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Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9954-9. doi: 10.1073/pnas.171098398. Epub 2001 Aug 07.

Role of glutamate delta -2 receptors in activity-dependent competition between heterologous afferent fibers.

Proceedings of the National Academy of Sciences of the United States of America

L Morando, R Cesa, R Rasetti, R Harvey, P Strata

Affiliations

  1. Rita Levi Montalcini Center for Brain Repair, Department of Neuroscience, University of Turin, Torino, Italy.

PMID: 11493687 PMCID: PMC55559 DOI: 10.1073/pnas.171098398

Abstract

A principle that regulates detailed architecture in the brain is that active terminals have a competitive advantage over less active terminals in establishing synaptic connections. This principle is known to apply to fibers within a single neuronal population competing for a common target domain. Here we uncover an additional rule that applies when two neuronal populations compete for two contiguous territories. The cerebellar Purkinje cell dendrites have two different synaptic domains with spines innervated by two separate excitatory inputs, parallel fibers (PFs) and climbing fibers (CFs). Glutamate delta-2 receptors are normally present only on the PF spines where they are important for their innervation. After block of activity by tetrodotoxin, numerous new spines form in the CF domain and become innervated mainly by PFs; all spines, including those still innervated by the CFs, bear delta-2 receptors. Thus, in the absence of activity, PFs gain a competitive advantage over CFs. The entire dendritic arbor becomes a uniform territory with the molecular cues associated with the PFs. To access their proper territory and maintain synaptic contacts, CFs must be active and locally repress the cues of the competitor afferents.

References

  1. Neurosci Res. 1999 Sep;34(4):281-7 - PubMed
  2. Cell. 1995 Apr 21;81(2):245-52 - PubMed
  3. Neuron. 2000 Feb;25(2):269-78 - PubMed
  4. Science. 2000 Mar 31;287(5462):2479-82 - PubMed
  5. Trends Neurosci. 2000 May;23(5):198 - PubMed
  6. Neuron. 2000 May;26(2):473-82 - PubMed
  7. Science. 2000 Dec 15;290(5499):2155-9 - PubMed
  8. Nat Rev Neurosci. 2001 Jan;2(1):24-32 - PubMed
  9. Brain Res. 1967 May;5(1):15-30 - PubMed
  10. Brain Res. 1975 Nov 21;98(3):574-81 - PubMed
  11. J Comp Neurol. 1991 Jun 22;308(4):536-54 - PubMed
  12. FEBS Lett. 1993 Jan 11;315(3):318-22 - PubMed
  13. Cell. 1993 Jan;72 Suppl:77-98 - PubMed
  14. J Comp Neurol. 1993 Jul 15;333(3):417-34 - PubMed
  15. Prog Neurobiol. 1996 May;49(1):53-71 - PubMed
  16. Science. 1996 Nov 15;274(5290):1133-8 - PubMed
  17. Brain Res. 1997 Jan 16;745(1-2):231-42 - PubMed
  18. Neuron. 1997 Jul;19(1):63-76 - PubMed
  19. Nature. 1997 Aug 21;388(6644):769-73 - PubMed
  20. J Neurosci. 1997 Jan 15;17(2):834-42 - PubMed
  21. J Neurosci. 1997 Dec 15;17(24):9613-23 - PubMed
  22. J Neurosci. 1998 Jul 15;18(14):5517-28 - PubMed
  23. Trends Neurosci. 1998 Sep;21(9):401-7 - PubMed
  24. Trends Neurosci. 1998 Sep;21(9):407-13 - PubMed
  25. Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1704-9 - PubMed
  26. J Neurosci. 1999 Sep 15;19(18):7999-8008 - PubMed
  27. Neuron. 1993 Oct;11(4):771-87 - PubMed
  28. Biochem Biophys Res Commun. 1993 Dec 30;197(3):1267-76 - PubMed
  29. Science. 1995 Mar 17;267(5204):1662-6 - PubMed
  30. J Neurosci. 2000 Jan 15;20(2):685-95 - PubMed

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