LTP and LTD in the visual cortex require the activation of NOX2.
J Neurosci
; 34(38): 12778-87, 2014 Sep 17.
Article
in En
| MEDLINE
| ID: mdl-25232114
ABSTRACT
Reactive oxygen species (ROS) are signaling factors involved in many intracellular transduction pathways. In the nervous system, ROS are thought to modulate various mechanisms of synaptic plasticity. One important source of ROS production in the brain is the NADPH oxidase complex. Stimulation of NMDA receptors activates NADPH oxidase, which provides selective oxidative responses accompanying the induction of synaptic changes. The activity of NADPH oxidase is known to be crucial for the induction of LTP in the hippocampus. However, the involvement of this complex in cortical synaptic plasticity is still unclear. Here we provide evidence that genetic ablation of NOX2 (the prototypical member of NADPH oxidase family of proteins) suppresses LTP and LTD in the primary visual cortex of the mouse. We also found that the involvement of NOX2 on LTP is partially age-dependent, as the activity of this complex is not critical for mechanisms of synaptic potentiation occurring in immature animals. Furthermore, we show that inhibition of NOX2 reduces the NMDA receptor function, suggesting a possible mechanism that could be the basis of the effects on synaptic plasticity.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Visual Cortex
/
Aging
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Membrane Glycoproteins
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Long-Term Potentiation
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NADPH Oxidases
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Long-Term Synaptic Depression
Limits:
Animals
Language:
En
Journal:
J Neurosci
Year:
2014
Document type:
Article