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At least 145 records · Page 8Linked to original sources
PubMed2000

Propagation of spontaneous synchronized activity in cortical slice cultures recorded by planar electrode arrays.

The spatial propagation of synchronized activity in cortical slice cultures was characterized by multi-site extracellular recording. Spontaneous activity was studied in normal culture medium, and in bicuculline- or kainic acid-containing media. A common feature in all these conditions was that activity was generated first in superficial layers (i.e., layer I/II) before spreading over the whole area of the slice. In culture medium or bicuculline-containing medium, the initiation site of the activity was not constant and showed a large variety of patterns of horizontal propagation. Kainic acid induced epileptiform activity, consisting of intense initial bursts followed by repetitive after-discharges. Though the patterns of spatial propagation of the bursts were variable as in the other conditions, the after-discharges followed a constant path. Cross-correlation analysis indicated that the network moved in a graded fashion to a steady state during the sequence of after-discharges.

Animals↗
PubMed1997

The K-complex: its slow (<1-Hz) rhythmicity and relation to delta waves.

The K-complex is a major graphoelement of sleep EEG. This report demonstrates that K-complexes emerge from a cortically generated slow (<1-Hz) oscillation. Human EEG as well as cat cellular and field potential recordings converge into demonstrating that the K-complex results from a synchronized cortical network that imposes periodic excitatory and inhibitory actions on cortical neurons. We additionally show the correspondence between neuronal activities and the shape of the K-complex. Spectral analysis confirms the periodic recurrence of human K-complexes, with main peaks at 0.5 to 0.7 Hz. It is also shown that the spectral content in the delta band (1 to 4 Hz) is partially due to the shape and duration of the K-complex.

Action Potentials↗
PubMedDate not supplied

[Shifts in spatial synchronization of rabbit cortical potentials evoked by applying acetylcholine and amizil to the visual area].

Acetylcholine solution application to the visual cortex of walking unrestrained rabbit led approximately in 5 minutes to a certain increase of the spatial synchronization of the cortical potentials at the small conditions, the the cortex, 24 EEG channels being used. Under the same conditions, the application of muscarinic antagonist amizil had an opposite more distinct effect. Endogenous cholinergic input increasing the spatial synchronization is supposed to play an important role in the formation of the spatiotemporal cortical potentials' organization necessary for the occurrence of complex behavioural acts.

Acetylcholine↗
PubMed1987

The interaction between EEG and transient muscle activity during sleep in humans.

The EEG and EMG were recorded during 14 nights of sleep for 5 young normal adults and were analyzed automatically with a lab computer system. From the EEG one parameter was computed which is based on the joint frequency-amplitude distribution of EEG waves. The temporal sequence of parameter values displays the time course of the sleep EEG. Another parameter, which results from the automatic analysis of the EMG, represents transient EMG activity, i.e. shortlasting changes of the muscle tone. A comparison of the automatically analyzed EEG and EMG data revealed a close correspondence between both parameters. A peak of EMG transient activity was observed in virtually each ultradian sleep cycle at a well-defined turning point between the phase of EEG synchronization and the subsequent phase of EEG desynchronization. Before and after this turning point there was a gradual decrease in the rate of transient EMG activity with minimal activity immediately preceding the turning point. The results suggest that cortical synchronization during sleep is incompatible with transient activity in the muscle system while desynchronization is invariably accompanied by a high rate of transient EMG activity.

Adult↗
PubMed1982

Somatosensory rhythms in the awake cat: a single unit exploration of their thalamic concomitant in nucleus ventralis posterior and vicinity.

A microelectrode study was performed in n. ventralis posterior (VP) of the fully alert cat, to study the correlation between thalamic unit activity and the cortical synchronized 14 c/sec rhythms that develop in the somatic area I for forepaw and wrist projections, when the animal is in a state of "quiet waking". (i) Only a small proportion of VP cells underwent changes during the studied cortical rhythms. (ii) None of these cells were typical thalamo-cortical relay cells carrying tactile messages to the cortex. (iii) Cells altering their discharge were of two types, rhythmic (R) cells, discharging at the frequency of the cortical rhythms, and tonic (T) cells, displaying an overall, sustained change during the whole sequence of cortical 14 c/sec. (iv) Among R cells, some were long axon thalamo-cortical cells and others, likely to be interneurones. (v) Some T cells increased their firing rate during rhythmic trains, others came into silence during the same period. (vi) The thalamic circuitry responsible for this particular set of "quiet waking rhythms" is discussed.

