Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Journal of Comparative Neurology |
| Vol/bind | 281 |
| Udgave nummer | 1 |
| Sider (fra-til) | 40-53 |
| Antal sider | 13 |
| ISSN | 0021-9967 |
| DOI | |
| Status | Udgivet - 1989 |
| Udgivet eksternt | Ja |
Bibliografisk note
Keywords: Animals; Glutamate Decarboxylase; Hippocampus; Immunohistochemistry; Ischemic Attack, Transient; Male; Rats; Rats, Inbred Strains; Time FactorsAdgang til dokumentet
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I: Journal of Comparative Neurology, Bind 281, Nr. 1, 1989, s. 40-53.
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Immunocytochemical investigation of L-glutamic acid decarboxylase in the rat hippocampal formation: the influence of transient cerebral ischemia.
AU - Johansen, Flemming Fryd
AU - Lin, C T
AU - Schousboe, A
AU - Wu, J Y
N1 - Keywords: Animals; Glutamate Decarboxylase; Hippocampus; Immunohistochemistry; Ischemic Attack, Transient; Male; Rats; Rats, Inbred Strains; Time Factors
PY - 1989
Y1 - 1989
N2 - The hippocampus is especially vulnerable to ischemic damage. Neurons in the CA3c region and dentate hilus demonstrate fast progressive damage while CA1 pyramidal cells demonstrate delayed neuronal damage. The delayed CA1 pyramidal cell loss could be caused by postischemic neuronal hyperactivity if hippocampal interneurons are lost after ischemia. Therefore we have counted the L-glutamic acid decarboxylase (GAD)-immunoreactive neurons in the hippocampus from control rats and rats surviving 4 or 11 days after 20 minutes of cerebral ischemia. All rats were injected intraventricularly with colchicine before they were killed. The hippocampal cell counts showed an increase in GAD-immunoreactive somata visualized on the fourth postischemic day. Eleven days after ischemia, the number of GAD-immunoreactive neurons visualized in the hippocampus CA1 and CA3c region decreased. GAD-immunoreactive baskets were visualized in the pyramidal cell layer and the granule cell layer in controls and 4 days after ischemia, but not in the CA1 and CA3c pyramidal cell layer 11 days after ischemia. We suggest the number of GAD-immunoreactive neurons visualized on the fourth postischemic day increases because somatal GAD accumulation increases and, therefore, ischemia may enhance GAD production. Our previous counts of CA1 interneurons 21 days after ischemia in toluidine-stained semithin sections demonstrated no interneuron loss. Therefore we suggest that the decreased number of CA1 and CA3c GAD-immunoreactive neurons visualized 11 days after ischemia is related to a decreased GAD production. It is possible at this stage after ischemia that the interneurons have decreased their GAD production because they have lost their input and/or target cells. We conclude that our counts of GAD-immunoreactive neurons visualized after ischemia express changes in the content of somatal GAD rather than the actual number of GAD-immunoreactive somata. Finally, we conclude that the delayed loss of CA1 pyramidal cells seen 4 days after ischemia is not preceded by loss of hippocampal GAD-immunoreactive neurons.
AB - The hippocampus is especially vulnerable to ischemic damage. Neurons in the CA3c region and dentate hilus demonstrate fast progressive damage while CA1 pyramidal cells demonstrate delayed neuronal damage. The delayed CA1 pyramidal cell loss could be caused by postischemic neuronal hyperactivity if hippocampal interneurons are lost after ischemia. Therefore we have counted the L-glutamic acid decarboxylase (GAD)-immunoreactive neurons in the hippocampus from control rats and rats surviving 4 or 11 days after 20 minutes of cerebral ischemia. All rats were injected intraventricularly with colchicine before they were killed. The hippocampal cell counts showed an increase in GAD-immunoreactive somata visualized on the fourth postischemic day. Eleven days after ischemia, the number of GAD-immunoreactive neurons visualized in the hippocampus CA1 and CA3c region decreased. GAD-immunoreactive baskets were visualized in the pyramidal cell layer and the granule cell layer in controls and 4 days after ischemia, but not in the CA1 and CA3c pyramidal cell layer 11 days after ischemia. We suggest the number of GAD-immunoreactive neurons visualized on the fourth postischemic day increases because somatal GAD accumulation increases and, therefore, ischemia may enhance GAD production. Our previous counts of CA1 interneurons 21 days after ischemia in toluidine-stained semithin sections demonstrated no interneuron loss. Therefore we suggest that the decreased number of CA1 and CA3c GAD-immunoreactive neurons visualized 11 days after ischemia is related to a decreased GAD production. It is possible at this stage after ischemia that the interneurons have decreased their GAD production because they have lost their input and/or target cells. We conclude that our counts of GAD-immunoreactive neurons visualized after ischemia express changes in the content of somatal GAD rather than the actual number of GAD-immunoreactive somata. Finally, we conclude that the delayed loss of CA1 pyramidal cells seen 4 days after ischemia is not preceded by loss of hippocampal GAD-immunoreactive neurons.
U2 - 10.1002/cne.902810105
DO - 10.1002/cne.902810105
M3 - Journal article
C2 - 2925901
SN - 0021-9967
VL - 281
SP - 40
EP - 53
JO - Journal of Comparative Neurology
JF - Journal of Comparative Neurology
IS - 1
ER -