Physiol Rep. 2015 Dec;3(12). doi: 10.14814/phy2.12623.
The most sensitive inputs to cutaneous representing regions of primary somatosensory cortex do not change with behavioral training.
Physiological reports
David T Blake, Elsie Spingath
PMID: 26634900
PMCID: PMC4760438 DOI: 10.14814/phy2.12623
Abstract
Learning a sensory detection task leads to an increased primary sensory cortex response to the detected stimulus, while learning a sensory discrimination task additionally leads to a decreased sensory cortex response to the distractor stimulus. Neural responses are scaled up, and down, in strength, along with concomitant changes in receptive field size. The present work considers neural response properties that are invariant to learning. Data are drawn from two animals that were trained to detect and discriminate spatially separate taps delivered to positions on the skin of their fingers. Each animal was implanted with electrodes positioned in area 3b, and responses were derived on a near daily basis over 84 days in animal 1 and 202 days in animal 2. Responses to taps delivered in the receptive field were quantitatively measured each day, and receptive fields were audiomanually mapped each day. In the subset of responses that had light cutaneous receptive fields, a preponderance of the days, the most sensitive region of the field was invariant to training. This skin region was present in the receptive field on all, or nearly all, occasions in which the receptive field was mapped, and this region constituted roughly half of the most sensitive region. These results suggest that maintaining the most sensitive inputs as dominant in cortical receptive fields provide a measure of stability that may be transformationally useful for minimizing reconstruction errors and perceptual constancy.
© 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
Keywords: Implant; map plasticity; receptive field; somatosensory
References
- Bull Johns Hopkins Hosp. 1959 Sep;105:133-62 - PubMed
- Annu Rev Neurosci. 1998;21:149-86 - PubMed
- Annu Rev Neurosci. 1995;18:129-58 - PubMed
- Nature. 2001 Aug 2;412(6846):549-53 - PubMed
- J Neurophysiol. 1957 Jul;20(4):408-34 - PubMed
- Somatosens Mot Res. 2002;19(4):347-57 - PubMed
- J Neurosci Methods. 2012 Oct 15;211(1):114-24 - PubMed
- Nature. 1995 Nov 2;378(6552):71-5 - PubMed
- J Comp Neurol. 1984 Apr 20;224(4):591-605 - PubMed
- Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):10114-9 - PubMed
- J Neurophysiol. 2002 Apr;87(4):1867-88 - PubMed
- J Neurophysiol. 1991 Sep;66(3):1048-58 - PubMed
- J Neurophysiol. 2013 Feb;109(4):1036-44 - PubMed
- J Physiol. 1978 Aug;281:101-25 - PubMed
- J Neurophysiol. 1992 May;67(5):1031-56 - PubMed
- Neuron. 2006 Oct 19;52(2):371-81 - PubMed
- Proc Natl Acad Sci U S A. 2010 Sep 7;107(36):15927-32 - PubMed
- J Neurophysiol. 1995 Dec;74(6):2685-706 - PubMed
- Behav Brain Res. 2005 Jul 30;162(2):207-21 - PubMed
- PLoS One. 2011 Jan 31;6(1):e15342 - PubMed
- Cereb Cortex. 1999 Apr-May;9(3):264-76 - PubMed
- Neuron. 2001 Oct 25;32(2):359-74 - PubMed
- J Comp Neurol. 1978 Sep 1;181(1):41-73 - PubMed
- J Physiol Paris. 1996;90(3-4):277-87 - PubMed
- J Neurophysiol. 2005 Sep;94(3):2239-50 - PubMed
- Physiol Rep. 2015 Dec;3(12): - PubMed
- Nat Rev Neurosci. 2004 Apr;5(4):279-90 - PubMed
- J Neurosci Methods. 1999 Oct 30;93(1):27-35 - PubMed
- J Physiol. 1970 Feb;206(2):419-36 - PubMed
- Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14828-32 - PubMed
- Science. 1957 Mar 22;125(3247):549-50 - PubMed
- J Neurophysiol. 1990 Jan;63(1):82-104 - PubMed
- Brain Res. 1976 Nov 5;116(2):181-204 - PubMed
- J Neurophysiol. 2009 Sep;102(3):1843-53 - PubMed
- J Neurosci Methods. 2007 Mar 30;161(1):62-74 - PubMed
- Med Biol Eng Comput. 1988 Jan;26(1):96-101 - PubMed
- J Neurophysiol. 1992 May;67(5):1015-30 - PubMed
- Cereb Cortex. 2008 Jul;18(7):1676-94 - PubMed
- J Neurosci. 1995 Mar;15(3 Pt 1):1631-47 - PubMed
Publication Types