Action Potentials↗
PubMed2003

Progressive degradation and subsequent refinement of acoustic representations in the adult auditory cortex.

Correlated neuronal activity is believed to play an important role in refining and maintaining cortical circuitry during early development. Here we provide evidence that globally and locally correlated activity mediate different forms of adult plasticity. Pulses of broad-spectrum noise were used to activate time-locked responses across large areas of the rat auditory cortex, globally synchronizing cortical activity. Brief tone pips were used to activate relatively small groups of neurons, generating locally correlated activity. Pairing pulsed noises with nucleus basalis (NB) stimulation in awake rats for 4 weeks broadened spectral tuning, disrupted tonotopic maps, and reduced spontaneous discharge correlation in the primary auditory cortex (AI), as examined under anesthesia. Those effects caused AI neurons to appear qualitatively similar to neurons in nonprimary auditory fields of naive animals. Subsequent pairing of tone pips with NB stimulation for a period of 4 weeks completely reversed these effects induced by previous noise-NB pairing. These findings further demonstrate that the adult auditory cortex retains a substantial capacity for receptive field plasticity and tonotopic map reorganization and that locally correlated activity plays an important role in plasticity in the adult, as in the developing cortex.

Acoustic Stimulation↗
PubMed1996

Cooperative structures for visually guided reach.

In this introductory commentary, it is argued that the many areas in the cerebral cortex, cerebellum, and elsewhere that are active during reaching movements must interact to generate the appropriate neuronal drive for any given reach trajectory. Cooperative interaction among dispersed neuronal groups may be facilitated by synchronization of intrinsic oscillatory cycles of excitability. In sensorimotor cortex, intervals of oscillatory activity in relatively high frequency bands have been linked to the preparation phase of limb movements. Moreover, synchronization of oscillatory cycles in different loci of frontal and parietal cortex has been reported. Oscillation frequencies change abruptly at the onset of movement, which could reflect altered cerebellar influences on motor thalamocortical circuits. Since relaxation coupling within the thalamus is a probable mechanism of cortical synchronization, it is postulated that cerebellar output contributes to synchronization patterns.

Animals↗
PubMed1996

Inhibition synchronizes sparsely connected cortical neurons within and between columns in realistic network models.

Networks of compartmental model neurons were used to investigate the biophysical basis of the synchronization observed between sparsely-connected neurons in neocortex. A model of a single column in layer 5 consisted of 100 model neurons: 80 pyramidal and 20 inhibitory. The pyramidal cells had conductances that caused intrinsic repetitive bursting at different frequencies when driven with the same input. When connected randomly with a connection density of 10%, a single model column displayed synchronous oscillatory action potentials in response to stationary, uncorrelated Poisson spike-train inputs. Synchrony required a high ratio of inhibitory to excitatory synaptic strength; the optimal ratio was 4 : 1, within the range observed in cortex. The synchrony was insensitive to variation in amplitudes of postsynaptic potentials and synaptic delay times, even when the mean synaptic delay times were varied over the range 1 to 7 ms. Synchrony was found to be sensitive to the strength of reciprocal inhibition between the inhibitory neurons in one column: Too weak or too strong reciprocal inhibition degraded intra-columnar synchrony. The only parameter that affected the oscillation frequency of the network was the strength of the external driving input which could shift the frequency between 35 to 60 Hz. The same results were obtained using a model column of 1000 neurons with a connection density of 5%, except that the oscillation became more regular. Synchronization between cortical columns was studied in a model consisting of two columns with 100 model neurons each. When connections were made with a density of 3% between the pyramidal cells of each column there was no inter-columnar synchrony and in some cases the columns oscillated 180 degrees out of phase with each other. Only when connections from the pyramidal cells in each column to the inhibitory cells in the other column were added was synchrony between the columns observed. This synchrony was established within one or two cycles of the oscillation and there was on average less than 1 ms phase difference between the two columns. Unlike the intra-columnar synchronization, the inter-columnar synchronization was found to be sensitive to the synaptic delay: A mean delay of greater than 5 ms virtually abolished synchronization between columns.

