Changes in cytochrome oxidase in the piriform cortex after status epilepticus in adult rats

The piriform cortex is involved in genesis and propagation of temporal lobe seizures. Degenerating neurons demonstrated by FluoroJade B staining are visible early after status epilepticus (SE) as well as after longer intervals. Furthermore, the piriform cortex is activated during an early phase of experimental temporal seizures, as described by magnetic resonance imaging (MRI) studies. It indicates that the early activity of the piriform cortex should be accompanied by increased adenosine triphosphate (ATP) production. Cytochrome oxidase activity in the brain may be used as an endogenous metabolic marker for neurons. The present research studied activity of the cytochrome oxidase separately in the rostral and caudal parts of the piriform cortex after lithium chloride-pilocarpine-induced SE in adult rats.

SE was induced by a single dose of pilocarpine (40 mg/kg) in LiCl-pretreated adult Wistar rats. Cytochrome oxidase activity was mapped by optical density on sections stained with histochemistry separately in the rostral and caudal parts of the piriform cortex.

Optical density of the rostral part of the piriform cortex remained nearly unchanged at both 1 week (0.284 +/- 0.009 in SE group vs. 0.297 +/- 0.005 in controls) and 3 months (0.318 +/- 0.007 in SE group vs. 0.333 +/- 0.004 in controls) after SE intervals. The caudal part of the piriform cortex showed a decrease of optical density in both groups at 1 week (0.265 +/- 0.007 in SE group vs. 0.285 +/- 0.009 in controls) and 3 months after SE (0.292 +/- 0.006 in SE animals vs. 0.310 +/- 0.003 in controls), respectively. Nissl-stained sections demonstrated a marked neuronal loss and gliosis and/or necrotic cavities through the caudal piriform cortex 1 week after SE.

Our results demonstrated that damage of the piriform cortex is not homogeneous and thus that its parts are differently involved in epileptic activity.