ArticleAlcoholism, clinical and experimental research2011
Ethanol alters BDNF-induced Rho GTPase activation in axonal growth cones.
Article in Alcoholism, clinical and experimental research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 27 citations in OpenAlex.
- Impact of alcohol exposure on neural development and network formation in human cortical organoids.Molecular psychiatry · 2023Article
- The potential therapeutic roles of Rho GTPases in substance dependence.Frontiers in molecular neuroscience · 2023Article
- CB1R regulates CDK5 signaling and epigenetically controls Rac1 expression contributing to neurobehavioral abnormalities in mice postnatally exposed to ethanol.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Ethanol exposure inhibits hepatocyte lipophagy by inactivating the small guanosine triphosphatase Rab7.Hepatology communications · 2017Article
- Developmental alcohol exposure leads to a persistent change on astrocyte secretome.Journal of neurochemistry · 2016Article
- Ibuprofen slows migration and inhibits bowel colonization by enteric nervous system precursors in zebrafish, chick and mouse.Developmental biology · 2016Article
- Effects of Ethanol on the Expression Level of Various BDNF mRNA Isoforms and Their Encoded Protein in the Hippocampus of Adult and Embryonic Rats.International journal of molecular sciences · 2015Article
- Microtopographical features generated by photopolymerization recruit RhoA/ROCK through TRPV1 to direct cell and neurite growth.Biomaterials · 2015Article
- Alterations of neocortical pyramidal neurons: turning points in the genesis of mental retardation.Frontiers in pediatrics · 2014Review
- Using microfluidic chip to form brain-derived neurotrophic factor concentration gradient for studying neuron axon guidance.Biomicrofluidics · 2014Article
- Ethanol neurotoxicity in the developing cerebellum: underlying mechanisms and implications.Brain sciences · 2013Article
- Activation of RhoA in alcohol-induced intestinal barrier dysfunction.Inflammation · 2013Article
- Moderate prenatal alcohol exposure increases total length of L1-expressing axons in E15.5 mice.Neurotoxicology and teratologyArticle
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3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe effects of ethanol on development of postmitotic neurons include altered neurite outgrowth and differentiation, which may contribute to neuropathology associated with fetal alcohol spectrum disorders. We previously reported that ethanol exposure alters axon growth dynamics in dissociated cultures of rat hippocampal pyramidal neurons. Given the important regulatory role of small Rho guanosine triphosphatases (GTPases) in cytoskeletal reorganization associated with axon growth, and reports that ethanol alters whole cell Rho GTPase activity in other cell types, this study explored the hypothesis that ethanol alters Rho GTPase activity specifically in axonal growth cones.
methodsFetal rat hippocampal pyramidal neurons were maintained in dissociated cultures for 1 day in control medium or medium containing 11 to 43 mM ethanol. Some cultures were also treated with brain-derived neurotrophic factor (BDNF), an activator of Rac1 and Cdc42 GTPases that promotes axon extension. Levels of active Rho GTPases in growth cones were measured using in situ binding assays for GTP-bound Rac1, Cdc42, and RhoA. Axon length, growth cone area, and growth cone surface expression of tyrosine kinase B (TrkB), the receptor for BDNF, were assessed by digital morphometry and immunocytochemistry.
resultsAlthough ethanol increased the surface area of growth cones, the levels of active Rho GTPases in axonal growth cones were not affected in the absence of exogenous BDNF. In contrast, ethanol exposure inhibited BDNF-induced Rac1/Cdc42 activation in a dose-dependent manner and increased RhoA activation at the highest concentration tested. Similar TrkB expression was observed on the surface of axonal growth cones of control and ethanol-treated neurons.
conclusionsThese results reveal an inhibitory effect of ethanol on growth cone signaling via small Rho GTPases during early stages of hippocampal development in vitro, and suggest a mechanism whereby ethanol may disrupt neurotrophic factor regulation of axon growth and guidance.
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