PARVALBUMIN IMMUNOREACTIVITY IN THE HIPPOCAMPUS OF THE GERBIL AFTER TRANSIENT FOREBRAIN ISCHEMIA - A QUALITATIVE AND QUANTITATIVE SEQUENTIAL STUDY

Citation
A. Tortosa et I. Ferrer, PARVALBUMIN IMMUNOREACTIVITY IN THE HIPPOCAMPUS OF THE GERBIL AFTER TRANSIENT FOREBRAIN ISCHEMIA - A QUALITATIVE AND QUANTITATIVE SEQUENTIAL STUDY, Neuroscience, 55(1), 1993, pp. 33-43
Citations number
70
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03064522
Volume
55
Issue
1
Year of publication
1993
Pages
33 - 43
Database
ISI
SICI code
0306-4522(1993)55:1<33:PIITHO>2.0.ZU;2-A
Abstract
Parvalbumin immunoreactivity is examined in the hippocampus of the Mon golian gerbil (Meriones unguiculatus) in controls and in animals subje cted to 20 min of forebrain ischaemia produced by bilateral clipping o f the carotids. In comparison with other species, the hippocampus of t he gerbil is characterized by strong immunoreactivity of the (presumab ly excitatory) perforant pathway, and weak immunoreactivity (low numbe rs of neurons and scarce dendritic arbors) in nonpyramidal nerve cells (inhibitory neurons) of the CA1 area. These properties may play some role in the development and maintenance of seizures in this susceptibl e species. Parvalbumin immunoreactivity is rapidly and ephemerally inc reased in the hippocampus 15 min after reperfusion. Later on, there is a transitory decrease of parvalbumin immunoreactivity which is follow ed by an increase 6 h later in the stratum granulare hilus and CA3 are a, and not until the first and second days in the CA1 area. This incre ase significantly surpasses the number of immunoreactive neurons in co ntrol animals in CA1 and CA3 from 48 h after reperfusion onwards. The effect is similar using different anaesthetics and does not occur in s ham-operated animals. In contrast with these findings, the number of p arvalbumin-immunoreactive neurons in the somatosensory cortex is not a ffected in our model of forebrain ischaemia. On the other hand, GABA-i mmunoreactive neurons in CA1 are preserved during the first week after reperfusion, although an increase in the number of these cells occurs at the end of this period. Delayed neuronal death occurs in the CA1 a rea 48 h after ischaemia, and marked reduction in the number of CA1 ne urons is found by the end of the first week. Eighty per cent of the re maining cells in CA1 at day 7, and 83% at day 15, are parvalbumin-immu noreactive nonpyramidal neurons in contrast to 3% parvalbumin-immunore active cells in control animals. These findings indicate that GABAergi c neurons in CA1 are preserved after forebrain ischaemia, and that par valbumin in CA1 neurons is associated with survival.