Sensory deprivation during early development causes an increased exploratory behavior in a whisker-dependent decision task.

Stylianos Papaioannou, Leeann Brigham, Patrik Krieger
Author Information
  1. Stylianos Papaioannou: Department of Neuroscience, Karolinska Institutet, Stockholm Brain Institute Stockholm, Sweden.

Abstract

Stimulation of sensory pathways is important for the normal development of cortical sensory areas, and impairments in the normal development can have long-lasting effect on animal's behavior. In particular, disturbances that occur early in development can cause permanent changes in brain structure and function. The behavioral effect of early sensory deprivation was studied in the mouse whisker system using a protocol to induce a 1-week sensory deprivation immediately after birth. Only two rows of whiskers were spared (C and D rows), and the rest were deprived, to create a situation where an unbalanced sensory input, rather than a complete loss of input, causes a reorganization of the sensory map. Sensory deprivation increased the barrel size ratio of the spared CD rows compared with the deprived AB rows; thus, the map reorganization is likely due, at least in part, to a rewiring of thalamocortical projections. The behavioral effect of such a map reorganization was investigated in the gap-crossing task, where the animals used a whisker that was spared during the sensory deprivation. Animals that had been sensory deprived performed equally well with the control animals in the gap-crossing task, but were more active in exploring the gap area and consequently made more approaches to the gap - approaches that on average were of shorter duration. A restricted sensory deprivation of only some whiskers, although it does not seem to affect the overall performance of the animals, does have an effect on their behavioral strategy on executing the gap-crossing task.

Keywords

References

  1. Nature. 2000 Apr 20;404(6780):876-81 [PMID: 10786794]
  2. J Comp Neurol. 1985 Aug 8;238(2):225-35 [PMID: 2413086]
  3. J Neurophysiol. 1986 Oct;56(4):1196-223 [PMID: 3783236]
  4. Cereb Cortex. 2008 Jun;18(6):1361-73 [PMID: 17921458]
  5. Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12864-8 [PMID: 11058162]
  6. Nature. 1993 Aug 12;364(6438):623-6 [PMID: 8102476]
  7. J Neurophysiol. 1994 Sep;72(3):1434-7 [PMID: 7807225]
  8. J Neurosci. 2003 Jan 1;23(1):358-66 [PMID: 12514235]
  9. Eur J Neurosci. 2009 Nov;30(10):1870-7 [PMID: 19912332]
  10. Nature. 1987 Apr 16-22;326(6114):694-7 [PMID: 3561512]
  11. BMC Neurosci. 2005 Mar 17;6:18 [PMID: 15774010]
  12. J Neurosci. 1992 May;12(5):1826-38 [PMID: 1578273]
  13. J Physiol Paris. 1996;90(3-4):263-9 [PMID: 9116680]
  14. Nat Neurosci. 2000 Sep;3(9):911-8 [PMID: 10966622]
  15. J Neurosci. 1996 Apr 15;16(8):2750-7 [PMID: 8786450]
  16. J Comp Neurol. 1976 Nov 1;170(1):53-66 [PMID: 977815]
  17. J Neurosci. 1999 Oct 15;19(20):9117-25 [PMID: 10516329]
  18. J Neurosci. 2001 Jun 1;21(11):3881-94 [PMID: 11356876]
  19. Science. 1973 Jan 26;179(4071):395-8 [PMID: 4682966]
  20. Cereb Cortex. 2008 Jul;18(7):1588-603 [PMID: 17998276]
  21. Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7587-91 [PMID: 10377459]
  22. Proc Natl Acad Sci U S A. 2007 Jan 23;104(4):1395-400 [PMID: 17227858]
  23. J Neurophysiol. 2005 Dec;94(6):3987-95 [PMID: 16093330]
  24. Science. 2005 Nov 4;310(5749):810-5 [PMID: 16272113]
  25. J Neurophysiol. 2008 Jul;100(1):504-15 [PMID: 18463190]
  26. Neurosci Res. 2002 Apr;42(4):243-50 [PMID: 11985876]
  27. Proc Natl Acad Sci U S A. 1993 Mar 1;90(5):2082-6 [PMID: 8446633]
  28. Nature. 1999 Jul 22;400(6742):367-71 [PMID: 10432115]
  29. J Neurophysiol. 2000 Oct;84(4):1971-81 [PMID: 11024090]
  30. Neuropharmacology. 1998 Apr-May;37(4-5):581-92 [PMID: 9704999]
  31. J Comp Neurol. 1999 Sep 13;412(1):83-94 [PMID: 10440711]
  32. J Neurodev Disord. 2010 Jun;2(2):62-9 [PMID: 22127855]
  33. Somatosens Mot Res. 1999;16(2):122-38 [PMID: 10449061]
  34. J Neurophysiol. 1996 Apr;75(4):1714-29 [PMID: 8727408]
  35. Exp Neurol. 2009 Oct;219(2):524-32 [PMID: 19619534]
  36. J Comp Neurol. 1984 Mar 1;223(3):424-47 [PMID: 6707253]
  37. Proc Natl Acad Sci U S A. 1980 Apr;77(4):2333-7 [PMID: 6246540]
  38. J Comp Neurol. 1991 Jan 8;303(2):211-24 [PMID: 2013636]
  39. J Comp Neurol. 2006 Jul 1;497(1):32-41 [PMID: 16680781]
  40. Science. 1994 Sep 23;265(5180):1885-8 [PMID: 8091215]
  41. Exp Brain Res. 1998 Nov;123(1-2):110-6 [PMID: 9835399]
  42. Neurosci Behav Physiol. 2010 Jul;40(6):671-7 [PMID: 20535568]
  43. Neuron. 2001 Aug 2;31(2):247-60 [PMID: 11502256]
  44. Neurosci Behav Physiol. 2006 Oct;36(8):883-8 [PMID: 16964468]
  45. J Neurophysiol. 2000 Oct;84(4):1781-9 [PMID: 11024070]
  46. J Comp Neurol. 2010 Nov 15;518(22):4629-48 [PMID: 20886626]
  47. J Neurosci. 2009 Feb 25;29(8):2384-92 [PMID: 19244514]
  48. Behav Brain Res. 1991 Jul 1;44(1):87-99 [PMID: 1910574]
  49. J Neurosci. 1994 Nov;14(11 Pt 2):6978-91 [PMID: 7965093]

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