The Pleiotropism of Nerve Growth Factor Sensorial Pathway: Supplemental Growth Stimuli Could be Required During Danger Signalization Like a Surviving “Proclaim”

Nerve growth factor (NGF) is the founder-member of neurotrophins family that provides growth and surviving effect not only for neuronal tissue but also for various non-neuronal cellular populations. It effectuates its physiologic or pathologic functions in sensorial neuronal system and some certain tissues through NGF-receptors such as tyrosinkinase A and p75, involving also transient receptor potential vanilloid 1, substance P and its receptor NK1 (members of NGF-pathways - NGFP). In different situations, such as stress-related or inflammatory pathologies (including allergy, asthma, depression, multiple chemical sensivity, stressful or dangerous events, etc), are reported elevated local and serologic concentrations of these mediators. Reflecting on the pleiotropic effects of mentioned substances, it could be suggested that over-regulation of NGFP mediators is generally required during identification of somatic or psycho-emotional integrity threatening like a surviving proclaim. In this context, the identification of a danger may induce NGFP-mediated growth stimuli to assure better surviving possibilities for the organism, maybe as a compensatory effect. Experiments in knockout animals with regards to genes of NGFP mediators could be helpful for the verification of its role as leader of information in the mentioned processes. Some investigations in such animals have demonstrated their abnormal passivity to fight for vital demands, whereas the behavior of subjects with down-regulation of aforementioned factors is associated with sensory or cognitive disorders such as congenital insensivity for pain with anhidrosis, schizophrenia, diabetes, or self-mutilatory behaviors. The last mentioned facts manifest the inability to recognize the situation of bodily and mental integrity during the NGFP insufficiency, leading to the necessity for further pharmacologic investigations with regards to NGFP mediators in the related pathologies.