Development of GABA and calcium binding proteins immunoreactivity in the rat hippocampus following neonatal anoxia.
The consequences of neonatal anoxia (N2 100% for 25 min at 30 h after birth) on the rat hippocampus were studied 7-60 days postnatally with immunocytochemistry for gamma-aminobutyric acid (GABA), parvalbumin (PV) and calbindin-D28k (CB). In both sham-treated and anoxic rats, GABA immunoreactivity presented a mature expression since early stages, while PV and CB immunoreactivity showed a major postnatal development. In anoxic animals, a significant reduction in the number of hippocampal GABA-immunoreactive neurons was observed at all time-points analysed, a transitory effect on PV immunoreactivity was seen at P7 and P21, while no modifications in the number of CB-immunoreactive neurons could be found. Thus, selective vulnerability of GABA-containing neurons and relative resistance of neurons in which PV or CB immunoreactivity is present or is expressed later, occur in the hippocampus after neonatal anoxia. The role of calcium binding proteins ( CBP) in nerve cell protection is discussed.[1]References
- Development of GABA and calcium binding proteins immunoreactivity in the rat hippocampus following neonatal anoxia. Dell'Anna, E., Geloso, M.C., Magarelli, M., Molinari, M. Neurosci. Lett. (1996) [Pubmed]
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