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Reversal of pentylenetetrazol‐induced potentiation phenomenon by theta pulse stimulation in the CA1 region of rat hippocampal slices
Author(s) -
Omrani Azar,
Fathollahi Yaghoub
Publication year - 2003
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.10250
Subject(s) - long term potentiation , excitatory postsynaptic potential , pentylenetetrazol , population spike , stimulation , population , hippocampal formation , chemistry , neuroscience , postsynaptic potential , adenosine , medicine , biology , receptor , inhibitory postsynaptic potential , epilepsy , biochemistry , anticonvulsant , environmental health
The effect of theta pulse stimulation (TPS) on pentylenetetrazol (PTZ)‐induced long‐term potentiation of population spikes was studied in the CA1 region of rat hippocampal slices. The field excitatory postsynaptic potential (fEPSP) and population spikes (PS) were recorded from strata radiatum and pyramidale, respectively, following stimulation of Schaffer collaterals. A transient PTZ application produced a long‐lasting enhancement of PS amplitude. A 3‐min episode of TPS delivered at test‐pulse intensity failed to reverse the PTZ potentiation. However, the same stimulation at a higher intensity produced complete reversal of the PTZ potentiation when delivered during the last minutes of PTZ application. Prior application of high‐intensity TPS also decreased the amount of PTZ potentiation, whereas it had no long‐lasting effect on baseline synaptic responses. High‐intensity TPS induced reversal was blocked by adenosine A1 receptor antagonist and, furthermore, was reduced by protein phosphatase 1 inhibitor. The results suggest that mechanism of PTZ‐induced LTP reversal involves activation of adenosine receptors and protein phosphatases. Synapse 50:83–94, 2003. © 2003 Wiley‐Liss, Inc.