| First Author | Velísek L | Year | 1995 |
| Journal | Brain Res | Volume | 671 |
| Issue | 2 | Pages | 245-53 |
| PubMed ID | 7743211 | Mgi Jnum | J:22929 |
| Mgi Id | MGI:70800 | Doi | 10.1016/0006-8993(94)01336-g |
| Citation | Velisek L, et al. (1995) Resistance of hippocampal synaptic transmission to hypoxia in carbonic anhydrase II-deficient mice. Brain Res 671(2):245-53 |
| abstractText | Mutant Car2n/Car2n mice deficient in carbonic anhydrase II (CA II; a major brain CA isozyme) suffer from systemic acidosis and are more resistant to experimental seizures than their normal littermates (+/+ or +/Car2n). The N-methyl-D-aspartate (NMDA) subtype of glutamate receptor has been shown to contribute to long-term potentiation (LTP) of synaptic transmission, hypoxic/ischemic neuronal injury and to be blocked by extracellular protons (acidosis). We compared the effects of hypoxia on synaptic transmission and LTP in field CA1 of hippocampal slices from CA II-deficient mice to their normal littermates. Slices were subjected to successive 5, 10 and 15 min-periods of hypoxia with 30 min-recovery periods in between. Hippocampal slices from mutant, CA II-deficient mice, were more resistant to all periods of hypoxia tested than slices from normal littermates. In a separate set of mutant and normal slices, there were no differences in LTP of population spike amplitude. The relative resistance of CA II-deficient mice to hypoxia-induced damage may be a consequence of severe interstitial acidosis. The sustained influence of increased extracellular proton concentrations may change the characteristics of NMDA receptors resulting in an increased resistance of synaptic transmission in CA II-deficient mice to hypoxia compared to controls. |
