Literature DB >> 9744953

Spike-wave complexes and fast components of cortically generated seizures. III. Synchronizing mechanisms.

D Neckelmann1, F Amzica, M Steriade.   

Abstract

The intracortical and thalamocortical synchronization of spontaneously occurring or bicuculline-induced seizures, consisting of spike-wave (SW) or polyspike-wave (PSW) complexes at 2-3 Hz and fast runs at 10-15 Hz, was investigated in cats under ketamine-xylazine anesthesia. We used single and dual simultaneous intracellular recordings from cortical areas 5 and 7, and extracellular recordings of unit firing and field potentials from neocortical areas 5, 7, 17, 18, as well as related thalamic nuclei. The evolution of time delays between paroxysmal depolarizing events in single neurons or neuronal pools recorded from adjacent and distant sites was analyzed by using 1) sequential cross-correlations between field potentials, 2) averaged activities triggered by the spiky component of cortical SW/PSW complexes, and 3) time histograms between neuronal discharges. In all instances, the paroxysmal activities recorded from the dorsal thalamus lagged the onset of seizures in neocortex. The time lags between simultaneously impaled cortical neurons were significantly smaller during SW complexes than during the prior epochs of slow oscillation. During seizures, as during the slow oscillation, the intracortical synchrony was reduced with increased distance between different cortical sites. Dual intracellular recordings showed that, during the same seizure, time lags were not constant and, instead, reflected alternating precession of the recorded foci. After transection between areas 5 and 7, the intracortical synchrony was lost, but corticothalamocortical volleys could partially restore seizure synchrony. These data show that the neocortex leads the thalamus during SW/PSW seizures, that time lags between cortical foci are not static, and that thalamus may assist synchronization of SW/PSW seizures after disconnection of intracortical synaptic linkages.

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Year:  1998        PMID: 9744953     DOI: 10.1152/jn.1998.80.3.1480

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.714


  23 in total

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2.  The GABAergic reticular nucleus: a preferential target of corticothalamic projections.

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

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5.  Spatial buffering during slow and paroxysmal sleep oscillations in cortical networks of glial cells in vivo.

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Journal:  J Neurosci       Date:  2002-02-01       Impact factor: 6.167

6.  Activity of thalamic reticular neurons during spontaneous genetically determined spike and wave discharges.

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8.  Synchronized oscillations caused by disinhibition in rodent neocortex are generated by recurrent synaptic activity mediated by AMPA receptors.

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Review 9.  Bursts modify electrical synaptic strength.

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Review 10.  The appearance of long-latency responses to a conditioned signal in the cortex is explained by strengthening of collateral connections between pyramidal neurons.

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