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

Lookup NU author(s): Dr Michelle Pierce, Professor Miles Whittington, Professor Mark Cunningham


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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.

Publication metadata

Author(s): Pierce ML, Whittington MA, Cunningham MO

Publication type: Conference Proceedings (inc. Abstract)

Publication status: Published

Conference Name: Young Life Scientists' Symposium 2009

Year of Conference: 2009


Notes: Given as an oral presentation