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Online edition:ISSN 2434-3404

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A study of regional cerebral blood flow (rCBF), distribution of benzodiazepine receptor and nueronal density and alteration after transient forebrain ischemia in the mongolian gerbil *

The response of many intracerebral receptors to ischemic insult is not known. In particular, there have been few reports comparing regional cerebral blood flow (rCBF) and the distribution of inhibitive benzodiazepine receptor (BZR) and neuronal density in the whole brain. Furthermore, there have only a few chronological experiments comparing rCBF following transient forebrain ischemia (five minutes) with the distribution of BZR. In the present experiment, we determined rCBF and the distributions of BZR and neurons employing the procedures of nuclear medicine and histology in normal mongolian gerbils. The binding of radioligands,N-isopropyl-p- 〔123 Ⅰ〕iodoamphetamine (123Ⅰ -IMP) and 125Ⅰ -iomazenil (125Ⅰ -IMZ), was determined autoradiographically to the brain to estimate the rCBF and BZR in each region. The density of neurons was determined by counting the number of neurons stained by hematoxylin - eosin (HE stain) in the corresponding regions to that examined by autoradiography (ARG). Then a model of transient forebrain ischemia was prepared to compare the CA1 region of the hippocampus, with a region which was demonstrated no change in neurons. In the CA1 region of the hippocampus, delayed neuronal death was occurred after five minutes of transient forebrain ischemia. It was observed that rCBF was high in regions where the density of neurons tended to be high except thalamus and dentate gyrus of the hippocampus. There was no confirmed relationship between the rates of accumulation of the BZR and the densities of neurons. It was suggested that the BZR distribution might be different in each neuron . After the ischemic treatment, the rCBF level was transiently elevated in the CA1 region of the hippocampus. No obvious reduction of BZR was observed in the CA1 region in spite of some neurons died. It was proved that the distribution of BZR in the acute phase after the ischemic insult do not always reflect the survival rate of neurons. (Accepted on October 31, 1997) Kawasaki Igakkaishi 23(3) : 175-184, 1997

Author
Nakamura H
Volume
23
Issue
3
Pages
175-184
DOI
10.11482/KMJ23(3)175-184.1997.pdf

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