networks are based on powerful monosynaptic connections (with delays of up to 2 msec) between large and small neurons. Most connections in distributed networks were between small neurons in local networks of the frontal cortex and large neurons in local networks in the motor cortex. Food deprivation for 24 h mainly affected late (with delays of 2-100 msec) cross-correlation interneuronal relationships in both local and distributed networks.

Functional organization of local neural networks in the cat neocortex. Relationship to the level of food motivation.

Implanted semimicroelectrodes were used to record multineuron activity--spike discharges from groups of close-lying neurons--in the deep layers of the frontal and motor cortex in conscious cats with different levels of food motivation. Spike activity from 4-7 neurons was extracted from multineuron activity, and interneuron interactions were studied by cross-correlation analysis. Neurons in local networks were divided into two subgroups: neurons with high-amplitude spikes with a predominance of output (divergent) connections, and neurons with low-amplitude spikes and a predominance of input (convergent) connections. Food deprivation lasting 24 h affected mainly the nature of interneuron interactions in the range of late cross-correlational connections (with delays of 2-100 msec).

Amplitude-Dependent Spike-Broadening and Enhanced Ca 2+ Signaling in GnRH-Secreting Neurons

In GnRH-secreting (GT1) neurons, activation of Ca 2+-mobilizing receptors induces a sustained membrane depolarization that shifts the profile of the action potential (AP) waveform from sharp, high-amplitude to broad, low-amplitude spikes. Here we characterize this shift in the firing pattern and its impact on Ca 2+ influx experimentally by using prerecorded sharp and broad APs as the voltage-clamp command pulse. As a quantitative test of the experimental data, a mathematical model based on the membrane and ionic current properties of GT1 neurons was also used. Both experimental and modeling results indicated that inactivation of the tetrodotoxin-sensitive Na + channels by sustained depolarization accounted for a reduction in the amplitude of the spike upstroke. The ensuing decrease in tetraethylammonium-sensitive K + current activation slowed membrane repolarization, leading to AP broadening. This change in firing pattern increased the total L-type Ca 2+ current and facilitated AP-driven Ca 2+ entry. The leftward shift in the current-voltage relation of the L-type Ca 2+ channels expressed in GT1 cells allowed the depolarization-induced AP broadening to facilitate Ca 2+ entry despite a decrease in spike amplitude. Thus the gating properties of the L-type Ca 2+ channels expressed in GT1 neurons are suitable for promoting AP-driven Ca 2+ influx in receptor- and non-receptor-depolarized cells.

Dipole analysis of epileptic source generator with manual zero potential shifting method.

The dipole tracing method is a technique whereby an electric source generator is estimated as an equivalent current dipole (ECD) based on potential distribution on the scalp. To estimate the electric source generator of low amplitude spikes, a manual zero potential shifting (MZPS) method was introduced in which a zero potential is set manually in dipole analysis. The subjects were three patients with localization-related epilepsy with temporal spikes. When low-amplitude spikes (< 50 microV) were analyzed by the conventional mean zero potential method, the dipolarity, an indicator of ECD reliability, had a low value and its locations were scattered. In contrast, when these low-amplitude spikes were analyzed by the MZPS method, ECD showed a high dipolarity value comparable to that obtained when high-amplitude spikes (> or = 50 microV) were analyzed by the mean zero potential method. Furthermore, the locations of the former ECD tended to converge and were almost identical to those of the latter ECD. These findings suggest the usefulness of the MZPS method in dipole analysis in terms of the dipolarity and ECD locations of low-amplitude spikes.

Fast Na+ spike generation in dendrites of guinea-pig substantia nigra pars compacta neurons.

