Neocortical synchronized oscillations induced by thalamic disinhibition in vivo.
Thalamocortical circuits are recognized as the main elements involved in the genesis of synchronized oscillations typical of certain generalized seizures. We addressed the capability of thalamic disinhibition to generate synchronized oscillations in neocortex. Microdialysis was used to infuse GABA(A) and GABA(B) receptor antagonists directly into the thalamus of anesthetized rats while recording cortical field potentials from 16 sites aligned perpendicular to the cortical surface, using 100 microm spaced linear array silicon probes. The results demonstrate that block of thalamic GABA(A) receptors induces continuous 3 Hz discharges in neocortex and that thalamic GABA(B) receptors mediate this activity. Also, during thalamic disinhibition sporadic long-lasting discharges at 12 Hz occur that do not depend on GABA(B) receptors. Current source density analysis of these activities revealed that the dynamics of sinks and sources for the 3 and 12 Hz discharges was quite distinct, in a way that suggests a different active involvement of the neocortex. The results indicate that intrathalamic inhibitory processes play an essential role in the generation of neocortical synchronized oscillatory activity that may be related to certain forms of generalized seizures.
Castro-Alamancos
M A
MA
Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A2B4 Canada.
D000818:Animals; D004594:Electrophysiology; D018756:GABA Antagonists / Q000494:pharmacology; D017551:Microdialysis; D019579:Neocortex / Q000502:physiology*; D010507:Periodicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology*; D018080:Receptors, GABA-B / Q000187:drug effects / Q000502:physiology*; D013788:Thalamus / Q000502:physiology*
D018756:GABA Antagonists; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B