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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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Arc−/− mice exhibit no ocular dominance plasticity as assessed by chronic VEP recordings after long–term monocular deprivation. (a) WT mice exhibit a significant depression in contralateral (deprived eye) responses (n = 7; Day 0=152±9.2 µV, 7 Day monocular deprivation = 89.5±11.5 µV, *p<0.003, paired t–test) and a significant potentiation in ipsilateral responses (n = 7; Day 0=84.9±9.8 µV, 7 Day monocular deprivation=114.2±10.1 µV, #p<0.05, paired t–test). Averaged waveforms are shown at top. (b)Arc−/− mice exhibit no changes in contralateral (n=6; Day 0=112±2.2 µV, 7 Day monocular deprivation=100±6 µV, p>0.1, paired t–test) or in ipsilateral responses (n=8; Day 0=96±8.6 µV, 3 Day monocular deprivation=84±10 µV, p>0.4, paired t–test). Averaged waveforms are shown at top (c) WT mice exhibit a significant shift in the C/I ratio (n=7; Day 0=1.9±0.14, 7 Day monocular deprivation=0.8±0.06, *p < 0.0001, paired t–test), whereas Arc−/− mice exhibit no significant shift in the C/I ratio (n=6; Day 0=1.2±0.1, 7 Day monocular deprivation=1.25±0.11, p>0.7, paired t–test). Arc−/− mice exhibit a significantly smaller baseline C/I ratio than WT mice (WT n=7, C/I ratio 1.87±0.14; Arc−/− n=6, C/I ratio 1.2±0.1, #p<0.003) (Error bars represent SEM).
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Figure 6: Arc−/− mice exhibit no ocular dominance plasticity as assessed by chronic VEP recordings after long–term monocular deprivation. (a) WT mice exhibit a significant depression in contralateral (deprived eye) responses (n = 7; Day 0=152±9.2 µV, 7 Day monocular deprivation = 89.5±11.5 µV, *p<0.003, paired t–test) and a significant potentiation in ipsilateral responses (n = 7; Day 0=84.9±9.8 µV, 7 Day monocular deprivation=114.2±10.1 µV, #p<0.05, paired t–test). Averaged waveforms are shown at top. (b)Arc−/− mice exhibit no changes in contralateral (n=6; Day 0=112±2.2 µV, 7 Day monocular deprivation=100±6 µV, p>0.1, paired t–test) or in ipsilateral responses (n=8; Day 0=96±8.6 µV, 3 Day monocular deprivation=84±10 µV, p>0.4, paired t–test). Averaged waveforms are shown at top (c) WT mice exhibit a significant shift in the C/I ratio (n=7; Day 0=1.9±0.14, 7 Day monocular deprivation=0.8±0.06, *p < 0.0001, paired t–test), whereas Arc−/− mice exhibit no significant shift in the C/I ratio (n=6; Day 0=1.2±0.1, 7 Day monocular deprivation=1.25±0.11, p>0.7, paired t–test). Arc−/− mice exhibit a significantly smaller baseline C/I ratio than WT mice (WT n=7, C/I ratio 1.87±0.14; Arc−/− n=6, C/I ratio 1.2±0.1, #p<0.003) (Error bars represent SEM).

Mentions: To address whether open eye potentiation occurs in Arc−/− mice we used intrinsic signal imaging to measure response magnitudes in mice deprived for 7 days. In response to deprivation, WT mice showed a significant shift in ODI (Fig. 5a). Consistent with previous reports, we found that this shift was mediated by a significant increase in open eye responses (Fig. 5b). The increase in open eye response was accompanied by a decrease in the deprived eye response (Fig. 5b). Strikingly, Arc−/− mice did not show a shift in ODI or significant open eye potentiation (Fig. 5a,c). Similar results were found with VEP recordings after 7 days of monocular deprivation. WT mice exhibited a robust ocular dominance shift that was due to both significant deprived eye depression and open eye potentiation (Fig. 6a, c). In contrast, Arc−/− mice did not exhibit an ocular dominance shift or any significant changes in deprived eye or open eye responses (Fig. 6b, c).


