Abstract
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 imlmunoreactivity 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 GABAimmunoreactive neurons
was observed at all tilme-points analysed, a transitory effect on PV immunoreactivity was seen at P7 and P21, while no modifications
in the number of CEI-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.
Lingua originale | English |
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pagine (da-a) | 93-96 |
Numero di pagine | 4 |
Rivista | Neuroscience Letters |
Volume | 1996 |
Stato di pubblicazione | Pubblicato - 1996 |
Keywords
- Calbindin
- Development
- Hippocampus
- Parvalbumin
- Perinatal asphyxia
- Vulnerability
- gamma-aminobutyric acid