“…Using fMRI in humans, it has been shown that topographic regions of V1 can be activated simply by asking normal subjects to imagine (with eyes closed) visual objects within particular areas of the visual field (i.e. in the absence of any direct stimulus to the retina). Additionally, evidence indicates that, in congenitally blind subjects….” —— Other inputs to V1 Besides the LGN, V1 receives a variety of other modulatory inputs both from subcortical and cortical areas. These inputs include serotonergic, noradrenergic, and cholinergic inputs from the brainstem and basal forebrain nuclei, respectively. The latter inputs show differences in density in the V1 layers, but show a much less specific pattern of innervation than do LGN inputs. Other input sources include the intralaminar nuclei of the thalamus and the pulvinar, both of which send broad projections most heavily to layers I and II of V1. Additionally, there are retinotopically more specific sources of input to V1, including from the claustrum and visual (V) areas 2, 3, 4, & 5 (V4 and V5 are also referred to as the dorsal lateral (DL) and middle temporal (MT) visual areas, respectively). , As a general rule any area to which V1 projects also sends feedback to V1. However, some higher-order visual areas in the temporal and parietal lobes that do not receive direct projections from V1 send axons to V1. With the exception of the claustrum, whose axons overlap with M and P axons in layer IVC, all of the other extrastriate visual inputs to V1 terminate outside of layer IVC. So why are there so many other inputs to V1 if the main drive comes from the LGN? As with the LGN described earlier, the numerous non-geniculate inputs to V1 regulate which visual signals will be transmitted to higher-order visual areas. An example of the impact that these non-LGN connections to V1 can have has been demonstrated using fMRI neural imaging methods. Using fMRI in humans, it has been shown that topographic regions of V1 can be activated simply by asking normal subjects to imagine (with eyes closed) visual objects within particular areas of the visual field (i.e. in the absence of any direct stimulus to the retina). Additionally, evidence indicates that, in congenitally blind subjects, major rearrangements of connections can take place such that somatosensory inputs can now activate V1, or changes in receptor distribution at the retina can cause rewiring of V1 ( Box 30.2 ). These findings argue that non-LGN inputs can have a strong impact on activity in V1 and that V1 is highly plastic during development.

“…Using fMRI in humans, it has been shown that topographic regions of V1 can be activated simply by asking normal subjects to imagine (with eyes closed) visual objects within particular areas of the visual field (i.e. in the absence of any direct stimulus to the retina). Additionally, evidence indicates that, in congenitally blind subjects….”
 
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Other inputs to V1
 
Besides the LGN, V1 receives a variety of other modulatory inputs both from subcortical and cortical areas. These inputs include serotonergic, noradrenergic, and cholinergic inputs from the brainstem and basal forebrain nuclei, respectively. The latter inputs show differences in density in the V1 layers, but show a much less specific pattern of innervation than do LGN inputs. Other input sources include the intralaminar nuclei of the thalamus and the pulvinar, both of which send broad projections most heavily to layers I and II of V1. Additionally, there are retinotopically more specific sources of input to V1, including from the claustrum and visual (V) areas 2, 3, 4, & 5 (V4 and V5 are also referred to as the dorsal lateral (DL) and middle temporal (MT) visual areas, respectively). , As a general rule any area to which V1 projects also sends feedback to V1. However, some higher-order visual areas in the temporal and parietal lobes that do not receive direct projections from V1 send axons to V1. With the exception of the claustrum, whose axons overlap with M and P axons in layer IVC, all of the other extrastriate visual inputs to V1 terminate outside of layer IVC.
 
So why are there so many other inputs to V1 if the main drive comes from the LGN? As with the LGN described earlier, the numerous non-geniculate inputs to V1 regulate which visual signals will be transmitted to higher-order visual areas. An example of the impact that these non-LGN connections to V1 can have has been demonstrated using fMRI neural imaging methods. Using fMRI in humans, it has been shown that topographic regions of V1 can be activated simply by asking normal subjects to imagine (with eyes closed) visual objects within particular areas of the visual field (i.e. in the absence of any direct stimulus to the retina). Additionally, evidence indicates that, in congenitally blind subjects, major rearrangements of connections can take place such that somatosensory inputs can now activate V1, or changes in receptor distribution at the retina can cause rewiring of V1 ( Box 30.2 ). These findings argue that non-LGN inputs can have a strong impact on activity in V1 and that V1 is highly plastic during development.

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