0000000000379402

AUTHOR

Olaf Ninnemann

showing 2 related works from this author

Precise Somatotopic Thalamocortical Axon Guidance Depends on LPA-Mediated PRG-2/Radixin Signaling

2016

Summary Precise connection of thalamic barreloids with their corresponding cortical barrels is critical for processing of vibrissal sensory information. Here, we show that PRG-2, a phospholipid-interacting molecule, is important for thalamocortical axon guidance. Developing thalamocortical fibers both in PRG-2 full knockout (KO) and in thalamus-specific KO mice prematurely entered the cortical plate, eventually innervating non-corresponding barrels. This misrouting relied on lost axonal sensitivity toward lysophosphatidic acid (LPA), which failed to repel PRG-2-deficient thalamocortical fibers. PRG-2 electroporation in the PRG-2−/− thalamus restored the aberrant cortical innervation. We ide…

0301 basic medicineNeuroscience(all)ThalamusGrowth ConesSensory systemBiologyArticle03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDiscrimination PsychologicalThalamusRadixinLysophosphatidic acidNeural PathwaysmedicineAnimalsPhosphorylationGrowth coneCerebral CortexMice KnockoutGeneral NeuroscienceMembrane ProteinsAxon GuidanceCytoskeletal Proteins030104 developmental biologymedicine.anatomical_structurechemistryCerebral cortexAxon guidanceSignal transductionLysophospholipidsNeuroscience030217 neurology & neurosurgerySignal TransductionNeuron
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An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration

2011

Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. We uncovered an unconventional role for the microRNA let-7, a highly abundant regulator of gene expression in the CNS, in which extracellular let-7 activates the RNA-sensing Toll-like receptor (TLR) 7 and induces neurodegeneration through neuronal TLR7. Cerebrospinal fluid (CSF) from individuals with Alzheimer’s disease contains increased amounts of let-7b, and extracellular introduction of let-7b into the CSF of wild-type mice by intrathecal injection resulted in neurodegeneration. Mice lacking TLR7 were resistant to this neurodegenerative effect, but thi…

Cell signalingApoptosisElectrophoretic Mobility Shift AssayBiologyReal-Time Polymerase Chain ReactionMiceAlzheimer DiseasemicroRNAExtracellularmedicineAnimalsHumansReceptorIn Situ HybridizationMice KnockoutNeuronsToll-like receptorMembrane GlycoproteinsMicroscopy ConfocalInnate immune systemGeneral NeuroscienceNeurodegenerationBrainvirus diseasesTLR7medicine.diseaseImmunohistochemistryMice Inbred C57BLMicroRNAsHEK293 CellsToll-Like Receptor 7Nerve DegenerationCancer researchSignal TransductionNature Neuroscience
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