Neuronal Projections from V1 to V2 in Amblyopia

Abstract

The mechanism of amblyopia in children with congenital cataract is not understood fully, but studies in macaques have shown that geniculate synapses are lost in striate cortex (V1). To search for other projection abnormalities in amblyopia, the pathway from V1 to V2 was examined using a triple-label technique in 3 animals raised with monocular suture. [3H]proline was injected into one eye to label the ocular dominance columns. Cholera toxin B-gold (CTB-Au) was injected in V2 to label V1 projection neurons. Alternate sections were processed for cytochrome oxidase (CO) and CTB-Au, or dipped for autoradiography. Eight fields of CTB-Au-labeled cells in V1 opposite injection sites were plotted in layers 2/3 or 4B. After thin stripe injection, labeled cells were concentrated in CO patches. Despite column shrinkage, cells in deprived and normal columns were equal in size and density, in both layer 2/3 and 4B. After pale or thick stripe injection, labeled cells were concentrated in interpatches. Only 23% of projection neurons originated from deprived columns. This reduction exceeded the degree of column shrinkage, a result explained by the fact that column shrinkage causes disproportionate loss of interpatch territory. These data indicate that early monocular form deprivation does not alter the segregation of patch and interpatch pathways to V2 stripes, or cause selective loss or atrophy of V1 projection neurons. The effect of shrinkage of geniculocortical afferents in layer 4C following visual deprivation is not amplified further by attenuation of the amblyopic eye’s projections from V1 to V2.

Covert spatial attention is functionally intact in amblyopic human adults

“…This may be due, at least in part, to a reduced strength of amblyopic eye input to higher level areas (Anderson, Holliday, & Harding, 1999; Anderson & Swettenham, 2006). Thus, whereas V1 anomalies may be at the root of amblyopic impairments, they are likely to be amplified by the progressive degradation of feed-forward neural signals in the dorsal and ventral pathways (Barnes, Hess, Dumoulin, Achtman, & Pike, 2001; Choi et al, 2001; Conner, Odom, Schwartz, & Mendola, 2007; El-Shamayleh, Kiorpes, Kohn, & Movshon, 2010; Goodyear, Nicolle, Humphrey, & Menon, 2000; Ho & Giaschi, 2009; Imamura et al, 1997; Kiorpes, 2006; Kiorpes et al, 1998; Kiorpes & Movshon, 1996; Levi, 2006; X. Li, Dumoulin, Mansouri, & Hess, 2007; Muckli et al, 2006; Secen, Culham, Ho, & Giaschi, 2011; Shooner et al, 2015; Sincich, Jocson, & Horton, 2012). Indeed, several studies have shown reduced levels of activation for amblyopes than neurotypical observers as far downstream as parietal and ventral temporal cortex (Ho & Giaschi, 2009; Hyvarinen, Hyvarinen, & Linnankoski, 1981; Lerner et al, 2006; Secen et al, 2011; review by Anderson & Swettenham, 2006).…”

From Basic Visual Science to Neurodevelopmental Disorders: The Voyage of Environmental Enrichment-Like Stimulation

“…Amblyopia is easily modeled in animals, keeping one eye deprived of pattern vision via prolonged eyelid suture (monocular deprivation (MD)), started during the CP and protracted until adulthood [32, 33]. The procedure causes a marked ocular dominance shift towards the open eye in the binocular neurons of the primary visual cortex, determined by functional and structural empowering of the inputs emerging from the ipsilateral/spared eye, at the expense of those from the contralateral/deprived one [34].…”

Amblyopia: neural basis and therapeutic approaches

“…Some researchers have speculated that cellular interactions in amblyopia are reduced in intensity, whereas others think that sensitivity and spatial resolution are both reduced in cortical neurons stimulated by foveal projections (63) . Furthermore, it has been speculated that the cortical deficits would not necessarily occur in V1 (64) ; perhaps the problem might lie only in V2 and V3, with normal processing in V1 (65) . The following hypothesis has also been proposed in the literature: The amblyopic projections are disordered, and there is a significant reduction (or loss) of spatial resolution of cortical neurons stimulated by projections from the fovea, which is thicker in subjects with amblyopia when evaluated by optical coherence tomography (1) .…”