ArticleHuman molecular genetics2011
The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Glioblastoma cell-derived exosomes induce cell death and oxidative stress in primary cultures of olfactory neurons. Role of redox stress.Molecular biology reports · 2023Article
- Neurotrophic factors in the physiology of motor neurons and their role in the pathobiology and therapeutic approach to amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2023Review
- Running and swimming prevent the deregulation of the BDNF/TrkB neurotrophic signalling at the neuromuscular junction in mice with amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2020Article
- TrkB agonists prevent postischemic emergence of refractory neonatal seizures in mice.JCI insight · 2020Article
- Overview of Impaired BDNF Signaling, Their Coupled Downstream Serine-Threonine Kinases and SNARE/SM Complex in the Neuromuscular Junction of the Amyotrophic Lateral Sclerosis Model SOD1-G93A Mice.Molecular neurobiology · 2019Article
- The p75Acta neuropathologica communications · 2019Article
- The Role of Altered BDNF/TrkB Signaling in Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2019Review
- Specific effects of c-Jun NH2-terminal kinase-interacting protein 1 in neuronal axons.Neural regeneration research · 2016Article
- Ablation of intact hypothalamic and/or hindbrain TrkB signaling leads to perturbations in energy balance.Molecular metabolism · 2015Article
- Suppression of adenosine 2a receptor (A2aR)-mediated adenosine signaling improves disease phenotypes in a mouse model of amyotrophic lateral sclerosis.Experimental neurology · 2015Article
- Genetically altering organismal metabolism by leptin-deficiency benefits a mouse model of amyotrophic lateral sclerosis.Human molecular genetics · 2014Article
- Role of BDNF in central motor structures and motor diseases.Molecular neurobiology · 2013Review
- Deletion of the BDNF truncated receptor TrkB.T1 delays disease onset in a mouse model of amyotrophic lateral sclerosis.PloS one · 2012Article
- Lingual innervation in male and female marmosets.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) are widely expressed in the vertebrate nervous system and play a central role in mature neuronal function. In vitro BDNF/TrkB signaling promotes neuronal survival and can help neurons resist toxic insults. Paradoxically, BDNF/TrkB signaling has also been shown, under certain in vitro circumstances, to render neurons vulnerable to insults. We show here that in vivo conditional deletion of TrkB from mature motor neurons attenuates mutant superoxide dismutase 1 (SOD1) toxicity. Mutant SOD1 mice lacking motor neuron TrkB live a month longer than controls and retain motor function for a longer period, particularly in the early phase of the disease. These effects are subserved by slowed motor neuron loss, persistence of neuromuscular junction integrity and reduced astrocytic and microglial reactivity within the spinal cord. These results suggest that manipulation of BDNF/TrkB signaling might have therapeutic efficacy in motor neuron diseases.
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