GABAergic neurons in the striatum are very sensitive to the effects of
ischemia. The progressive decline in striatal GABA following transien
t forebrain ischemia in gerbils may be secondary to either a decreased
production or an increase in reuptake mechanisms or both. The current
experiment was designed to evaluate release of GABA by stimulation wi
th K+ or inhibition of its uptake with nipecotic acid or their combina
tion (K+nipecotic) after repetitive forebrain ischemia in gerbils by i
n-vivo microdialysis on Days 1, 3, 5, and 14 following the insult. Inf
usion of nipecotic acid or potassium chloride, resulted in a significa
nt increase in extracellular GABA. This response was significantly dec
reased in the post-ischemic animals. The synergistic effect of increas
ed GABA concentrations by the infusion of nipecotic acid + potassium c
hloride seen in the controls was not evident in the post-ischemic anim
als. In conclusion, though there is a reduction in the extracellular G
ABA concentrations in the first week following an ischemic insult, res
torative mechanisms are operative in the second week as seen by the in
creasing GABA concentrations.