Abstracts

Rationale: At present it is unknown if histamine is released as consequence of seizure activity and its role in the subsequent brain damage. Experiments were designed to evaluate acute changes in the histamine release, mast cell number and neuronal damage in hippocampus induced by status epilepticus. We also investigated the neuroprotective effect of sodium cromoglycate in the pilocarpine-induced hippocampal damage as well its correlation with histamine, γ-aminobutyric acid (GABA) and glutamate release. Methods: Male Wistar rats previously implanted with a bipolar electrode coupled to a guide cannula into the right ventral hippocampus were used to evaluate the release of neurotransmitters during microdialysis experiments. A group of rats (SS-SE group, n=8) pretreated with methylscopolamine (2 mg/kg, i.p.) received the administration of pilocarpine to induce status epilepticus during the microdialysis procedure. A group of rats (CG-SE group, n=5) were pretreated with sodium cromoglycate 30 min before pilocarpine injection. A control group (n=6) was manipulated as described above for the SS-SE group, except that animals received vehicle administration instead of pilocarpine. Twenty-four hours after the status epilepticus, the brains were used to determine the neuronal damage (Fluoro-Jade staining) and the number of mast cells (toluidine blue staining) in hippocampus. Results: During the status epilepticus, SS-SE group showed an enhanced release of histamine (138.5%, p=0.005), GABA (331±91%, p≤0.001) and glutamate (467%, p≤0.001), an effect that was not modified by diazepam injection. One day after the status epilepticus, the hippocampus of the SS-SE group demonstrated increased number of mast cells (Stratum pyramidale of CA1, 88%, p<0.001) and neuronal damage (dentate gyrus, 417.3±127.1 cells/mm