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Nitric oxide synthase inhibition prevents neuronal death in the developing visual cortex
Yueting Zhang1, Jie Zhang, Baolu Zhao
1Laboratory of Visual Information Processing, Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, ChaoYang District, Beijing 100101, People's Republic of China.
The European Journal of Neuroscience
|November 5, 2004
Summary
Nitric oxide synthase (NOS) activity is crucial for visual cortex development in hamsters. Inhibiting NOS during early development reduces neuronal growth and triggers apoptosis, suggesting NO signals cell death for maturation.
Area of Science:
- Neuroscience
- Developmental Biology
- Biochemistry
Background:
- Postnatal visual cortex development involves transient increases in nitric oxide synthase (NOS) expression and activity.
- This period coincides with the formation of visual projections and cortical functional differentiation.
- Nitric oxide (NO) is implicated in the maturation of the visual cortex.
Purpose of the Study:
- To investigate the role of NOS in postnatal visual cortex development.
- To examine the effects of NOS inhibition on neuronal growth and apoptosis.
Main Methods:
- Used N-nitro-L-arginine (L-NNA), a NOS inhibitor, in newborn golden hamsters.
- Monitored body weight gain, nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) activity, and neuronal growth.
- Assessed apoptosis using terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assay.
Main Results:
- L-NNA treatment increased mortality and suppressed body weight gain and NADPH-d activity before postnatal day 14.
- Growth of NADPH-d-positive neurons in the visual cortex was inhibited by L-NNA.
- NOS inhibition significantly reduced neuronal apoptosis in cortical layers II and III.
Conclusions:
- NO may act as a signaling molecule that triggers apoptosis during visual cortex maturation.
- NOS activity plays a critical role in regulating neuronal development and cell death in the developing visual cortex.