Cerebral Cortex↗
PubMed2004

Impact of D1-class dopamine receptor on striatal processing of cortical input in experimental parkinsonism in vivo.

Recent in vivo electrophysiological studies suggest that chronic dopamine depletion alters profoundly the firing pattern of basal ganglia neurons. These changes may disrupt the processing of cortical information flow from the striatum to the output nuclei, and presumably underlie the clinical manifestations of Parkinson's disease. We have recently reported that chronic nigrostriatal lesions induce changes in the functional state of striatal medium-spiny neurons (MSNs) that could facilitate spreading of cortical synchronous activity (approximately 1 Hz) to striatal target nuclei. Here we show that systemic administration of D1 dopamine agonists was sufficient to restore the changes induced by chronic nigrostriatal lesions on striatal neuronal activity into the normal state. Following systemic administration of SKF38393 or SKF81279 the membrane potential of striatal MSNs was upheld into a more hyperpolarized value and action potential firing probability decreased. D1 agonists also increased the latency to the cortically driven plateau depolarization and reduced the peak potential of the short latency depolarizing postsynaptic response to a more hyperpolarized value. The present study provides in vivo evidence indicating that pharmacological stimulation of D1-class dopamine receptors can modulate the flow of cortical information through the striatum in the parkinsonian state.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2003

The biology of epilepsy genes.

Mutations in over 70 genes now define biological pathways leading to epilepsy, an episodic dysrhythmia of the cerebral cortex marked by abnormal network synchronization. Some of the inherited errors destabilize neuronal signaling by inflicting primary disorders of membrane excitability and synaptic transmission, whereas others do so indirectly by perturbing critical control points that balance the developmental assembly of inhibitory and excitatory circuits. The genetic diversity is now sufficient to discern short- and long-range functional convergence of epileptogenic molecular pathways, reducing the broad spectrum of primary molecular defects to a few common processes regulating cortical synchronization. Synaptic inhibition appears to be the most frequent target; however, each gene mutation retains unique phenotypic features. This review selects exemplary members of several gene families to illustrate principal categories of the disease and trace the biological pathways to epileptogenesis in the developing brain.

Animals↗
PubMed1981

Virus-induced electrotonic coupling: hypothesis on the mechanism of periodic EEG discharges in Creutzfeldt-Jakob disease.

Experimental evidence and computer modeling indicate that periodic synchronous cellular depolarizing bursts (interictal spikes) arise when the balance recurrent inhibition and local excitatory coupling is altered. Such a mechanism may explain the generalized periodic sharp waves that characterize the electroencephalogram of many patients with Creutzfeldt-Jakob disease. In Creutzfeldt-Jakob disease, fusions of neuronal processes, particularly dendrites, may lead to abnormal electrotonic coupling between cells, providing the basis for powerful excitatory interaction whereby large neuronal aggregates burst in near synchrony. Cortical synchronous discharges would give rise to sharp waves in the electroencephalogram, whereas similar discharges in brainstem, spinal cord, or elsewhere could lead to myoclonic jerks.

Animals↗
PubMedDate not supplied

[The effect of acetylcholine on shifts in the spatial synchronization of the cortical potentials in the rabbit evoked by the reversible interruption of the mammillary body connections].

To study the role of cholinergic transmitter system in the maintenance of sychronizing limbic influences, the dynamics of the spatial distribution of the changes of cross-correlation coefficients of rabbits EEG led by 24 electrodes, was estimated at application of acetylcholine solution to the visual cortical area in combination with anode polarization of mammillary bodies. Acetylcholine, which separate effect was connected with a restricted increase of the spatial synchronization of potentials, completely eliminated the effects of isolated polarization expressed in a significant decrease of a half of calculated correlation coefficients between EEGs of the visual and motor cortical areas. Nonspecific cholinergic synchronizing system is supposed to exist which is active under the conditions of the mammillo-thalamo-cortical connections being intact.

