Pentylenetetrazol-kindling induced synaptic plasticity in the CA1 region of rat hippocampus
Mohammad Reza Palizvan, Y Fath Elahi
Abstract
Mohammad Reza Palizvan, Y Fath Elahi
Abstract
The impact of pentylenetetrazol-induced kindling on the effectiveness of theta pattern primed-bursts (PBs) for the induction of long-term potentiation (LTP) of field excitatory postsynaptic potentials (fEPSP) and population spikes (PS) were investigated in hippocampal CA1 of pentylenetetrazol-kindled rats in vivo. The results showed that shortly after kindling, control animals had normal LTP of fEPSP slope and PS amplitude in response to PBs, but kindled rats lack LTP of fEPSP slope and PBs induced LTP of PS amplitude in most of kindled animals. At days 30-33 after kindling, PB potentiation was not observed in the stratum radiatum of kindled animals but PBs induced LTP of PS amplitude, which was significantly greater than that of control animals. The effect is compatible with the hypothesis, which postulates kindling-associated functional deficit in hippocampus, especially CA1, as an explanation for the behavioral deficits seen with the kindling model of epilepsy.
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The impact of pentylenetetrazol-induced kindling on the effectiveness of theta pattern primed-bursts (PBs) for the induction of long-term potentiation (LTP) of field excitatory postsynaptic potentials (fEPSP) and population spikes (PS) were investigated in hippocampal CA1 of pentylenetetrazol-kindled rats in vivo. The results showed that shortly after kindling, control animals had normal LTP of fEPSP slope and PS amplitude in response to PBs, but kindled rats lack LTP of fEPSP slope and PBs induced LTP of PS amplitude in most of kindled animals. At days 30-33 after kindling, PB potentiation was not observed in the stratum radiatum of kindled animals but PBs induced LTP of PS amplitude, which was significantly greater than that of control animals. The effect is compatible with the hypothesis, which postulates kindling-associated functional deficit in hippocampus, especially CA1, as an explanation for the behavioral deficits seen with the kindling model of epilepsy.
Key concepts: Pentylenetetrazol, Kindling, Long-term potentiation, Excitatory postsynaptic potential, Population spike, Hippocampal formation, Hippocampus, Neuroscience