How can an excessive production of nitric oxide be harmful to developing neurites?

[Karnage]

Hi. I have a question. How can an excessive production of nitric oxide be harmful to developing neurites? This is a question that I have had unanswered for a while. I know that a lack of nitric oxide production is harmful to neurites because it is essential for neuritogenesis. Thus a lack of nitric oxide will lead to cognitive deficits. However, I do not know how an excessive production of NO will be harmful to neurites. Does anyone know? Can anyone help me? Is there evidence to support nitric oxide toxicity to developing neurites?

[Karnage]

24 ppl have viewed it so far and no one can give me an answer...

[RyanJ]

Its not shure if this is correct but it seems to be alanagous to what happens when heamoglobyn is explosed to Carbon Monoxide. It seems that it bonds with the receptors and stops them form working correctly though I am not shure about this

 

Cheers,

 

Ryan Jones

[Karnage]

errrrrr . It seems a BIT way out there. But anyway, im looking to see the effects nitric oxide may have ie neurite death, stunted neurite growth, abnormal growth of neurites etc. Thnx for trying tho

[Mokele]

Use Google Scholar and see if there's any papers on it.

[Karnage]

Research on this field has been relatively to a minimun. I have not succeeded in finding any literature (scientific articles) that discuss this topic. Maybe there have been a few references but I have not been able to find them. Does any1 have any info about this subject?

[LucidDreamer]

"Nitric oxide acts as a slow-down and search signal in developing neurites.

 

Nitric oxide (NO) has been demonstrated to act as a signaling molecule during neuronal development, but its precise function is unclear. Here we investigate whether NO might function at the neuronal growth cone to affect growth cone motility. We have previously demonstrated that growth cones of identified neurons from the snail Helisoma trivolvis show a rapid and transient increase in filopodial length in response to NO, which was regulated by soluble guanylyl cyclase (sGC) [s. Van Wagenen and V. Rehder (1999) J. Neurobiol., 39, 168-185]. Because in vivo studies have demonstrated that growth cones have longer filopodia and advance more slowly in regions where pathfinding decisions are being made, this study aimed to establish whether NO could function as a combined 'slow-down and search signal' for growth cones by decreasing neurite outgrowth. In the presence of the NO donor NOC-7, neurites of B5 neurons showed a concentration-dependent effect on neurite outgrowth, ranging from slowing at low, stopping at intermediate and collapsing at high concentrations. The effects of the NO donor were mimicked by directly activating sGC with YC-1, or by increasing its product with 8-bromo-cGMP. In addition, blocking sGC in the presence of NO with NS2028 blocked the effect of NO, suggesting that NO affected outgrowth via sGC. Ca2+ imaging of growth cones with Fura-2 indicated that [Ca2+]i increased transiently in the presence of NOC-7. These results support the hypothesis that NO can function as a potent slow/stop signal for developing neurites. When coupled with transient filopodia elongation, this phenomenon emulates growth cone searching behavior."

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15009128&query_hl=1

[Karnage]

OK thanks for the info. Its not exactly what I was looking for but its a good start