Acetylcholine↗
PubMed2004

Cortical activation and synchronization during sentence comprehension in high-functioning autism: evidence of underconnectivity.

The brain activation of a group of high-functioning autistic participants was measured using functional MRI during sentence comprehension and the results compared with those of a Verbal IQ-matched control group. The groups differed in the distribution of activation in two of the key language areas. The autism group produced reliably more activation than the control group in Wernicke's (left laterosuperior temporal) area and reliably less activation than the control group in Broca's (left inferior frontal gyrus) area. Furthermore, the functional connectivity, i.e. the degree of synchronization or correlation of the time series of the activation, between the various participating cortical areas was consistently lower for the autistic than the control participants. These findings suggest that the neural basis of disordered language in autism entails a lower degree of information integration and synchronization across the large-scale cortical network for language processing. The article presents a theoretical account of the findings, related to neurobiological foundations of underconnectivity in autism.

Autistic Disorder↗
PubMed1999

Synchronized paroxysmal activity in the developing thalamocortical network mediated by corticothalamic projections and "silent" synapses.

In mouse thalamocortical slices in vitro, the potassium channel blocker 4-AP and GABAA receptor antagonist bicuculline together induced spontaneous prolonged depolarizations in layer VI neurons from postnatal day 2 (P2), in ventroposterior nucleus neurons (VP) from P7, and in reticular nucleus neurons (RTN) from P8. Dual whole-cell recordings revealed that prolonged bursts were synchronized in layer VI, VP, and RTN. Bursts were present in cortex isolated from thalamus, but not in thalamus isolated from cortex, indicating that bursts originated in cortex and propagated to thalamus. Prolonged bursts were synchronized in layer VI when vertical cuts extended from pia mater through layers IV or V, but were no longer synchronized when cuts extended through layer VI and white matter. In voltage-clamp recordings before P10, burst conductance of all three neuronal populations was dominated by the NMDA receptor-mediated conductance, and therefore synapses were "silent". In cortex and RTN, after P10, bursts were associated with strong AMPA/kainate receptor-mediated conductances, and synapses had become "functional"; silent synapses persisted in a large proportion of VP cells after P10. Before P9, the NMDA receptor antagonist APV or the non-NMDA receptor antagonist CNQX blocked the prolonged bursts. After P9, CNQX continued to block the prolonged bursts, but APV merely shortened their duration. Thus, NMDA receptor-based silent synapses are essential for paroxysmal corticothalamic activity during early postnatal development, and connections between layer VI neurons are sufficient for horizontal cortical synchronization.

4-Aminopyridine↗
PubMed1997

Magnetoencephalographic cortical rhythms.

We have characterized the magnetic 10- and 20-Hz rhythms recorded with a whole-scalp neuromagnetometer during different conditions. Sources of the posterior 10-Hz (alpha) rhythm clustered mainly around the parieto-occipital sulcus and, to a lesser extent, around the calcarine sulci, with several generators. Temporal Spectral Evolution (TSE) analysis, used to follow event-related changes in the different frequency bands, showed strong dampening of the alpha within 200 ms after the appearance of a visual stimulus and also during visual imagery. Suppression was often followed by a rebound above the baseline level. The rolandic mu rhythm consisted of 10- and 20-Hz components with different reactivity and source locations. The 10-Hz component seems to be mainly somatosensory in origin whereas the 20-Hz signal also receives contributions from the motor cortex, and even shows 'motorotopy' in its reactivity: the source locations depend in a somatotopical manner on the site of the moving body part. The frequency composition of the posterior spontaneous activity was disturbed in patients with small infarcts of the medial thalamus. It is shown with simulations that a surprisingly small number of synchronized cortical neurons could generate the major part of the recorded oscillatory signal. Finally, some clarifications are suggested to the terminology of brain rhythms.

Animals↗
PubMed1990

Burst generating and regular spiking layer 5 pyramidal neurons of rat neocortex have different morphological features.

