ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Brain-derived neurotrophic factor and trkB signaling in parasympathetic neurons: relevance to regulating alpha7-containing nicotinic receptors and synaptic function.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 76 citations in OpenAlex.
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- Aerobic exercise as a promising nonpharmacological therapy for the treatment of substance use disorders.Journal of neuroscience research · 2022Review
- Dysregulation of Neuronal Nicotinic Acetylcholine Receptor-Cholesterol Crosstalk in Autism Spectrum Disorder.Frontiers in molecular neuroscience · 2021Article
- In vitro evidence for post-insult neuroprotective activity of an evolutionarily conserved motif against excitotoxic neuronal cell death.Neuroreport · 2019Article
- Wheel running during chronic nicotine exposure is protective against mecamylamine-precipitated withdrawal and up-regulates hippocampal α7 nACh receptors in mice.British journal of pharmacology · 2018Article
- Knockdown of CXCL14 disrupts neurovascular patterning during ocular development.Developmental biology · 2017Article
- The DYX2 locus and neurochemical signaling genes contribute to speech sound disorder and related neurocognitive domains.Genes, brain, and behavior · 2015Article
- Neuronal somata and extrasomal compartments play distinct roles during synapse formation between Lymnaea neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Evidence that BDNF regulates heart rate by a mechanism involving increased brainstem parasympathetic neuron excitability.Journal of neurochemistry · 2014Article
- T-cell receptor activation decreases excitability of cortical interneurons by inhibiting α7 nicotinic receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Nicotine as a potential neuroprotective agent for Parkinson's disease.Movement disorders : official journal of the Movement Disorder Society · 2012Review
- Nerve injury increases brain-derived neurotrophic factor levels to suppress BK channel activity in primary sensory neurons.Journal of neurochemistry · 2012Article
- Targeted deletion of Hand2 in enteric neural precursor cells affects its functions in neurogenesis, neurotransmitter specification and gangliogenesis, causing functional aganglionosis.Development (Cambridge, England) · 2011Article
- Abelson family tyrosine kinases regulate the function of nicotinic acetylcholine receptors and nicotinic synapses on autonomic neurons.Molecular pharmacology · 2011Article
- Targeted deletion of Hand2 in cardiac neural crest-derived cells influences cardiac gene expression and outflow tract development.Developmental biology · 2010Article
- PACAP/PAC1R signaling modulates acetylcholine release at neuronal nicotinic synapses.Molecular and cellular neurosciences · 2010Article
- Multiple roles for nicotine in Parkinson's disease.Biochemical pharmacology · 2009Review
- Nicotine is neuroprotective when administered before but not after nigrostriatal damage in rats and monkeys.Journal of neurochemistry · 2009Article
- Pituitary adenylate cyclase-activating polypeptide (PACAP) alters parasympathetic neuron gene expression in a time-dependent fashion.Journal of molecular neuroscience : MN · 2008Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Parasympathetic neurons do not require neurotrophins for survival and are thought to lack high-affinity neurotrophin receptors (i.e., trks). We report here, however, that mRNAs encoding both brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tropomyosin-related kinase B (trkB) are expressed in the parasympathetic chick ciliary ganglion (CG) and that BDNF-like protein is present in the ganglion and in the iris, an important peripheral target of ciliary neurons. Moreover, CG neurons express surface trkB and exogenous BDNF not only initiates trk-dependent signaling, but also alters nicotinic acetylcholine receptor (nAChR) expression and synaptic transmission. In particular, BDNF applied to CG neurons rapidly activates cAMP-dependent response element-binding protein (CREB), and over the long-term selectively upregulates expression of alpha7-subunit-containing, homomeric nAChRs (alpha7-nAChRs), increasing alpha7-subunit mRNA levels, alpha7-nAChR surface sites, and alpha7-nAChR-mediated whole-cell currents. At nicotinic synapses formed on CG neurons in culture, brief and long-term BDNF treatments also increase the frequency of spontaneous EPSCs, most of which are mediated by heteromeric nAChRs containing alpha3, alpha5, beta4, and beta2 subunits (alpha3*-nAChRs) with a minor contribution from alpha7-nAChRs. Our findings demonstrate unexpected roles for BDNF-induced, trk-dependent signaling in CG neurons, both in regulating expression of alpha7-nAChRs and in enhancing transmission at alpha3*-nAChR-mediated synapses. The presence of BDNF-like protein in CG and iris target coupled with that of functional trkB on CG neurons raise the possibility that signals generated by endogenous BDNF similarly influence alpha7-nAChRs and nicotinic synapses in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.