Abstract
The functions of nitric oxide (NO) in primary somatosensory neurons are reviewed. During the early development of these neurons the neuronal isoform of nitric oxide synthase (nNOS) is expressed during neurite extension. As their axons extend peripherally and start to take up nerve growth factor (NGF), nNOS starts to disappear from the majority of these neurons. A small number (less than 5%) continue to express nNOS, and for this small population NO may have a role in synaptic transmission. Following peripheral nerve section in adult rats, nNOS is reexpressed in many small peptidergic DRG neurons that have been axotomized. At the same time cGMP synthesis is increased in satellite glia cells. From culture studies, it was established that NGF negatively regulates nNOS synthesis in DRG neurons and that block of NO production leads to neuronal death. Further recent data is reviewed that supports the view that NO has a neuroprotective action preventing loss of DRG neurons and facilitates regeneration.
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