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The Journal of Neuroscience, December 15, 2000, 20(24):9195-9206
Origin of Synchronized Oscillations Induced by Neocortical
Disinhibition In Vivo
Manuel A.
Castro-Alamancos
Department of Neurology and Neurosurgery, Montreal
Neurological Institute, McGill University, Montreal, Quebec H3A
2B4, Canada
During disinhibition, the neocortex generates synchronous
activities. Block of GABAA receptors in neocortex
transforms cortical slow-wave oscillations into large-amplitude ~1 Hz
discharges consisting of a negative spike or multiple negative spikes
riding on a positive wave. Further block of GABAB receptors
in neocortex slows the discharges to ~0.5 Hz and increments the
number of negative spikes forming rhythmic ~10 Hz neocortical
oscillations. Although the thalamus responds robustly to these
neocortical discharges, these are unaffected by thalamic inactivation
using tetrodotoxin. Thus, an important problem relates to the origin of
these activities within the neocortex. Current source density analysis
and intracellular recordings revealed that the first negative spike in
a discharge corresponded to a current sink that reflected a paroxysmal
depolarizing shift (PDS) and could originate in the lower layers or in
the upper layers. Regardless of the origin (upper or lower layer), the
initial current sink always spreads to the same site in upper layer
V-IV. In contrast, the ~10 Hz oscillation that follows the initial
negative spike corresponds to current sinks that always originate in
the lower layers but do not spread to upper layer V-IV, jumping
directly to the upper layers. Each current sink in the ~10 Hz
oscillation reflects a small PDS and is followed by a current source
that reflects the repolarization after each PDS.
Key words:
epilepsy; seizure; oscillations; thalamus; neocortex; -aminobutyric acid; GABAA receptors; GABAB
receptors; CGP35348
Copyright © 2000 Society for Neuroscience 0270-6474/00/20249195-12$05.00/0
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