US EPA

5388303 

Journal Article 

Accumulation of calcium in substantia nigra lesions induced by status epilepticus. A microprobe analysis 

Inamura, K; Martins, E; Themner, K; Tapper, S; Pallon, J; Lövestam, G; Malmqvist, KG; Siesjö, BK 

1990 

Yes 

Brain Research
ISSN: 0006-8993
EISSN: 1872-6240 

514 

1 

49-54 

English 

2357529 

10.1016/0006-8993(90)90434-d 

Status epilepticus of sufficient duration (greater than 30 min) causes a unique lesion of substantia nigra pars reticulata (SNPR), and of globus pallidus (GP). This lesion, which encompasses a pan-necrotic destruction of neurons and glial cells seems to develop during ongoing seizures. We decided to investigate if the lesion is accompanied by net calcium accumulation. Seizures of 20 and 60 min duration were induced by the administration of flurothyl, and the tissue was frozen in situ either at the end of the seizure periods, or after recovery periods of 15 or 120 min. The total calcium and potassium contents of caudoputamen, neocortex, GP and SNPR were measured using particle induced X-ray emission (PIXE) in the microprobe mode. Seizures of 20 min duration did not cause net accumulation of calcium. When the duration of seizures was extended to 60 min the results varied depending on the location. In caudoputamen, which does not incur neuronal damage, no calcium accumulation was observed. In GP and SNPR, such a rise was unequivocally demonstrated, with calcium content increasing to about 150% of controls. The increase in calcium correlated to a decrease in potassium content. It is concluded that epileptic cell death occurs pari passu with accumulation of calcium although it cannot be stated that this accumulation is the cause of the cell death. It is speculated that seizures increase the permeability of the blood-brain barrier to calcium, and that enhanced blood to tissue transfer increases the calcium load of metabolically strained cells.