Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parallel streams from the primary visual cortex (V1) to the second visual area (V2) are thought to mediate different aspects of visual perception in primates. One hypothesis is that the projection from cytochrome oxidase patches to thin stripes is responsible for color, whereas a separate pathway from interpatches to pale stripes mediates form. Recently, the notion of segregated pathways has been challenged by a report showing that patches and interpatches project equally to thin stripes. We made injections of a retrograde tracer, cholera toxin-B (CTB-Au), into macaque V2 thin stripes and counted the number of labeled cells in patches versus interpatches in layer 2/3. Analysis of eight thin-stripe injections showed that a mean of 81% of labeled cells were located in patches (defined as 33% of the surface area of V1). This result confirms that the projection to thin stripes arises predominately from patches. To assess the segregation of patch and interpatch projections, we injected CTB-Au in a pale stripe and horseradish peroxidase in an adjacent thin stripe. In both successful cases, interdigitated fields of labeled cells were present in V1. Less than 1% of cells were double-labeled, indicating that the populations of cells supplying thin stripes and pale stripes are quite independent. This finding means that different signals are likely conveyed by patches and interpatches to V2.
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PMID:Input to V2 thin stripes arises from V1 cytochrome oxidase patches. 1626 15

In the primate, connections between primary visual cortex (V1) and the second visual area (V2) are segregated according to the characteristic pattern of cytochrome oxidase (CO) activity in each of these cortical areas. Patches supply thin stripes, whereas interpatches supply pale stripes and thick stripes. Previously, the projection from patches to thin stripes was reported to arise exclusively from layer 2/3. In this present report, we made injections of a retrograde tracer, cholera toxin-B (CTB-Au), into macaque V2 thin stripes to re-examine the laminar origin of their input from V1. While the great majority of cells indeed resided in layer 2/3, small populations were also present in layers 4A, 4B, and 5/6. The location of CTB-filled cells in each layer was analyzed to determine the relationship with CO patches. Cells in layers 2/3, 4A, and 4B were aggregated into patches, forming columns that project to thin stripes. Surprisingly, cells in layer 5/6 were scattered, seemingly at random. These findings confirm that the main V1 projection to V2 stripes emanates from patches in layer 2/3. However, multiple V1 layers innervate V2 thin stripes, and the projection from layer 5/6 does not respect the patch/interpatch dichotomy.
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PMID:Neurons in V1 patch columns project to V2 thin stripes. 1674 May 82

In this study, we examined the topography of projections from facial afferents to the trigeminal brainstem nuclear complex (TBNC) in naked mole-rats using the neuronal tracer CTB-HRP. Tracer injections were made in a ventral to dorsal sequence that included the tooth pulp and dental ligament, ventral buccal pad, vibrissae, and the forehead. Labeled terminals were identified throughout the rostrocaudal extent of the TBNC, including the principal nucleus (Pr5), pars oralis (Sp5O), pars interpolaris (Sp5I), and pars caudalis (Sp5C) of the spinal trigeminal nucleus. Injections that labeled afferents from the tooth pulp and dental ligament resulted in heavy transport to dorsomedial portions of the TBNC, whereas injections made into progressively more dorsal regions of the face resulted in labeled terminals progressively more ventral and lateral in the nuclei. Injections that included dental afferents also labeled the mesencephalic nucleus of V, whereas injections into the skin of the face labeled cell bodies in the facial nucleus, and in most cases the motor nucleus of 5. Dental afferents in more rostral portions of the TBNC were coextensive with a cytochrome oxidase-dense region visible in alternate sections processed for chemoarchitecture.
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PMID:Central projections of trigeminal afferents innervating the face in naked mole-rats (Heterocephalus glaber). 1846 95

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 three animals raised with monocular suture. [(3)H]proline was injected into one eye to label the ocular dominance columns. Cholera toxin B subunit conjugated to gold (CTB-Au) was injected into 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 layers 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.
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PMID:Neuronal projections from V1 to V2 in amblyopia. 2235 49