Intracellular recordings were obtained from pyramidal neurons in layer 5 of rat somatosensory and visual cortical slices maintained in vitro. When directly depolarized, one subclass of pyramidal neurons had the capacity to generate intrinsic burst discharges and another generated regular trains of single spikes. Burst responses were triggered in an all-or-none manner from depolarizing afterpotentials in most bursting neurons. Regular spiking cells responded to electrical stimulation of ascending afferents with a typical EPSP-IPSP sequence, whereas IPSPs were hard to detect in bursting cells. Orthodromic activation of the latter evoked a prominent voltage-dependent depolarization that could trigger a burst response. Intracellularly labelled bursting and regular spiking cells were located in layer 5b, but had distinctly different morphologies. Bursting neurons had a large pyramidal soma, a gradually emerging apical dendrite, and an extensive apical and basal dendritic tree. Their axonal collateral arborization was predominantly limited to layers 5/6. In contrast, regular spiking cells had a more rounded soma with abruptly emerging apical dendrite, a smaller dendritic arborization, and 2 to 8 ascending axonal collaterals that arborized widely in the supragranular layers. Both bursting and regular spiking cells had main axons that entered the subcortical white matter. These data show that some subgroups of pyramidal neurons within the deeper parts of layer 5 of rat cortex are morphologically and physiologically distinct and have different intracortical connections. Bursting cells presumably function to amplify and synchronize cortical outputs, whereas regular spiking output neurons provide excitatory feedback to neurons at all cortical levels and receive a more effective orthodromic inhibitory input. These data support the hypothesis that differences in gross neuronal structure, perhaps even the subtle differences that distinguish subclasses of neurons in a given lamina, are predictive of underlying differences in the type and distribution of ion channels in the nerve cell membrane and connections of cells within the cortical circuit.

Animals↗
PubMedDate not supplied

Toward an integrated continuum model of cerebral dynamics: the cerebral rhythms, synchronous oscillation and cortical stability.

Continuum models of cerebral cortex with parameters derived from physiological data, provide explanations of the cerebral rhythms, synchronous oscillation, and autonomous cortical activity in the gamma frequency range, and suggest possible mechanisms for dynamic self-organization in the brain. Dispersion relations and derivations of power spectral response for the models, show that a low frequency resonant mode and associated travelling wave solutions of the models' equations of state can account for the predominant 1/f spectral content of the electroencephalogram (EEG). Large scale activity in the alpha, beta, and gamma bands, is accounted for by thalamocortical interaction, under regulation by diffuse cortical excitation. System impulse responses can be used to model Event-Related Potentials. Further classes of local resonance may be generated by rapid negative feedbacks at active synapses. Activity in the gamma band around 40 Hz, associated with large amplitude oscillations of pulse density, appears at higher levels of cortical activation, and is unstable unless compensated by synaptic feedbacks. Control of cortical stability by synaptic feedbacks offers a partial account of the regulation of autonomous activity within the cortex. Synchronous oscillation occurs between concurrently excited cortical sites, and can be explained by analysis of wave motion radiating from each of the co-active sites. These models are suitable for the introduction of learning rules-most notably the coherent infomax rule.

Cerebral Cortex↗
PubMed1988

Post-hypoxic action (intention) myoclonus: a clinico-electroencephalographic study.

A patient with post-hypoxic action myoclonus classified as reticular reflex myoclonus was subjected to an electrophysiological investigation. The myoclonic movements involved mainly the legs but could also affect the whole body. Somatosensory evoked responses were not increased and electroencephalography (EEG) was normal when the patient was relaxed. Startle, self-paced movement or movement on command induced repetitive myoclonic jerks preceded and accompanied by repetitive small spikes in the EEG with phase reversal in the midline at the vertex or slightly posterior to it, regardless of the limb moved. The central spiking subsided considerably earlier than the myoclonic jerks as shown by polygraphic recordings. The EEG spikes were also provoked by mere imagination of movement and persisted in spite of a dramatic reduction of myoclonic activity after treatment with clonazepam. The observations suggest that the vertex spiking in post-hypoxic action myoclonus indicates synchronous cortical activation, but is not closely coupled with activation of the Betz cells of layer V where the pyramidal pathway originates.

Aorta, Abdominal↗