Different Mechanisms May Be Required For Maintenance Of Nimda Receptor-dependent And Independent Forms Of Long-term Potentiation

Different Mechanisms May Be Required For Maintenance Of Nimda Receptor-dependent And Independent Forms Of Long-term Potentiation

Grover L M; Teyler T J

Synapse

1995

1995-02

In hippocampal area CA1, long-term potentiation (LTP) is induced by tetanic stimulation protocols that activate N-methyl-D-aspartate (NMDA) receptors. In addition, some stimulation protocols can induce LTP during NMDA receptor blockade. An initial signal in both NMDA receptor-dependent and independent LTPs is increased intracellular Ca2+ concentration in postsynaptic neurons. It therefore seems possible that subsequent steps leading to expression and maintenance of potentiation are shared whether or not LTP is induced through NMDA receptor activation. We tested this hypothesis by applying a broad spectrum protein kinase inhibitor, previously shown to inhibit NMDA receptor-dependent LTP. In agreement with earlier reports, we found that H-7 inhibited NMDA receptor-dependent LTP when applied either during tetanic stimulation, or beginning 30 min following tetanic stimulation. In contrast, NMDA receptor-independent LTP was not inhibited by H-7 applied during or following tetanic stimulation. We also tested for mutual occlusion between NMDA receptor-dependent and independent LTPs. Although induction of NMDA receptor-independent LTP did not occlude later induction of NMDA receptor-dependent LTP, induction of NMDA receptor-dependent LTP did occlude NMDA receptor-independent LTP. While the kinase inhibitor experiment showed a clear difference between NMDA receptor-dependent and independent LTPs, the occlusion experiments suggest an interaction between the signalling pathways for the two LTPs. (C) 1995 Wiley-Liss, Inc.

activation; area; ca1; calcium; calcium channels; calmodulin inhibitors; d-aspartate receptors; dentate gyrus; depression; glutamate; hippocampal slice; induction; Neurosciences & Neurology; protein kinase; protein-kinase-c; rat hippocampal slices

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