Abstracts

Rationale: Epileptic events elicit an increase in neuronal metabolism and an increase in cerebral blood flow (CBF), bringing oxygenated hemoglobin to the activated neurons. Our previous studies have suggested that CBF has a monophonic increase in the focus and biphasic transient decrease in the surround. For the tissue oxygen, seizures induce a transient dip flowed by an increase in the focus and a sustained increase in the surround. The brain energy need is met predominantly through oxygen consumption mediated by the mitochondrial respiratory chain. Whether local oxygen consumption is coupled to the seizure activity in the focus and surround is unknown. Methods: We induced acute focal seizures in the rat neocortex by 4-aminopyridine (4-AP, 15mM, 0.5 ?l) injection. Local field potential was recorded to identify ictal discharge. Partial pressure of tissue oxygen (pO2) and CBF were measured with one Clark-style polarographic oxygen microelectrode and a laser Doppler flowmetry probe placed close to the oxygen electrode, which located in the focus or surround. Cerebral metabolic oxygen consumption (CMRO2) was calculated from CBF and pO2 measurements using Gjedde s equation (2005). Results: The total of 127 seizures was recorded from 11 rats. CMRO2 increased to a maximum of 14.701 3.794 % of baseline (n=9 rats, 54 seizures) in the focus. In the surround region, CMRO2 decreased at a peak of -8.307 2.54 % in 5 of 8 rats (n=43 seizures) and decreased to -5.711 1.427 % after a transit increase of 6.298 1.279 % in 3 of 8 rats (n=39 seizures). Conclusions: These results demonstrated a significant increase of oxygen consumption rate in the focus and two types of CMRO2 decrease in the region of surround cortex. This surround oxygen consumption suppression may be responsible for circuit neuronal injury associated with epileptic events