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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
Pierce ML, Whittington MA, Cunningham MO
British Neuroscience Association Abstracts
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Gamma frequency (30-80 Hz) oscillations in the medial entorhinal cortex (mEC) are implicated in memory formation and processing. In the 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 EC slices (450µm) were prepared from adult male Wistar rats. Transient gamma oscillations (45.8 ± 1.8Hz, power=100.2 ± 21.4µV²) were elicited by ejecting 500nM kainate near an extracellular field electrode in the superficial mEC (n=11). Peak frequency of the evoked oscillation was positively correlated with the duration of kainate ejection over a 5-fold range of durations. Longer applications produced similar frequency oscillations to those evoked by the shortest applications (p>0.2). ATPA (1µM), a selective GluK1-containing KAR agonist, also induced gamma oscillations (43.1 ± 4.6Hz, power=102.0 ± 22.8µV²) whose frequency was positively correlated with ejection duration over at least a 20-fold range of ejection durations. All induced responses were blocked by the GABA
receptor antagonist GABAzine (1µM) as expected for an inhibition-based rhythm (n=3). Bath application of the NMDA receptor antagonist DAP5 (50µM) reduced the frequency (35.3 ± 2.5Hz, p<0.01) and power (19.4 ± 4.7µV², p<0.01) of kainate-induced oscillations, but did not abolish the correlation between frequency and ejection duration (n=6). In conclusion, transient gamma oscillation frequency in the mEC is closely linked to GluK1-containing KAR drive, and this relationship does not require NMDA receptors.
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