Contribution of ionotropic glutamate receptors and voltage-dependent calcium channels to the potentiation phenomenon induced by transient pentylenetetrazol in the CA1 region of rat hippocampal slices.

The role of ionotropic glutamate receptors and voltage-dependent calcium channels (VDCCs) in potentiation phenomenon and epileptic activity induced by a transient pentylenetetrazol (PTZ) application in the CA1 region of rat hippocampal slices was investigated. Also we examined whether adenosine as an inhibitory neuromodulator would interact with expression of the long-lasting effect of transient PTZ. Population spikes (PS) were recorded in the CA1 cell body layer of the hippocampal slices following stratum radiatum stimulation. Changes in the PS amplitude potentiation and number of extra PS, which induced by transient PTZ were used as indices to quantify the effects of drugs. PS input-output curve was significantly increased 10 min after PTZ application and persisted at least for 60 min after PTZ washout. Polyspikes also appeared, but did not persist. Both ketamine and APV reduced the extent of potentiation of PS amplitude but had no effect on number of extra PS. The selective non-NMDA receptor antagonist CNQX prevented the amplitude potentiation and the generation of extra PS. The blocker of VDCCs, verapamil, prevented the amplitude potentiation and inhibited polyspike activity. Co-application of adenosine and PTZ produced a rapid and reversible decrease in the PS amplitude, but PTZ-induced potentiation phenomenon was observed after washout. It is concluded that ionotropic glutamate receptors as well as VDCCs involve in the PTZ-induced LTP of PS amplitude. PTZ-induced LTP is also insensitive to adenosine. The epileptiform activity induced by a transient PTZ application could be attributed to VDCCs. The polyspikes mediated by VDCCs are dependent on prior activation of AMPA receptors.