Ephrin-B/EphB and Wnts are known to regulate synapse maturation and plasticity, besides serving as axon guidance molecules, but the relevance of such synaptic regulation to neural circuit functions in vivo remains unclear. In this study, we have examined the role of ephrin-B and Wnt signaling in regulating visual experience-dependent and developmental plasticity of receptive fields (RFs) of tectal cells in the developing Xenopus optic tectum. We found that repetitive exposure to unidirectional moving visual stimuli caused varying degrees of shift in the RFs in different regions of the tectum. By acute perfusion of exogenous antagonists and inducible transgene expression, we showed that ephrin-B signaling in presynaptic retinal ganglion cells and Wnt secretion from tectal cells are specifically responsible for the enhanced visual stimulation-induced changes in neuronal responses and RFs in the ventral and dorsal tectum, respectively. Thus, ephrin-B and Wnt signaling contribute to region-specific plasticity of visual circuit functions.
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http://dx.doi.org/10.1016/j.neuron.2010.03.008 | DOI Listing |
J Biol Chem
August 2022
Department of Biological Sciences, University of Delaware, Newark, Delaware, USA. Electronic address:
Ephrin-B signaling has been implicated in many normal and pathological processes, including neural crest development and tumor metastasis. We showed previously that proteolysis of ephrin-B ligands by the disintegrin metalloprotease ADAM13 is necessary for canonical Wnt signal activation and neural crest induction in Xenopus, but it was unclear if these mechanisms are conserved in mammals. Here, we report that mammalian ADAM9 cleaves ephrin-B1 and ephrin-B2 and can substitute for Xenopus ADAM13 to induce the neural crest.
View Article and Find Full Text PDFBone Rep
June 2022
Center for Translational and Clinical Research, Department of Proteomics, School of Medicine, University of Zagreb, Zagreb, Croatia.
Fibrodysplasia ossificans progressiva (FOP) is an extremely rare disease in which bone tissue forms in extraskeletal sites, which is known as heterotopic ossification (HO). Extracellular vesicles (EVs) are small phospholipid-enclosed particles released by various cells which have an emerging, but not completely understood role in various (patho)physiological processes. In order to further study the pathophysiology of FOP we conducted a small observational study comparing the proteomic profiles of EV cargo, derived from pooled plasma of four patient groups: FOP patient ( = 1) during active disease phase (flare-up), FOP patients during remission ( = 2), patients after long bone fracture ( = 20) and healthy controls ( = 10).
View Article and Find Full Text PDFAdv Exp Med Biol
February 2021
Department of General Surgery, Faculty of Medicine, Gazi University, Ankara, Turkey.
Alzheimer's disease (AD) is the most common neurodegenerative disorder and accounts for more than 60-80% of all cases of dementia. Loss of pyramidal neurons, extracellular amyloid beta (Abeta) accumulated senile plaques, and neurofibrillary tangles that contain hyperphosphorylated tau constitute the main pathological alterations in AD.Synaptic dysfunction and extrasynaptic N-methyl-D-aspartate receptor (NMDAR) hyperactivation contributes to excitotoxicity in patients with AD.
View Article and Find Full Text PDFJ Steroid Biochem Mol Biol
March 2014
Department of Pathology, University of Illinois at Chicago, Chicago, IL, USA.
Soy isoflavones are dietary components for which an association has been demonstrated with reduced risk of prostate cancer (PCa) in Asian populations. However, the exact mechanism by which these isoflavones may prevent the development or progression of PCa is not completely understood. There are a growing number of animal and in vitro studies that have attempted to elucidate these mechanisms.
View Article and Find Full Text PDFPLoS One
February 2014
Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, Virginia, United States of America.
Persons infected with HIV-1 often develop neurologic disorders despite receiving highly active anti-retroviral therapy. Although the underlying mechanism is largely undetermined, our previous RNA-seq-based study showed that the expression of many genes was altered in the central nervous system (CNS) of HIV-1 transgenic (HIV-1Tg) rats. Because nicotine, a natural agonist of nicotinic acetylcholine receptors, exhibits a neuroprotective effect, we presently tested the hypothesis that nicotine restores the expression of altered genes in the CNS of HIV-1Tg rats.
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