Abstract We examined the impact of hypoxia‐ischemia on high‐affinity [3H]glutamate uptake into a synaptosomal fraction prepared from immature rat corpus striatum. In 7‐day‐old pups the right carotid artery was ligated, and pups were exposed to 8% oxygen for 0, 0.5, 1, or 2.5 h, and allowed to recover for up to 24 h before they were killed. High‐affinity glutamate uptakes in striatal synaptosomes derived from tissue ipsilateral and contralateral to ligation were compared. After 1 h of hypoxia plus ischemia, high‐affinity glutamate uptake in the striatum was reduced by 54 ± 13% compared with values from the opposite (nonischemic) side of the brain (p < 0.01, t test versus ligates not exposed to hypoxia). There were similar declines after 2.5 h of hypoxiaischemia. Activity remained low after a 1 h recovery period in room air, but after 24 h of recovery, high‐affinity glutamate uptake was equal bilaterally. Kinetic analysis revealed that loss of activity could be attributed primarily to a 40% reduction in the number of uptake sites. Hypoxia alone had no effect on high‐affinity glutamate uptake although it reduced synaptosomal uptake of [3H]3,4‐dihydroxyphenyl‐ethylamine. Addition of 1 mg/ml of bovine serum albumin to the incubation medium preferentia'ly stimulated high‐affinity glutamate uptake in hypoxic‐ischemic brain compared with its effects in normal tissue. These studies demonstrate that hypoxia‐ischemia reversibly inhibits high‐affinity glutamate uptake and this occurs earlier than the time required to produce neuronal damage in the model.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Neurochemistry|
|State||Published - Nov 1986|
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience