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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Dendrites

 
 
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Disease relevance of Dendrites

 

Psychiatry related information on Dendrites

 

High impact information on Dendrites

  • We previously showed that collapsin response mediator protein-2 (CRMP-2) is critical for specifying axon/dendrite fate, possibly by promoting neurite elongation via microtubule assembly [11].
  • Dendrites of fry and trc mutants display excessive terminal branching and fail to avoid homologous dendritic branches, resulting in significant overlap of the dendritic fields [12].
  • We show here that neurexin alone is sufficient to induce glutamate postsynaptic differentiation in contacting dendrites [13].
  • Formation of synaptic connections requires alignment of neurotransmitter receptors on postsynaptic dendrites opposite matching transmitter release sites on presynaptic axons. beta-neurexins and neuroligins form a trans-synaptic link at glutamate synapses [13].
  • Biochemical and immunocytochemical analysis demonstrates that in VNO sensory dendrites M10s belong to large multi-molecular complexes that include pheromone receptors and beta2-microglobulin (beta2m) [14].
 

Chemical compound and disease context of Dendrites

  • The findings further suggest that the directional responses of DS ganglion cells are mediated in part by the directional release of gamma-aminobutyric acid from starburst dendrites and that the asymmetric distribution of the two cotransporters along starburst-cell dendrites mediates direction selectivity [15].
  • In this paper we show that in the Bomirski amelanotic melanoma system MSH and agents that raise intracellular cyclic AMP induce dendrite formation, inhibit cell growth, and cause substantial increases in tyrosinase activity without inducing melanin synthesis [16].
  • Our observations help explain the pharmacology of the competitive NMDA antagonists against NMDA receptor-mediated neurotoxicity but also suggest the possibility that, because the cell body and dendrites may be distinct sites for neurotoxicity, they might also involve different mechanisms of toxicity [17].
  • Central VP release from MNC somata and dendrites is stimulated by both dehydration and pituitary adenylate cyclase activating polypeptide (PACAP) [18].
  • The absence of reinnervation of bipolar cell dendrites by DA-IPCs may account for the persistence of the increased light sensitivity following retinal dopamine depletion [19].
 

Biological context of Dendrites

 

Anatomical context of Dendrites

 

Associations of Dendrites with chemical compounds

  • Dendrite growth increased by visual activity requires NMDA receptor and Rho GTPases [30].
  • Morphological substrates for DA storage exist in dendrites, as do dendro-dendritic and dendro-axonic contacts [29].
  • Here we show that neurotransmission-evoked calcium (Ca(2+)) release from intracellular stores stabilizes dendrites during the period of synapse formation [31].
  • At the molecular level, LTD appears to be caused by desensitization of receptor molecules in PC dendrites towards the PF neurotransmitter, presumably L-glutamate (Glu) [32].
  • Local calcium signalling by inositol-1,4,5-trisphosphate in Purkinje cell dendrites [33].
 

Gene context of Dendrites

  • In the developing cerebellum, DNER is highly expressed in Purkinje cell dendrites, which are tightly associated with radial fibers of Bergmann glia expressing Notch [34].
  • We found that the cell-surface molecules Frazzled and Robo work as guidance molecules not only for axons but also for dendrites as they navigate within the CNS [35].
  • Baz, Par-6 and aPKC are not required for axon or dendrite specification in Drosophila [36].
  • Using 12P3, we demonstrate that a brief exposure of a rat cerebellar slice to AMPA leads to transient phosphorylation of the GluR subunits in Purkinje cell dendrites [37].
  • Destabilization of cortical dendrites and spines by BDNF [38].
 

Analytical, diagnostic and therapeutic context of Dendrites

References

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  22. Protein kinase C modulates NMDA receptor trafficking and gating. Lan , J.Y., Skeberdis, V.A., Jover, T., Grooms, S.Y., Lin, Y., Araneda, R.C., Zheng, X., Bennett, M.V., Zukin, R.S. Nat. Neurosci. (2001) [Pubmed]
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