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. Author manuscript; available in PMC: 2015 Jul 18.
Published in final edited form as: Acta Neurol Scand Suppl. 2013;(197):9–18. doi: 10.1111/ane.12099

Figure 2.

Figure 2

Electrophysiological recording from a guinea-pig hippocampal slice in the presence of 50 µM picrotoxin. Top (black) traces are intracellular recordings from CA3 pyramidal neurons; bottom (blue) traces are extracellular recordings from the stratum pyramidale. Bath application of the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV, 200 µM) eliminates late bursting but does not affect the triggering of the initial epileptiform discharge. However, when the AMPA receptor antagonist CNQX (20 µM) is added, epileptiform activity is eliminated, indicating that AMPA receptors alone are sufficient to bring about the synchronized bursting underlying the primary burst (in the presence of blockade of GABAA receptors and in neurons that have intrinsic bursting properties of CA3 pyramidal neurons). Adapted from (15), with permission of John Wiley & Sons.