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)

Arc−/− mice exhibit no ocular dominance plasticity as assessed by chronic VEP recordings after long–term monocular deprivation. (a) WT mice exhibit a significant depression in contralateral (deprived eye) responses (n = 7; Day 0=152±9.2 µV, 7 Day monocular deprivation = 89.5±11.5 µV, *p<0.003, paired t–test) and a significant potentiation in ipsilateral responses (n = 7; Day 0=84.9±9.8 µV, 7 Day monocular deprivation=114.2±10.1 µV, #p<0.05, paired t–test). Averaged waveforms are shown at top. (b)Arc−/− mice exhibit no changes in contralateral (n=6; Day 0=112±2.2 µV, 7 Day monocular deprivation=100±6 µV, p>0.1, paired t–test) or in ipsilateral responses (n=8; Day 0=96±8.6 µV, 3 Day monocular deprivation=84±10 µV, p>0.4, paired t–test). Averaged waveforms are shown at top (c) WT mice exhibit a significant shift in the C/I ratio (n=7; Day 0=1.9±0.14, 7 Day monocular deprivation=0.8±0.06, *p < 0.0001, paired t–test), whereas Arc−/− mice exhibit no significant shift in the C/I ratio (n=6; Day 0=1.2±0.1, 7 Day monocular deprivation=1.25±0.11, p>0.7, paired t–test). Arc−/− mice exhibit a significantly smaller baseline C/I ratio than WT mice (WT n=7, C/I ratio 1.87±0.14; Arc−/− n=6, C/I ratio 1.2±0.1, #p<0.003) (Error bars represent SEM).
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Figure 6: Arc−/− mice exhibit no ocular dominance plasticity as assessed by chronic VEP recordings after long–term monocular deprivation. (a) WT mice exhibit a significant depression in contralateral (deprived eye) responses (n = 7; Day 0=152±9.2 µV, 7 Day monocular deprivation = 89.5±11.5 µV, *p<0.003, paired t–test) and a significant potentiation in ipsilateral responses (n = 7; Day 0=84.9±9.8 µV, 7 Day monocular deprivation=114.2±10.1 µV, #p<0.05, paired t–test). Averaged waveforms are shown at top. (b)Arc−/− mice exhibit no changes in contralateral (n=6; Day 0=112±2.2 µV, 7 Day monocular deprivation=100±6 µV, p>0.1, paired t–test) or in ipsilateral responses (n=8; Day 0=96±8.6 µV, 3 Day monocular deprivation=84±10 µV, p>0.4, paired t–test). Averaged waveforms are shown at top (c) WT mice exhibit a significant shift in the C/I ratio (n=7; Day 0=1.9±0.14, 7 Day monocular deprivation=0.8±0.06, *p < 0.0001, paired t–test), whereas Arc−/− mice exhibit no significant shift in the C/I ratio (n=6; Day 0=1.2±0.1, 7 Day monocular deprivation=1.25±0.11, p>0.7, paired t–test). Arc−/− mice exhibit a significantly smaller baseline C/I ratio than WT mice (WT n=7, C/I ratio 1.87±0.14; Arc−/− n=6, C/I ratio 1.2±0.1, #p<0.003) (Error bars represent SEM).
Mentions: To address whether open eye potentiation occurs in Arc−/− mice we used intrinsic signal imaging to measure response magnitudes in mice deprived for 7 days. In response to deprivation, WT mice showed a significant shift in ODI (Fig. 5a). Consistent with previous reports, we found that this shift was mediated by a significant increase in open eye responses (Fig. 5b). The increase in open eye response was accompanied by a decrease in the deprived eye response (Fig. 5b). Strikingly, Arc−/− mice did not show a shift in ODI or significant open eye potentiation (Fig. 5a,c). Similar results were found with VEP recordings after 7 days of monocular deprivation. WT mice exhibited a robust ocular dominance shift that was due to both significant deprived eye depression and open eye potentiation (Fig. 6a, c). In contrast, Arc−/− mice did not exhibit an ocular dominance shift or any significant changes in deprived eye or open eye responses (Fig. 6b, c).

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