Premium
Long‐term lithium treatment increases intracellular and extracellular brain‐derived neurotrophic factor ( BDNF ) in cortical and hippocampal neurons at subtherapeutic concentrations
Author(s) -
DePaula Vanessa J.,
Gattaz Wagner F.,
Forlenza Orestes V.
Publication year - 2016
Publication title -
bipolar disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.285
H-Index - 129
eISSN - 1399-5618
pISSN - 1398-5647
DOI - 10.1111/bdi.12449
Subject(s) - neurotrophic factors , neuroprotection , hippocampal formation , lithium (medication) , brain derived neurotrophic factor , neurotrophin , neuroscience , hippocampus , extracellular , endocrinology , medicine , psychology , biology , microbiology and biotechnology , receptor
Objectives The putative neuroprotective effects of lithium treatment rely on the fact that it modulates several homeostatic mechanisms involved in the neurotrophic response, autophagy, oxidative stress, inflammation, and mitochondrial function. Lithium is a well‐established therapeutic option for the acute and long‐term management of bipolar disorder and major depression. The aim of this study was to evaluate the effects of subtherapeutic and therapeutic concentrations of chronic lithium treatment on brain‐derived neurotrophic factor ( BDNF ) synthesis and secretion. Methods Primary cultures of cortical and hippocampal neurons were treated with different subtherapeutic (0.02 and 0.2 mM) and therapeutic (2 mM ) concentrations of chronic lithium treatment in cortical and hippocampal cell culture. Results Lithium treatment increased the intracellular protein expression of cortical neurons (10% at 0.02 mM) and hippocampal neurons (28% and 14% at 0.02 mM and 0.2 mM, respectively). Extracellular BDNF of cortical neurons increased 30% and 428% at 0.02 and 0.2 mM , respectively and in hippocampal neurons increased 44% at 0.02 mM . Conclusion The present study indicates that chronic, low‐dose lithium treatment up‐regulates BDNF production in primary neuronal cell culture.