Quantitative receptor autoradiography was used to measure the binding of
gamma-aminobutyric acid (
GABA) and
benzodiazepine receptors after
ischemia by means of transient occlusion of bilateral common carotid arteries in the gerbil. [3H]
Muscimol was used to label the GABAA receptors and [3H]
flunitrazepam to label central type
benzodiazepine receptors. In the superolateral convexities of the frontal cortices, [3H]
muscimol binding was increased in 60% of the animals killed 3 days after
ischemia, and decreased in 67% of the animals killed 27 days after
ischemia. Twenty-seven days after
ischemia, [3H]
flunitrazepam binding in the substantia nigra pars reticulata increased to 252% of the control, though the increase in [3H]
muscimol binding was not significant. In the dorsolateral region of the caudate putamen, marked neuronal
necrosis and depletion of both [3H]
muscimol and [3H]
flunitrazepam binding sites were observed 27 days after
ischemia, the ventromedial region being left intact. In spite of the depletion of pyramidal cells in the CA1 region of the hippocampus, both [3H]
muscimol and [3H]
flunitrazepam binding sites were preserved 27 days after
ischemia. Since our previous study revealed that
adenosine A1 binding sites were depleted in the CA1 subfield of the hippocampus after
ischemia correlating with neuronal damage, GABAA and
benzodiazepine receptors may not be distributed predominantly on the pyramidal cells in the CA1 region.