K. Alici et al., COMPARISON OF EFFECTS INDUCED BY TOXIC APPLICATIONS OF KAINATE AND GLUTAMATE AND BY GLUCOSE DEPRIVATION ON AREA CA1 OF RAT HIPPOCAMPAL SLICES, Brain research, 738(1), 1996, pp. 109-120
Baseline and stimulus-induced changes in [Ca2+](o) and [K+](o) as well
as field potentials (fp's) were studied during application of the exc
itatory amino acids kainate or glutamate, or during glucose deprivatio
n in area CA1 and CA3 of rat hippocampal slices. Bath application of k
ainate in concentrations of 1, 2, 5, 8 and 10 mM induced a sudden rapi
d fall of [Ca2+](o) in area CA1, associated with a negative shift of t
he slow fp. Kainate induced disappearance of stratum radiatum (SR) as
well as alveus stimulation-evoked postsynaptic fp's, with partial reco
very after application of up to 2 mM kainate, but no recovery after 5
mM kainate. Only afferent volleys and repetitive SR stimulation-induce
d decreases of [Ca2+](o) recovered after 5 mM kainate. Similar observa
tions were made with glutamate. Only when glutamate was applied with 2
0 mM, irreversible disappearance of postsynaptic fp's was noted. Gluco
se deprivation for 60-90 min led to an initial slow decline of [Ca2+](
o) in area CA1 and CA3, associated with increases in [K+](o), but no s
ignificant changes in the fp baseline. Before reaching the lowest leve
l in [Ca2+](o), stimulation of afferent and efferent fibres in area CA
1 and CA3 evoked epileptiform discharges. After reaching the lowest le
vel in [Ca2+](o), all postsynaptic potential components were irreversi
bly abolished, sparing afferent volleys and SR stimulation-induced dec
reases in [Ca2+](o). The application of the glutamate receptor antagon
ists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 30 mu M) and L-2-amin
o-5-phosphonovalerate (2APV, 30 mu M) during glucose deprivation did n
ot prevent irreversible loss of alveus and SR stimulation-induced post
synaptic signals. These findings suggest that glutamate release during
glucose deprivation is not the main factor of acute cell damage.