ArticleTranslational neuroscience2010
ALTERED CALCIUM CURRENTS AND AXONAL GROWTH IN Nf1 HAPLOINSUFFICIENT MICE.
Article in Translational neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Recent advances of epilepsy associated with neurofibromatosis type 1.Frontiers in neurology · 2025Review
- snRNA-seq of human cutaneous neurofibromas before and after selumetinib treatment implicates role of altered Schwann cell states, inter-cellular signaling, and extracellular matrix in treatment response.Acta neuropathologica communications · 2024Article
- Early-life immune activation is a vulnerability factor for adult epileptogenesis in neurofibromatosis type 1 in male mice.Frontiers in neurology · 2024Article
- Loss ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Role of nerves in neurofibromatosis type 1-related nervous system tumors.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Renal manifestations in children with neurofibromatosis type 1.European journal of pediatrics · 2021Article
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- Review
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- CRMP2-Neurofibromin Interface Drives NF1-related Pain.Neuroscience · 2018Article
- CRMP2 and voltage-gated ion channels: potential roles in neuropathic pain.Neuronal signaling · 2018Article
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- Article
- Sensitization of Ion Channels Contributes to Central and Peripheral Dysfunction in Neurofibromatosis Type 1.Molecular neurobiology · 2017Review
- Epilepsy Mechanisms in Neurocutaneous Disorders: Tuberous Sclerosis Complex, Neurofibromatosis Type 1, and Sturge-Weber Syndrome.Frontiers in neurology · 2017Review
- N-type calcium current, Cav2.2, is enhanced in small-diameter sensory neurons isolated from Nf1+/- mice.Neuroscience · 2014Article
- Opening Pandora's jar: a primer on the putative roles of CRMP2 in a panoply of neurodegenerative, sensory and motor neuron, and central disorders.Future neurology · 2012Article
- Inhibition of transmitter release and attenuation of anti-retroviral-associated and tibial nerve injury-related painful peripheral neuropathy by novel synthetic Ca2+ channel peptides.The Journal of biological chemistry · 2012Article
- Prevention of posttraumatic axon sprouting by blocking collapsin response mediator protein 2-mediated neurite outgrowth and tubulin polymerization.Neuroscience · 2012Article
- Delayed calcium dysregulation in neurons requires both the NMDA receptor and the reverse Na+/Ca2+ exchanger.Neurobiology of disease · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations of the neurofibromin gene (NF1) cause neurofibromatosis type 1 (NF1), a disease in which learning disabilities are common. Learning deficits also are observed in mice with a heterozygous mutation of Nf1 (Nf1(+/-)). Dysregulation of regulated neurotransmitter release has been observed in Nf1(+/-) mice. However, the role of presynaptic voltage-gated Ca(2+) channels mediating this release has not been investigated. We investigated whether Ca(2+) currents and transmitter release were affected by reduced neurofibromin in Nf1(+/-) mice. Hippocampal Ca(2+) current density was greater in neurons from Nf1(+/-) mice and a greater fraction of Ca(2+) currents was activated at less depolarized potentials. In addition, release of the excitatory neurotransmitter, glutamate, was increased in neuronal cortical cultures from Nf1(+/-) mice. Dendritic complexity and axonal length were also increased in neurons Nf1(+/-) mice compared to wild-type neurons, linking loss of neurofibromin to developmental changes in hippocampal axonal/cytoskeletal dynamics. Collectively, these results show that altered Ca(2+) channel density and transmitter release, along with increased axonal growth may account for the abnormal nervous system functioning in NF1.
Identifiers
What OpenQuestion holds
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.