INT22269
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
There was a significant negative correlation between FPQ scores and Eso-PT on V1 (r = -0.57, P = 0.05). | |||||||||||||||
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Finally, aside from dorsal V4, the retinotopic organization of macaque early visual cortex (V1, V2, V3, V3A, and ventral V4) is remarkably similar to that observed in human fMRI studies. | |||||||||||||||
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As expected, strong activation of non-lesioned parts of V1 was preserved throughout the course of our experiments, whereas inside the lesioned V1 area coherence remained consistently at noise levels (? | |||||||||||||||
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Confirming the observation of a preserved cortical organization in a human blindsight subject [30], our data from V1 lesioned monkeys also demonstrate that the retinotopic structure of V1 cortex surrounding the lesion has not changed (Figure 4). | |||||||||||||||
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Note the excellent correspondence between the eccentricities in the part of V1 to be lesioned (V1 region between the arrowheads) and the LPZ in area V2. | |||||||||||||||
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As expected, strong activation of non-lesioned parts of V1 was preserved throughout the course of our experiments, whereas inside the lesioned V1 area coherence remained consistently at noise levels (? | |||||||||||||||
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Characterization of the V1 lesion | |||||||||||||||
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An important question that remains is whether higher cortical areas, particularly those with fast response latencies (such as V5/MT or FEF) play a role in generating the persisting activity in areas V2, V3 after V1 lesions. | |||||||||||||||
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To investigate whether the retinotopic organization of areas V1, V2, V3 is changed (e.g. reorganized) after V1 lesioning, we compared visual eccentricity versus cortical distance plots (Materials and Methods) across these areas both in the lesioned and the intact hemispheres. | |||||||||||||||
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Note that despite the V1 lesion, significant visually driven modulation remains in both the V2 and V3 LPZ. | |||||||||||||||
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Monitoring the LPZ activity over time starting one month following the V1 lesion did not reveal systematic changes in BOLD signal amplitude. | |||||||||||||||
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Similar to the extent of the V1 lesion, the LPZs in V2 and V3 covered an area equal to ? | |||||||||||||||
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Moreover, there is evidence from EBS studies in animals that the electrical stimulation of V1 produces a change of activity in neural structures that are known to be connected with the V1 (e.g., areas V2, V3, and MT) (Tolias et al., 2005). | |||||||||||||||
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Moreover, there is evidence from EBS studies in animals that the electrical stimulation of V1 produces a change of activity in neural structures that are known to be connected with the V1 (e.g., areas V2, V3, and MT) (Tolias et al., 2005). | |||||||||||||||
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They used a model with the following form to explain the responses of V1 neurons to plaid stimuli made of two superimposed sinusoidal gratings:(1) | |||||||||||||||
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There were good correlations between UV (corrected for dose) and the reciprocals of V1, Vdbeta, Vss, and plasma clearance of thiopental. | |||||||||||||||
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This analysis did confirm the expression of v1 (EU562295) and identified another alternatively spliced variant v3 (EU562297) which is widely expressed in adult tissues (Fig. 1D). | |||||||||||||||
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-RACE product of brain and testis as template and primers specific to v1 (v1F/R4 and v1F0/R4; Fig. 1C right panel), to check whether v1 was expressed in normal tissues. | |||||||||||||||
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We further assessed its expression in 33 normal human adult and fetal tissues by semi-quantitative PCR with specific primers targeting the v1, v2, or common exons (exon 2 and 3) (Fig. 1B), respectively. | |||||||||||||||
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Our results also reveal that OPCML transcripts v1 and v2 have different tissue expression patterns. | |||||||||||||||
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General Comments
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