Neuronal expression of brain derived neurotrophic factor in the injured telencephalon of adult zebrafish
Brain‐derived neurotrophic factor (BDNF) is a member of neurotrophin (NT) family. NTs comprise, in addition to BDNF, the nerve growth factor (NGF), NT‐3, NT‐4/5, NT 6/7. The binding to three distinct tyrosine kinase receptors (Trk) A, B and C mediates their activities concerning neuronal proliferation, survival, differentiation and plasticity in many neuronal populations of central and peripheral nervous system (Reichardt, 2006). However, all NTs also bind with low affinity to the common p75 receptor.
In the brain, BDNF plays multiple and important roles. An indirect evidence is given by a common single‐nucleotide polymorphism in the human BDNF gene, resulting in a valine to methionine substitution in the prodomain (Val66Met), which has been shown to lead to memory impairment and susceptibility to neuropsychiatric disorders (Bath & Lee, 2006). In schizophrenia, patients showed in brain tissue reduced BDNF mRNA serum levels (Wysokinski, 2016). In depressed patients BDNF levels appeared lower, and treatment with antidepressants increased serum BDNF levels compared to controls (for a review see Molendijk et al., 2014). During human normal ageing, BDNF plasma levels significantly decreased. In animal models, BDNF content was unchanged or increased in the hippocampus of aged Sprague Dawley or Wistar rats, although its receptors levels were decreased, thus certainly resulting in a weaker BDNF action (Silhol, Bonnichon, Rage, & Tapia‐Arancibia, 2005).
BDNF has also beneficial effects. In Alzheimer disease, in vitro and in vivo studies in rats indicated that BDNF has neuronal protective effects against neurotoxicity caused by amyloid β‐peptide accumulation. In fact BDNF could act as an antioxidative factor since it is known that it increases the level of activity of some antioxidant enzymes (for a review see Tapia‐Arancibia, Aliaga, Silhol, & Arancibia, 2008). Finally, in the treatment of multiple sclerosis, BDNF plays a role in mechanism of re‐myelination (KhorshidAhmad et al., 2016).
In experimental traumatic brain injury (TBI) performed in rodents, BDNF protein expression is modified (Yang et al., 1996; Hicks, Numan, Dhillon, Prasad, & Seroogy, 1997; Hicks et al., 1999; Griesbach, Hovda, Molteni, & Gomez‐Pinilla, 2002; Rostami et al.