Regulation of Injury-Induced Neurogenesis by Nitric Oxide

I think this is more important and easier to get thru the regulatory hoops than stem cells. So ask your researcher when neurogenesis will have a specific protocol.
http://scholar.google.com/scholar_url?hl=en&q=http://downloads.hindawi.com/journals/sci/2012/895659.pdf&sa=X&scisig=AAGBfm3eI1kL72LmUjKTh0Mtvoirn8STYQ&oi=scholaralrt
The finding that neural stem cells (NSCs) are able to divide, migrate, and differentiate into several cellular types in the adult
brain raised a new hope for restorative neurology. Nitric oxide (NO), a pleiotropic signaling molecule in the central nervous
system (CNS), has been described to be able to modulate neurogenesis, acting as a pro- or antineurogenic agent. Some authors
suggest that NO is a physiological inhibitor of neurogenesis, while others described NO to favor neurogenesis, particularly under
inflammatory conditions. Thus, targeting the NO system may be a powerful strategy to control the formation of new neurons.
However, the exact mechanisms by which NO regulates neural proliferation and differentiation are not yet completely clarified.
In this paper we will discuss the potential interest of the modulation of the NO system for the treatment of neurodegenerative
diseases or other pathological conditions that may affect the CNS.
1. Introduction
Neurogenesis is not limited to embryonic development as
previously thought and occurs throughout the entire adult
life of mammals, including humans. New neurons are continuously
added to neural circuits and originate at two
principal brain regions: the subventricular zone (SVZ) of the
lateral ventricles, which generates olfactory bulb (OB) neurons,
and the subgranular zone (SGZ) of the dentate gyrus
(DG) of the hippocampus. Both regions harbor neural stem
cells (NSCs) that can be isolated and cultured in vitro in the
presence of growth factors, such as basic fibroblast growth
factor (bFGF), epidermal growth factor (EGF), or both. The
absence of growth factors results in the differentiation of cells
into neurons, astrocytes, or oligodendrocytes as discussed
in [1]. Neurogenesis has been exhaustively studied over the
past years, and despite the great progress that has been
achieved, the knowledge of the multiple aspects controlling
proliferation, differentiation, or survival of NSCs is far
from being known or understood. It was shown that neurogenesis
decreases with aging and is impaired in several
pathological conditions affecting the brain. Whether the
insult is acute, such as ischemic brain stroke, traumatic
brain injury, or epileptic seizures, or is a slow-progressing
disease like Alzheimer’s disease, Huntington’s disease, or
Parkinson’s disease, all these conditions are accompanied by
an inflammatory response in the brain [2]. Furthermore, the
blockade of neuroinflammation restores adult neurogenesis
[3, 4]. When an inflammatory response in the brain appears
following an injury, activation of the brain immune cells
takes place, particularly microglial cells. In inflammatory
conditions, microglial cells become “activated”, and among
a plethora of morphological and immunological alterations,
they are able to express the inducible nitric oxide synthase
(iNOS), producing high levels of nitric oxide (NO).
2. Neurogenesis following Brain Injury
Adult neurogenesis is implicated in many forms of plasticity
in the CNS. The neurogenic process can be summarized
in five main stages: (a) precursor cell proliferation, (b) fate
determination, (c) migration, (d) differentiation and integration,
and (e) survival.
3. Injury and Neuroinflammation
    3.1. Neurodegeneration
    3.2. Neuroinflammation and Production of New Neurons.
     3.2.1. Impaired Formation of New Neurons.
     3.2.2. Enhancement of Neurogenesis.
     3.2.3. Dual Role of Inflammation in Neurogenesis.
4. Nitric Oxide
     4.1. NO as an Inflammatory Mediator.
     4.2. Neuronal Death.
     4.3. Nitric Oxide and Neurogenesis.
5. Potential Neurogenic Targets in Nitrergic Pathways
      5.1. Nitric Oxide-Releasing Drugs.
      5.1.1. Nitric Oxide Donors.
      5.1.2. Nitric Oxide-Releasing Nonsteroidal Anti-Inflammatory
Drugs.
      5.2. PDE Inhibitors.
6. Future Prospects

Its only 15 pages, rest at the link.  Even though you'll know more than your doctor after this, NO self-medication.