Abstract
In Mg 2+-free aCSF, bursting discharges were induced in the posterior telencephalon of zebrafish following an electrical stimulation of the anterior telencephalon. The bursting discharges were partially reduced by CNQX (10 μM), an AMPA receptor antagonist, and the remaining activity was completely blocked by an additional treatment of APV (50 μM), an NMDA receptor antagonist. Long-term potentiation that lasted more than 1 h was also induced after 20 min of perfusion with KCl (10 mM). The degree of KCl-induced long-term potentiation (K-LTP) was reduced when a concomitant electrical stimulation was not delivered during a KCl perfusion. K-LTP was blocked by APV (50 μM) but not by nifedipine (10 μM), an L-type Ca 2+ channel blocker. Furthermore, K-LTP was not induced in the presence of a broad spectrum inhibitor for protein kinases, H-7 (10 μM). These results suggest that NMDA receptors and protein kinases play important roles in the synaptic plasticity of the zebrafish brain.
Published Version
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