Electric fields were applied to study the regenerative properties of substantia nigra pars compacta neurons in guinea-pig brain slices. Two types of spikes, of high or low amplitude, were generated in both the soma-hyperpolarizing and the soma-depolarizing directions of the field. The different sensitivity of the spikes to somatic polarization suggested that the high-amplitude spikes were generated near the cell body, whereas the low-amplitude spikes were generated at a distance from the soma. Application of tetrodotoxin or intracellular injection of QX 314 abolished both types of spike. The spikes were not inhibited in the presence of glutamate receptor antagonists or during Ca2+ channel blockade. Blockers of gap junctional conductance (sodium propionate, octanol and halothane) did not affect the field-induced spikes. The spike generation was highly sensitive to changes in membrane conductance induced by current injection in the soma or by external field application. The ability of a conditioning field stimulation to affect the spike generation in different neuronal compartments suggested that a transient outward current was generated in the dendrites. The field-induced spikes were facilitated by synaptic stimulation and, in some neurons, low-amplitude spikes were generated by synaptic potentials in the absence of field application. These results suggest that channels responsible for Na+ spike generation reside in the dendrites, and are influenced by spatially distributed voltage-dependent K+ currents and by synaptic input.

EEG findings in acetazolamide-responsive hereditary paroxysmal ataxia

EEG studies were performed in six family members affected by acetazolamide-responsive paroxysmal ataxia. Intermittent rhythmic delta activity was found at rest in five of them; low amplitude spikes were associated with delta waves in two cases, resulting in irregular spike and wave patterns. Slowing of background activity was present in three patients. EEG abnormalities were activated by hyperventilation and modified neither by intermittent photic stimulation, nor by acetazolamide therapy. Our results suggest that EEG may be helpful to recognize this rare, but well defined, treatable disorder.

Dendritic electrogenesis in rat hippocampal CA1 pyramidal neurons: functional aspects of Na+ and Ca2+ currents in apical dendrites.

The regenerative properties of CA1 pyramidal neurons were studied through differential polarization with external electrical fields. Recordings were obtained from somata and apical dendrites in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), DL-2-amino-5-phosphonovaleric acid (APV), and bicuculline. S+ fields hyperpolarized the distal apical dendrites and depolarized the rest of the cell, whereas S divided by fields reversed the polarization. During intradendritic recordings, S+ fields evoked either fast spikes or compound spiking. The threshold response consisted of a low-amplitude fast spike and a slow depolarizing potential. At higher field intensities the slow depolarizing potential increased in amplitude, and additional spikes of high amplitude appeared. During intrasomatic recordings, S+ field evoked repetitive firing of fast spikes, whereas S divided by fields evoked a slow depolarizing potential on top of which high- and low-amplitude spikes were evoked. Tetrodotoxin (TTX) blocked all types of responses in both dendrites and somata. Perfusion with Ca(2+)-free, Co(2+)-containing medium increased the frequency and amplitude of fast spikes evoked by S+ field and substantially reduced the slow depolarizing potential evoked by S+ field and substantially reduced the slow depolarizing potential evoked by S divided by fields. Antidromic stimulation revealed that an all-or-none dendritic component was activated in the distal apical dendrites by back-propagating somatic spikes. The dendritic component had an absolute refractory period of about 4 ms and a relative refractory period of 10-12 ms. Ca(2+)-dependent spikes in the dendrites were followed by a long-lasting afterhyperpolarization (AHP) and a decrease in membrane input resistance, during which dendritic excitability was selectively reduced. The data suggest that generation of fast Na+ currents and slow Ca2+ currents in the distal part of apical dendrites is highly sensitive to the dynamic state of the dendritic membrane. Depending on the mode and frequency of activation these currents can exert a substantial influence on the input-output behavior of the pyramidal neurons.

Use of running fractal dimension for the analysis of changing patterns in electroencephalograms

Running fractal dimensions were measured on four channels of an electroencephalogram (EEG) recorded from a normal volunteer. The changes in the background activity due to eye closure were clearly differentiated by the fractal method. The compressed spectral array (CSA) and the running fractal dimensions of the EEG showed corresponding changes with respect to change in the background activity. The fractal method was also successful in detecting low amplitude spikes and the changes in the patterns in the EEG. The effects of different window lengths and shifts on the running fractal dimension have also been studied. The utility of fractal method for EEG data compression is highlighted.