We investigated the postischemic alterations in [3H]
MK-801, [3H]
muscimol, and [3H]
naloxone binding in the gerbil brain, and examined the effect of
pentobarbital against these alterations. [3H]
MK-801, [3H]
muscimol, and [3H]
naloxone were used to label
N-methyl-D-aspartate (
NMDA), gamma-aminobutyric acidA (GABAA), and
opiate receptors, respectively.
Transient cerebral ischemia was induced for 10 min, and
pentobarbital (40 mg/kg) was administered intraperitoneally 30 min before
ischemia. Five hours after
ischemia, no conspicuous alteration in [3H]
MK-801, [3H]
muscimol, and [3H]
naloxone binding was found in the striatum and hippocampus. Seven days after
ischemia, [3H]
MK-801 and [3H]
naloxone binding was significantly decreased in the striatum and hippocampal area where histological neuronal damage was noted. By contrast, no significant change in [3H]
muscimol binding was seen in the above regions except for the hippocampal CA3 sector. The treatment of
pentobarbital caused a significant alteration in the binding of [3H]
naloxone and [3H]
muscimol in various brain areas 5 h after
ischemia. However, this
drug showed no significant change in [3H]
MK-801 binding in the brain. Seven days after
ischemia,
pentobarbital partly ameliorated a significant reduction in [3H]
MK-801 and [3H]
naloxone binding in the striatum and hippocampus. A histological study also showed that
pentobarbital afforded neuronal protection against the damage to the brain except for the hippocampal CA1 sector 7 days after
ischemia. These results suggest that
NMDA and
opiate receptors are damaged after
ischemia, whereas GABAA receptors are unaffected. They also demonstrate that
opiate receptors are severe affected by the treatment of
pentobarbital, compared with
NMDA and GABAA receptors. These findings are of interest in relation to the mechanism of ischemic neuronal damage.