POOR CORRELATION BETWEEN DELAYED NEURONAL DEATH INDUCED BY TRANSIENT FOREBRAIN ISCHEMIA, AND IMMUNOREACTIVITY FOR PARVALBUMIN AND CALBINDIND-28K IN DEVELOPING GERBIL HIPPOCAMPUS

Citation
A. Tortosa et I. Ferrer, POOR CORRELATION BETWEEN DELAYED NEURONAL DEATH INDUCED BY TRANSIENT FOREBRAIN ISCHEMIA, AND IMMUNOREACTIVITY FOR PARVALBUMIN AND CALBINDIND-28K IN DEVELOPING GERBIL HIPPOCAMPUS, Acta Neuropathologica, 88(1), 1994, pp. 67-74
Citations number
40
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00016322
Volume
88
Issue
1
Year of publication
1994
Pages
67 - 74
Database
ISI
SICI code
0001-6322(1994)88:1<67:PCBDND>2.0.ZU;2-M
Abstract
In the normal developing hippocampus of the gerbil, parvalbumin-immuno reactive neurons first appear in the stratum pyramidale of CA3 at post natal day 15 (P15), and in CA2 and hilus of the dentate gyrus from P21 onwards. Immunoreactive terminals also follow the same sequence from CA3 to CA1 to reach adult patterns by the end of the 1st month. Calbin din D-28k immunoreactivity is seen in the external part of the upper b lade of the dentate gyrus at P5, and progresses to the granule cell an d molecular layers of the whole gyrus by P15, except for a thin band o f immature cells located at the base of the granule cell layer which a re calbindin negative. Calbindin immunoreactivity in messy fibers prog resses from the external to the hilar region of CA3 during the same pe riod. A few immunoreactive cells are also found in the stratum radiatu m/lacunare of the CA3, but no calbindin-immunoreactive cells are obser ved in the CA1 and CA2 subfields. The adult pattern of calbindin immun oreactivity is reached at P21. Vulnerability following transient foreb rain ischemia for 20 min was examined in the hippocampal formation of gerbils during postnatal development. No cellular damage was seen in a nimals aged 7 days. Dying cells were observed at the base of the granu le cell layer of the dentate gyrus in animals aged 15, 21 and 30 days. Pyramidal cells in the CA3 subfield were also sensitive to ischemia i n gerbils aged 15 days, and less frequently in animals aged 21 days. T he adult pattern of cellular damage, characterized by selective vulner ability of the CA1 subfield, was seen from day 30 onwards. These findi ngs show that the pattern of selective vulnerability following transie nt forebrain ischemia is different in young and adult gerbils, and sug gest that little, if any, correlation exists between resistance to del ayed cellular damage and parvalbumin and calbindin D-28k content in th e hippocampus of young gerbils.