Transient cortical gamma oscillations: a role for GluK1-containing kainate receptors

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  2. Dr Michelle Pierce
  3. Professor Miles Whittington
  4. Dr Mark Cunningham
Author(s)Pierce ML, Whittington MA, Cunningham MO
Editor(s)
Publication type Conference Proceedings (inc. Abstract)
Conference NameYoung Life Scientists' Symposium 2009
Conference LocationBristol, UK
Year of Conference2009
Legacy Date14 May 2009
Volume
Pages
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Cortical gamma (30-80 Hz) oscillations are essential for normal cognitive function. In the medial entorhinal cortex (mEC) in vitro, kainate receptors (KARs) containing the GluK1 subunit generate gamma activity whose frequency depends on the degree of KAR activation. Here, we use transient pressure ejections of KAR agonists to construct dose response curves illustrating this relationship - and its pharmacology - in detail. Horizontal temporal lobe slices (450mm) were prepared from adult male Wistar rats. Transient gamma oscillations were elicited by ejecting kainate (500nM; 45.6 ±1.8Hz, power=100.2 ±21.4mV², n=11) or the selective GluK1-containing KAR agonist ATPA (1mM; 43.1 ±4.6Hz, power=102.0 ±22.8mV², n=7) near an extracellular field electrode in the superficial mEC. Peak frequency of the induced oscillation was positively correlated with agonist ejection duration. In the presence of 25mM SYM2206, an AMPA receptor antagonist, transient oscillations persisted but the correlation was abolished. Induced oscillations were abolished by the GABAA receptor antagonist gabazine (1mM; n=4). The NMDA receptor antagonist D-AP5 (50mM) either abolished responses (n=10) or reduced their frequency without affecting the frequency-duration correlation (n=5). Therefore, in the mEC, the relationship between transient gamma oscillation frequency and GluK1-containing KAR drive requires AMPA but not NMDA receptors.
URLhttp://www.younglifescientist.org/programme/programme.asp?Meeting=YLS2009Pro
NotesGiven as an oral presentation