Morphofunctional changes in field CA1 of the rat hippocampus after pentylenetetrazole and lithium-pilocarpine induced seizures

Animal models of seizures and epilepsy are very diverse and instrumental for elucidating the mechanisms that underlie convulsive states and epileptogenesis. A single injection of pentylenetetrazole (PTZ) induces seizures, however, does not raise the risk of further development of epilepsy. Pilocarpine, immediately after injection, evokes epileptical state and, following a latent period, results in the development of spontaneous seizures, i.e. the drug triggers epileptogenesis. Assuming that in the PTZ model morphofunctional changes are mainly transient, while changes in the lithium-pilocarpine (PC) model may indicate the brain epileptization, we set ourselves the task of comparing morphological and functional characteristics of the hippocampal field CA1 in control and two experimental animal groups in 24 h after injection of the convulsants. We revealed the changes specific to the PC model and indicating neurodegeneration: a decrease in the cell spacing density, a diminution in the number of the viable NeuN-expressing neurons, an increased activity of the proapoptotic protease caspase-3. A characteristic feature of the PTZ model was the appearance of hyperchromic neurons with normal viability. In both models, the expression of the excitatory amino acid carrier EAAT1 increased by about 40% as compared to control. These morphofucntional correlates of reversible changes in the nervous tissue caused by seizures, as well as the early disorders leading to long-term brain epileptization can be used as indicators allowing assessment of a therapeutic potential of novel anticonvulsive drugs.