Selective vulnerability in the gerbil hippocampus: Morphological changes after 5-min ischemia and long survival times

Abstract

The morphology of the hippocampus of Mongolian gerbils was investigated by light and electron microscopy after 5-min forebrain ischemia and survival times of up to 10 months. After 3 weeks recirculation only 5.8% of pyramidal neurons of the CA1 (cornu ammonis 1) sector had survived but the thickness of the inner and outer hippocampal layers did not change. After recirculation times of 6 and 10 months the number of surviving neurons declined no further but all layers of the CA1 subfield shrank markedly. Ultrastructurally, many but not all surviving CA1 neurons were altered. After 3 weeks both "dark" and "pale" type neurons were present, while after 6 and 10 months only the "pale" type of injury persisted. Axonal enlargements and myelin breakdown were observed at all survival times up to 10 months of recirculation. The astrocytes of CA1 sector contained numerous glial fibrils which were most pronounced after the longer recirculation times. The stratum radiatum presented intact presynaptic terminals densely packed with an abundance of clear vesicles even after survival of 10 months. Initially, morphologically damaged postsynaptic structures were still attached to these terminals but they disappeared after longer recirculation times. However, even after 10 months some intact synapses were observed involving dendrites which probably originated from surviving CA1 neurons. In CA3 sector and dentate gyrus no ultrastructural changes occurred at any survival time.(ABSTRACT TRUNCATED AT 250 WORDS)

Delayed neuronal death in the CA1 pyramidal cell layer of the gerbil hippocampus following transient ischemia is apoptosis

“…Until the present, various morphological, physiological, and biochemical changes have been noted in the CA1 pyramidal neurons after brief ischemia (Ito et al, 1975;Pulsinelli and Brierley, 1979;Kirino, 1982;Suzuki et al, 1983a,b;Kirino and Sano, 1984;Arai et al, 1986;Monmaur et al, 1986;Petit0 et al, 1987;Bonnekoh et al, 1990); however, there has been no accurate definition as to what reversible or irreversible alterations are in the neurons after brief ischemia. The in vitro study of neonatal sympathetic neurons has shown that the decrease in protein synthesis of the cultured neurons after nerve growth factor deprivation is insufficient to cause subsequent death, whereas DNA fragmentation of the neurons occurs close to the neuronal death (Deckwerth and Johnson, 1993).…”

“…Physiological as well as biochemical analyses using animal models have demonstrated that the CA1 pyramidal neurons are normal 24 hr after brief forebrain ischemia (Suzuki et al, 1983a,b;Arai et al, 1986;Monmaur et al, 1986). The CA1 pyramidal neurons of gerbil hippocampus degenerate within 2 to 4 d after transient ischemia (Petit0 et al, 1987) and only 5.8% of the neurons survive 3 weeks later (Bonnekoh et al, 1990). There has been no evidence whether this delayed neuronal death is necrosis or apoptosis.…”

Zonisamide: Pharmacology and Clinical Efficacy in Epilepsy

“…In the gerbil, a 5-min ischemic insult produced substantial damage to the CA1 sector of the hippocampus (6,36). During a brief ischemic insult, there was a rise in extracellular glutamate levels in the hippocampus (5,68) which caused pyramidal cell damage and impairment of cognitive memory task (65).…”

Apoptosis: The History and Trends of Its Studies.

“…Different from permanent ischemia in the central nervous system, transient brain or forebrain ischemia induces delayed neuronal death in the CAl pyramidal layer of the hippocampus (ITo et al, 1975;PULSINELLI and BRIERLEY, et al, 1979;KIRINO, 1982;KIRINO and SANG, 1984a, b;PETITO et al, 1987;BONNEKOH et al, 1990). The CA1 pyramidal cells are known to be physiologically intact 24h after ischemic insult, while they disappear from the CAl layer from 3 to 7 days after ischemic insult.…”