Increased aspartic acid release from the iron-induced epileptogenic focus.
Evidence has been growing in recent years for the involvement of excitatory neurotransmitter amino acids in the etiology of epilepsy. The precise mechanism of this involvement, however, remains unknown. In the present study, in vitro release and uptake of [3H]aspartic acid and [3H]glutamic acid were investigated in focal cerebral cortex in the iron-induced model of post-traumatic epilepsy in the rat. The animals were injected with FeCl3 or saline into the cerebral cortex and release and uptake studied in cortical slices from both acute and chronic foci (30 min and 3 weeks post injection, respectively), using a superfusion system. The results showed: (a) a significant increase in K(+)-stimulated aspartic acid release from the acute iron injected focus as compared to the corresponding saline injected cortex; and (b) no significant differences in the release of glutamic acid or in the uptake of glutamic acid and aspartic acid between the iron injected and the saline injected cortex. The finding of increased aspartic acid release suggests that this amino acid may play a role in the mechanism of iron-induced epilepsy in the rat.
Janjua
N A
NA
Department of Neurochemistry, Okayama University Medical School, Japan.
Mori
A
A
Hiramatsu
M
M
D000208:Acute Disease; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D002908:Chronic Disease; D004827:Epilepsy / Q000139:chemically induced* / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D007501:Iron; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D005971:Glutamates; D001224:Aspartic Acid; D018698:Glutamic Acid; D007501:Iron