High-frequency gamma oscillations coexist with low-frequency gamma oscillations in the rat visual cortex in vitro.
Synchronization of neuronal activity in the visual cortex at low (30-70 Hz) and high gamma band frequencies (> 70 Hz) has been associated with distinct visual processes, but mechanisms underlying high-frequency gamma oscillations remain unknown. In rat visual cortex slices, kainate and carbachol induce high-frequency gamma oscillations (fast-gamma; peak frequency approximately 80 Hz at 37 degrees C) that can coexist with low-frequency gamma oscillations (slow-gamma; peak frequency approximately 50 Hz at 37 degrees C) in the same column. Current-source density analysis showed that fast-gamma was associated with rhythmic current sink-source sequences in layer III and slow-gamma with rhythmic current sink-source sequences in layer V. Fast-gamma and slow-gamma were not phase-locked. Slow-gamma power fluctuations were unrelated to fast-gamma power fluctuations, but were modulated by the phase of theta (3-8 Hz) oscillations generated in the deep layers. Fast-gamma was spatially less coherent than slow-gamma. Fast-gamma and slow-gamma were dependent on gamma-aminobutyric acid (GABA)(A) receptors, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and gap-junctions, their frequencies were reduced by thiopental and were weakly dependent on cycle amplitude. Fast-gamma and slow-gamma power were differentially modulated by thiopental and adenosine A(1) receptor blockade, and their frequencies were differentially modulated by N-methyl-D-aspartate (NMDA) receptors, GluK1 subunit-containing receptors and persistent sodium currents. Our data indicate that fast-gamma and slow-gamma both depend on and are paced by recurrent inhibition, but have distinct pharmacological modulation profiles. The independent co-existence of fast-gamma and slow-gamma allows parallel processing of distinct aspects of vision and visual perception. The visual cortex slice provides a novel in vitro model to study cortical high-frequency gamma oscillations.
Oke
Olaleke O
OO
Neuronal Networks, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK.
Magony
Andor
A
Anver
Himashi
H
Ward
Peter D
PD
Jiruska
Premysl
P
Jefferys
John G R
JG
Vreugdenhil
Martin
M
D058916:Adenosine A1 Receptor Antagonists; D000818:Animals; D002491:Central Nervous System Agents / Q000494:pharmacology; D017629:Gap Junctions / Q000187:drug effects / Q000502:physiology; D008297:Male; D008839:Microelectrodes; D010507:Periodicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D043682:Receptor, Adenosine A1 / Q000378:metabolism; D018091:Receptors, AMPA / Q000378:metabolism; D011963:Receptors, GABA-A / Q000378:metabolism; D018092:Kainic Acid Receptors / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D015222:Sodium Channels / Q000378:metabolism; D013696:Temperature; D013826:Theta Rhythm; D014793:Visual Cortex / Q000187:drug effects / Q000502:physiology*
D058916:Adenosine A1 Receptor Antagonists; D002491:Central Nervous System Agents; D043682:Receptor, Adenosine A1; D018091:Receptors, AMPA; D011963:Receptors, GABA-A; D018092:Kainic Acid Receptors; D016194:Receptors, N-Methyl-D-Aspartate; D015222:Sodium Channels