title: Visual motion processing by neurons in area MT of macaque monkeys with experimental amblyopia.
abstract: Early experience affects the development of the visual system. Ocular misalignment or unilateral blur often causes amblyopia, a disorder that has become a standard for understanding developmental plasticity. Neurophysiological studies of amblyopia have focused almost entirely on the first stage of cortical processing in striate cortex. Here we provide the first extensive study of how amblyopia affects extrastriate cortex in nonhuman primates. We studied macaque monkeys (Macaca nemestrina) for which we have detailed psychophysical data, directly comparing physiological findings to perceptual capabilities. Because these subjects showed deficits in motion discrimination, we focused on area MT/V5, which plays a central role in motion processing. Most neurons in normal MT respond equally to visual stimuli presented through either eye; most recorded in amblyopes strongly preferred stimulation of the nonamblyopic (fellow) eye. The pooled responses of neurons driven by the amblyopic eye showed reduced sensitivity to coherent motion and preferred higher speeds, in agreement with behavioral measurements. MT neurons were more limited in their capacity to integrate motion information over time than expected from behavioral performance; neurons driven by the amblyopic eye had even shorter integration times than those driven by the fellow eye. We conclude that some, but not all, of the motion sensitivity deficits associated with amblyopia can be explained by abnormal development of MT.
authors.affiliation: Center for Neural Science, New York University, New York, New York 10003, USA.
authors.forename: Yasmine
authors.initials: Y
authors.lastname: El-Shamayleh
authors.forename: Lynne
authors.initials: L
authors.lastname: Kiorpes
authors.forename: Adam
authors.initials: A
authors.lastname: Kohn
authors.forename: J Anthony
authors.initials: JA
authors.lastname: Movshon
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000550:Amblyopia / Q000473:pathology* / Q000503:physiopathology*; D000818:Animals; D004192:Discrimination, Psychological / Q000502:physiology; D004195:Disease Models, Animal; D023882:Dominance, Ocular / Q000502:physiology; D004569:Electroencephalography / Q000379:methods; D008254:Macaca nemestrina; D009039:Motion Perception / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D010775:Photic Stimulation / Q000379:methods; D011336:Probability; D011601:Psychophysics; D012684:Sensory Thresholds / Q000502:physiology; D013997:Time Factors; D014793:Visual Cortex / Q000473:pathology*
references.citation: J Neurosci. 1996 Oct 15;16(20):6537-53
references.pmid: 8815931
references.citation: Eur J Neurosci. 1992;4(3):235-242
references.pmid: 12106369
references.citation: Vision Res. 2002 Jan;42(1):29-39
references.pmid: 11804629
references.citation: Neurosci Lett. 1997 Apr 11;225(3):173-6
references.pmid: 9147398
references.citation: Vision Res. 2002 Jan;42(2):169-79
references.pmid: 11809471
references.citation: Vision Res. 2003 Mar;43(6):729-38
references.pmid: 12604110
references.citation: J Neurosci. 2002 Nov 1;22(21):9475-89
references.pmid: 12417672
references.citation: J Neurophysiol. 2002 Nov;88(5):2530-46
references.pmid: 12424292
references.citation: J Vis. 2008 Apr 04;8(4):1.1-23
references.pmid: 18484840
references.citation: J Neurosci. 1998 Aug 15;18(16):6411-24
references.pmid: 9698332
references.citation: Nat Neurosci. 2005 Feb;8(2):220-8
references.pmid: 15657600
references.citation: Nature. 2001 Dec 20-27;414(6866):905-8
references.pmid: 11780062
references.citation: J Neurosci. 1999 Mar 15;19(6):2224-46
references.pmid: 10066275
references.citation: Invest Ophthalmol Vis Sci. 2005 Aug;46(8):3008-12
references.pmid: 16043878
references.citation: J Neurophysiol. 1986 Jun;55(6):1328-39
references.pmid: 3734858
references.citation: J Neurosci. 1987 May;7(5):1340-51
references.pmid: 3572484
references.citation: Vision Res. 1984;24(4):293-9
references.pmid: 6740951
references.citation: Vision Res. 1999;39(25):4152-60
references.pmid: 10755153
references.citation: J Neurophysiol. 1963 Nov;26:1003-17
references.pmid: 14084161
references.citation: J Neurosci. 1988 Jun;8(6):2201-11
references.pmid: 3385495
references.citation: J Neurophysiol. 2003 Jan;89(1):246-56
references.pmid: 12522176
references.citation: J Neurosci. 2002 Sep 15;22(18):8334-45
references.pmid: 12223588
references.citation: Vis Neurosci. 2006 Mar-Apr;23(2):247-56
references.pmid: 16638176
references.citation: J AAPOS. 2006 Dec;10(6):540-6
references.pmid: 17189148
references.citation: Vision Res. 1993 Nov;33(16):2301-11
references.pmid: 8273294
references.citation: Vision Res. 1986;26(12):1959-68
references.pmid: 3617536
references.citation: Vision Res. 2006 Aug;46(16):2571-80
references.pmid: 16530244
references.citation: J Neurosci. 1992 Dec;12(12):4745-65
references.pmid: 1464765
references.citation: Vision Res. 1999 Jan;39(1):19-30
references.pmid: 10211392
references.citation: Vis Neurosci. 2003 Sep-Oct;20(5):577-88
references.pmid: 14977336
references.citation: Vision Res. 2005 Feb;45(4):449-60
references.pmid: 15610749
references.citation: Philos Trans R Soc Lond B Biol Sci. 1977 Apr 26;278(961):377-409
references.pmid: 19791
references.citation: J Neurosci. 1996 Feb 15;16(4):1486-510
references.pmid: 8778300
references.citation: Nature. 1990 Jul 12;346(6280):174-7
references.pmid: 2366872