Abstract
Recent evidence has suggested that cyclosporin A (CsA), an immunosuppressive agent, has neuroprotective properties. However, its mechanisms associated with this activity remain unclear. We have previously shown that post-ischemic administration of CsA daily for 14 days prevented the decrease of muscarinic acetylcholine receptor binding in the hippocampus in the gerbil model of 5-min transient forebrain ischemia. In the present study, CsA (5 mg/kg, subcutaneously) was administered to each animal just after, 2 and 6 h after ischemia so as not to exert its immunosuppressive effect. Initial CsA treatment significantly restored the declined muscarinic acetylcholine receptor binding of the hippocampus 14 days after ischemia similar to the previous report. However, CsA did not alter reactive changes of astrocytes and microgila in the CA1 area of the hippocampus, which had been suppressed by daily administration. These results indicate that CsA could positively modulate the hippocampal acetylcholine neurotransmission system broken down through the ischemia-induced pyramidal cell death and its action mechanism may have no relation to the immunosuppressive properties.
| Original language | English |
|---|---|
| Pages (from-to) | 9-13 |
| Number of pages | 5 |
| Journal | Neurochemical Research |
| Volume | 24 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1999 |
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Keywords
- Acetylcholine receptor
- Cyclosporin A
- Gerbil
- Hippocampus
- Ischemia
ASJC Scopus subject areas
- Neuroscience(all)
- Biochemistry
Cite this
Early treatment with cyclosporin a ameliorates the reduction of muscarinic acetylcholine receptors in gerbil hippocampus after transient forebrain ischemia. / Kondo, Yoichi; Asanuma, Masato; Iwata, Emi; Kondo, Fumio; Miyazaki, Ikuko; Ogawa, Norio.
In: Neurochemical Research, Vol. 24, No. 1, 1999, p. 9-13.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Early treatment with cyclosporin a ameliorates the reduction of muscarinic acetylcholine receptors in gerbil hippocampus after transient forebrain ischemia
AU - Kondo, Yoichi
AU - Asanuma, Masato
AU - Iwata, Emi
AU - Kondo, Fumio
AU - Miyazaki, Ikuko
AU - Ogawa, Norio
PY - 1999
Y1 - 1999
N2 - Recent evidence has suggested that cyclosporin A (CsA), an immunosuppressive agent, has neuroprotective properties. However, its mechanisms associated with this activity remain unclear. We have previously shown that post-ischemic administration of CsA daily for 14 days prevented the decrease of muscarinic acetylcholine receptor binding in the hippocampus in the gerbil model of 5-min transient forebrain ischemia. In the present study, CsA (5 mg/kg, subcutaneously) was administered to each animal just after, 2 and 6 h after ischemia so as not to exert its immunosuppressive effect. Initial CsA treatment significantly restored the declined muscarinic acetylcholine receptor binding of the hippocampus 14 days after ischemia similar to the previous report. However, CsA did not alter reactive changes of astrocytes and microgila in the CA1 area of the hippocampus, which had been suppressed by daily administration. These results indicate that CsA could positively modulate the hippocampal acetylcholine neurotransmission system broken down through the ischemia-induced pyramidal cell death and its action mechanism may have no relation to the immunosuppressive properties.
AB - Recent evidence has suggested that cyclosporin A (CsA), an immunosuppressive agent, has neuroprotective properties. However, its mechanisms associated with this activity remain unclear. We have previously shown that post-ischemic administration of CsA daily for 14 days prevented the decrease of muscarinic acetylcholine receptor binding in the hippocampus in the gerbil model of 5-min transient forebrain ischemia. In the present study, CsA (5 mg/kg, subcutaneously) was administered to each animal just after, 2 and 6 h after ischemia so as not to exert its immunosuppressive effect. Initial CsA treatment significantly restored the declined muscarinic acetylcholine receptor binding of the hippocampus 14 days after ischemia similar to the previous report. However, CsA did not alter reactive changes of astrocytes and microgila in the CA1 area of the hippocampus, which had been suppressed by daily administration. These results indicate that CsA could positively modulate the hippocampal acetylcholine neurotransmission system broken down through the ischemia-induced pyramidal cell death and its action mechanism may have no relation to the immunosuppressive properties.
KW - Acetylcholine receptor
KW - Cyclosporin A
KW - Gerbil
KW - Hippocampus
KW - Ischemia
UR - http://www.scopus.com/inward/record.url?scp=0032938491&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032938491&partnerID=8YFLogxK
U2 - 10.1023/A:1020915727119
DO - 10.1023/A:1020915727119
M3 - Article
C2 - 9973231
AN - SCOPUS:0032938491
VL - 24
SP - 9
EP - 13
JO - Neurochemical Research
JF - Neurochemical Research
SN - 0364-3190
IS - 1
ER -