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Loss of Arc renders the visual cortex impervious to the effects of sensory experience or deprivation.

McCurry CL, Shepherd JD, Tropea D, Wang KH, Bear MF, Sur M - Nat. Neurosci. (2010)

Bottom Line: A myriad of mechanisms have been suggested to account for the full richness of visual cortical plasticity.We found that visual cortex lacking Arc is impervious to the effects of deprivation or experience.These data suggest that Arc is required for the experience-dependent processes that normally establish and modify synaptic connections in visual cortex.

View Article: PubMed Central - PubMed

Affiliation: Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

ABSTRACT
A myriad of mechanisms have been suggested to account for the full richness of visual cortical plasticity. We found that visual cortex lacking Arc is impervious to the effects of deprivation or experience. Using intrinsic signal imaging and chronic visually evoked potential recordings, we found that Arc(-/-) mice did not exhibit depression of deprived-eye responses or a shift in ocular dominance after brief monocular deprivation. Extended deprivation also failed to elicit a shift in ocular dominance or open-eye potentiation. Moreover, Arc(-/-) mice lacked stimulus-selective response potentiation. Although Arc(-/-) mice exhibited normal visual acuity, baseline ocular dominance was abnormal and resembled that observed after dark-rearing. These data suggest that Arc is required for the experience-dependent processes that normally establish and modify synaptic connections in visual cortex.

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Loss of Arc does not affect V1 responsiveness and organization. (a) Intrinsic signal imaging of V1 (left inset) in WT and Arc−/− mice. (Top) Ocular dominance map of V1, in a WT mouse (left) and an Arc−/− mouse (right); MZ=monocular zone, BZ=binocular zone. Scale at right illustrates binocularity index of pixels. Scale bar= 500 µm. V1 in Arc−/− mice is similar to that in WT mice in total area (WT n=6, area=1.401±0.07 mm2; Arc−/− n=10, area=1.270±0.15 mm2; p>0.5, t–test). (Bottom) Retinotopic organization of V1 in a WT mouse (left), and an Arc−/− mouse (right). Each image shows the mapping of elevation according to scale at top right. (b) Scatter analysis of 50×50 pixel area within white box in A, for WT and Arc−/− mice. The receptive field center (phase) difference between sets of 5 adjacent pixels is shown in histogram at right. The precision of local mapping is comparable between WT and Arc−/− mice.
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Figure 1: Loss of Arc does not affect V1 responsiveness and organization. (a) Intrinsic signal imaging of V1 (left inset) in WT and Arc−/− mice. (Top) Ocular dominance map of V1, in a WT mouse (left) and an Arc−/− mouse (right); MZ=monocular zone, BZ=binocular zone. Scale at right illustrates binocularity index of pixels. Scale bar= 500 µm. V1 in Arc−/− mice is similar to that in WT mice in total area (WT n=6, area=1.401±0.07 mm2; Arc−/− n=10, area=1.270±0.15 mm2; p>0.5, t–test). (Bottom) Retinotopic organization of V1 in a WT mouse (left), and an Arc−/− mouse (right). Each image shows the mapping of elevation according to scale at top right. (b) Scatter analysis of 50×50 pixel area within white box in A, for WT and Arc−/− mice. The receptive field center (phase) difference between sets of 5 adjacent pixels is shown in histogram at right. The precision of local mapping is comparable between WT and Arc−/− mice.

Mentions: We used intrinsic signal imaging to test whether loss of Arc altered V1 responses and retinotopic organization32, 33. Because previous studies implicated Arc protein in regulation of AMPARs, the major contributors to excitatory synaptic transmission, we asked whether loss of Arc protein would influence the strength of response to visual stimulation in mouse V1. Mice were shown a periodic moving bar of light and cortical responses to contralateral and ipsilateral eye stimulation were assessed with optical imaging of intrinsic signals to create an ocular dominance map of V1 (see Methods). V1 in Arc−/− mice was similar to that in WT mice in area and organization of binocular and monocular zones (Fig. 1a). To examine whether loss of Arc protein might impact retinotopic organization (Fig. 1a), we evaluated scatter within the retinotopic (phase) maps (Fig. 1b). Map organization in Arc−/− mice was indistinguishable from WT mice (Supplementary Fig. 2a). In addition, there was no significant difference in the magnitude of response to binocular stimulation in V1 (Supplementary Fig. 2b), nor were there differences in responses from the monocular zone of V1 (data not shown). These data demonstrate that loss of Arc protein does not grossly disrupt the development of V1 organization. We assessed visual acuity in Arc−/− mice by measuring VEPs in response to sinusoidal gratings at various spatial frequencies, a well established method of assessing visual function in mice27, 34. There was no significant difference between WT and Arc−/− mice in evoked responses at high spatial frequencies, regardless of whether responses were evoked binocularly or monocularly through either eye, suggesting that Arc−/− mice have normal visual acuity and responsiveness (Supplementary Fig. 3).


