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Long-term potentiation is reduced in mice that are doubly mutant in endothelial and neuronal nitric oxide synthase
被引:362
作者:
Son, H
Hawkins, RD
Martin, K
Kiebler, M
Huang, PL
Fishman, MC
Kandel, ER
机构:
[1] COLUMBIA UNIV,COLL PHYS & SURG,CTR NEUROBIOL & BEHAV,NEW YORK,NY 10032
[2] MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,CHARLESTOWN,MA 02129
[3] HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129
来源:
关键词:
D O I:
10.1016/S0092-8674(00)81796-1
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Nitric oxide (NO) has been implicated in hippocampal long-term potentiation (LTP), but LTP is normal in mice with a targeted mutation in the neuronal form of NO synthase (nNOS(-)). LTP was also normal in mice with a targeted mutation in endothelial NOS (eNOS(-)), but LTP in stratum radiatum of CA1 was significantly reduced in doubly mutant mice (nNOS(-)/eNOS(-)). By contrast, LTP in stratum oriens was normal in the doubly mutant mice. These results provide the first genetic evidence that NOS is involved in LTP in stratum radiatum and suggest that the neuronal and endothelial forms can compensate for each other in mice with a single mutation. They further suggest that there is also a NOS-independent component of LTP in stratum radiatum and that LTP in stratum oriens is largely NOS independent.
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页码:1015 / 1023
页数:9
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