Glial cell line-derived neurotrophic factor (GDNF) is regarded as a potent neuroprotector and a corrector of neural network activity in stress conditions. This work aimed to investigate the effect of GDNF on primary hippocampal cultures during acute normobaric hypoxia. Hypoxia induction was performed using day 14 in vitro cultures derived from mouse embryos (E18) with the preventive addition of GDNF (1 ng/ml) to the culture medium 10 min before oxygen deprivation. An analysis of spontaneous bioelectrical activity that included defining the internal neural network structure, morphological studies, and viability tests was performed during the post-hypoxic period. This study revealed that GDNF does not influence spontaneous network activity during normoxia but protects cultures from cell death and maintains the network activity during hypoxia. GDNF created unique conditions that supported the viability of cells even in cases of cellular mitochondrial damage. GDNF partially negated the consequences of hypoxia by influencing synaptic plasticity. Intravital mRNA detection identified fewer GluR2 mRNA-positive cells, whereas GDNF preserved the number of these cells in the post-hypoxic period. Activation of the synthesis of GluR2 subunits of AMPA-receptors is one possible mechanism of the neuroprotective action of GDNF.
Glial cell line-derived neurotrophic factor (GdNF) is one of the most important factors participating in the neuronal survival as well as promoting the differentiation and maintenance of various cellular populations in the central and peripheral nervous systems. in contrast to other neurotrophic factors, GdNF does not directly bind to its receptor. For the implementation of GdNF biological functions, the presence of coreceptor, acting as a mediator in the interaction with the receptor, is necessary required. Receptor with tyrosine kinase activity (Ret) regarded as the main receptor to GdNF, able to subsequent launch an intracellular molecular cascade. Particular attention to GdNF investigation caused by the fact that, among other neurotrophic factors GdNF has potent neuroprotective effect. Therefore, GdNF is considered as a possible factor for the correction of various nervous system disorders, including neurodegenerative diseases. in this review basic information concerning the molecular structure of GdNF and its receptors as well as the mechanisms for implementation the main functions of GdNF from the beginning of active receptor complex formation to the subsequent launching of intracellular signaling cascades until appropriate cellular response achieving, is collected. Furthermore, the review contains the data, indicating the possible GdNF effect on synaptogenesis.
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