期刊
JOURNAL OF MOLECULAR NEUROSCIENCE
卷 39, 期 1-2, 页码 9-21出版社
HUMANA PRESS INC
DOI: 10.1007/s12031-008-9169-0
关键词
NOS blockers; cGMP; sGC blocker; Hilar neurons; Dentate granule cells
资金
- Faculty of Veterinary Science, University of Liverpool
- Department of Pathology
- Safety Assessment
- AstraZeneca
- Macclesfield, UK
- Medical Research Council [G0701003] Funding Source: researchfish
- MRC [G0701003] Funding Source: UKRI
The dentate gyrus (DG) of the normal rat brain contains activity-dependent neuroprotective protein (ADNP) which is widely distributed in the cytoplasm of neurons and astrocytes. Treatment with nitric oxide (NO) synthase (NOS) inhibitor N-G-nitro-l-arginine methyl ester (l-NAME) caused a decrease in ADNP expression in granule cells which persisted 3 days post-treatment. However, treatment with neuronal-specific NOS inhibitor, 7-nitroindazole (7-NI), or soluble guanylyl cyclase inhibitor, ODQ, did not change ADNP expression in the DG. We have previously shown that kainic acid (KA)-induced seizure increases neuronal NOS in neurons and inducible NOS in glia cells and suppresses ADNP in the hippocampus (Cosgrave et al., Neurobiol Dis 30(3):281-292, 2008). In the DG, l-NAME treatment prior to KA causes ADNP synthesis in granule cells by 3 h which was later restricted to the subgranular zone by 3 days. 7-NI and ODQ had no effect. Double immunostaining for neuronal marker NeuN and ADNP revealed a significant decrease of both ADNP(+) neurons and of total neuron numbers (NeuN(+)) in the hilus of animals having KA-induced seizure that had been pretreated with l-NAME implying that NO and ADNP may act together to protect hilar neurons. Overall, these observations suggest that NO regulates ADNP in the DG under both basal and pathophysiological conditions.
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