Chapter 7 Modulation of Adult Neurogenesis by the Nitric Oxide System

Only 36 pages for your doctor to come up with a useful stroke protocol. and don't let excuses like nobody has done anything like this yet stop you from demanding action from your doctor.
You do want new neurons, don't you?
http://cdn.intechopen.com/pdfs/44261/InTech-Modulation_of_adult_neurogenesis_by_the_nitric_oxide_system.pdf

1. Introduction

Nitric oxide (NO) is a gaseous free radical that acts as a second messenger having an importantbiological role in intercellular communication and in intracellular signaling in many tissues, including the brain (reviewed by [

1

]). NO is synthesized by the nitric oxide synthase (NOS) family of enzymes, which convert L-arginine to L-citrulline and NO. There are three different

isoforms of NOS: a) neuronal NOS (nNOS or NOS I), b) endothelial NOS (eNOS or NOS III),and c) inducible NOS (iNOS or NOS II) (reviewed by [2]). Different members of the NOS family control different functions of NO (reviewed by [1]).  In the central nervous system (CNS), NO has been linked to the regulation of synaptic plasticity and cognitive functions, and it is also associated with the control of biological functions including sleep-wake cycle, appetite, body temperature, and modulation of hormone release as reviewed by [3]. In the last decade, there has been a growing interest in

the study of the role of NO in neurogenesis, the process by which new neurons are formed in the brain. NO regulates neurogenesis in diverse ways, and the different NO synthases are important players in the different effects on neurogenesis. Under physiological conditions NO synthesized from nNOS acts as a negative regulator of neurogenesis [4-9], while in inflammatory conditions, such as neurodegenerative disorders or acute brain insults, a decrease in nNOS and an increase in iNOS expression may act as a

mechanism to enhance neurogenesis [8,10-13]. In fact, depending on the source, NO has a pro-neurogenic effect either by promoting neural stem cell (NSC) proliferation, as recently described by our group [13,14], but also by favoring other steps of neurogenesis such as migration [15], differentiation and survival [10,16]. Although the exact molecular mechanisms underlying this dual effect of NO on neurogenesis are not fully clarified, the

modulation of the NO system seems be a good target for the development of strategies to improve endogenous neurogenesis following brain damage.