Loss of Arc renders the visual cortex impervious to the effects of sensory experience or deprivation.

McCurry CL, Shepherd JD, Tropea D, Wang KH, Bear MF, Sur M - Nat. Neurosci. (2010)

Loss of Arc does not affect V1 responsiveness and organization. (a) Intrinsic signal imaging of V1 (left inset) in WT and Arc−/− mice. (Top) Ocular dominance map of V1, in a WT mouse (left) and an Arc−/− mouse (right); MZ=monocular zone, BZ=binocular zone. Scale at right illustrates binocularity index of pixels. Scale bar= 500 µm. V1 in Arc−/− mice is similar to that in WT mice in total area (WT n=6, area=1.401±0.07 mm2; Arc−/− n=10, area=1.270±0.15 mm2; p>0.5, t–test). (Bottom) Retinotopic organization of V1 in a WT mouse (left), and an Arc−/− mouse (right). Each image shows the mapping of elevation according to scale at top right. (b) Scatter analysis of 50×50 pixel area within white box in A, for WT and Arc−/− mice. The receptive field center (phase) difference between sets of 5 adjacent pixels is shown in histogram at right. The precision of local mapping is comparable between WT and Arc−/− mice.
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Figure 1: Loss of Arc does not affect V1 responsiveness and organization. (a) Intrinsic signal imaging of V1 (left inset) in WT and Arc−/− mice. (Top) Ocular dominance map of V1, in a WT mouse (left) and an Arc−/− mouse (right); MZ=monocular zone, BZ=binocular zone. Scale at right illustrates binocularity index of pixels. Scale bar= 500 µm. V1 in Arc−/− mice is similar to that in WT mice in total area (WT n=6, area=1.401±0.07 mm2; Arc−/− n=10, area=1.270±0.15 mm2; p>0.5, t–test). (Bottom) Retinotopic organization of V1 in a WT mouse (left), and an Arc−/− mouse (right). Each image shows the mapping of elevation according to scale at top right. (b) Scatter analysis of 50×50 pixel area within white box in A, for WT and Arc−/− mice. The receptive field center (phase) difference between sets of 5 adjacent pixels is shown in histogram at right. The precision of local mapping is comparable between WT and Arc−/− mice.
Mentions: We used intrinsic signal imaging to test whether loss of Arc altered V1 responses and retinotopic organization32, 33. Because previous studies implicated Arc protein in regulation of AMPARs, the major contributors to excitatory synaptic transmission, we asked whether loss of Arc protein would influence the strength of response to visual stimulation in mouse V1. Mice were shown a periodic moving bar of light and cortical responses to contralateral and ipsilateral eye stimulation were assessed with optical imaging of intrinsic signals to create an ocular dominance map of V1 (see Methods). V1 in Arc−/− mice was similar to that in WT mice in area and organization of binocular and monocular zones (Fig. 1a). To examine whether loss of Arc protein might impact retinotopic organization (Fig. 1a), we evaluated scatter within the retinotopic (phase) maps (Fig. 1b). Map organization in Arc−/− mice was indistinguishable from WT mice (Supplementary Fig. 2a). In addition, there was no significant difference in the magnitude of response to binocular stimulation in V1 (Supplementary Fig. 2b), nor were there differences in responses from the monocular zone of V1 (data not shown). These data demonstrate that loss of Arc protein does not grossly disrupt the development of V1 organization. We assessed visual acuity in Arc−/− mice by measuring VEPs in response to sinusoidal gratings at various spatial frequencies, a well established method of assessing visual function in mice27, 34. There was no significant difference between WT and Arc−/− mice in evoked responses at high spatial frequencies, regardless of whether responses were evoked binocularly or monocularly through either eye, suggesting that Arc−/− mice have normal visual acuity and responsiveness (Supplementary Fig. 3).

Bottom Line: A myriad of mechanisms have been suggested to account for the full richness of visual cortical plasticity.We found that visual cortex lacking Arc is impervious to the effects of deprivation or experience.These data suggest that Arc is required for the experience-dependent processes that normally establish and modify synaptic connections in visual cortex.

View Article: PubMed Central - PubMed

Affiliation: Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

ABSTRACT
A myriad of mechanisms have been suggested to account for the full richness of visual cortical plasticity. We found that visual cortex lacking Arc is impervious to the effects of deprivation or experience. Using intrinsic signal imaging and chronic visually evoked potential recordings, we found that Arc(-/-) mice did not exhibit depression of deprived-eye responses or a shift in ocular dominance after brief monocular deprivation. Extended deprivation also failed to elicit a shift in ocular dominance or open-eye potentiation. Moreover, Arc(-/-) mice lacked stimulus-selective response potentiation. Although Arc(-/-) mice exhibited normal visual acuity, baseline ocular dominance was abnormal and resembled that observed after dark-rearing. These data suggest that Arc is required for the experience-dependent processes that normally establish and modify synaptic connections in visual cortex.

Show MeSH
Related in: MedlinePlus