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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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Related in: MedlinePlus

Chronic VEP recordings show that Arc−/− mice do not exhibit ocular dominance plasticity after short–term monocular deprivation. (a) WT mice exhibit a significant depression in contralateral (deprived eye) responses (n=11; Day 0=149±8.8 µV, 3 Day monocular deprivation=75.4±8.8 µV, *p< <0.0001, paired t–test). No significant change was observed in ipsilateral responses (n=11; Day 0=70.4±6.4 µV, 3 Day monocular deprivation=68.8±8 µV, p>0.8, paired t–test). Averaged waveforms across all mice are shown at top. (b)Arc−/− mice exhibit no changes in contralateral responses (n=8; Day 0=121±14.7 µV, 3 Day monocular deprivation=111.3±13.5 µV, p>0.2, paired t–test) or in ipsilateral responses (n=8; Day 0=92.5±15 µV, 3 Day monocular deprivation=85.8±10.7 µV, p>0.7, paired t–test). Averaged waveforms are shown at top. (c) WT mice exhibit a significant shift in the C/I ratio (n=11; Day 0=2.2±0.16, 3 Day monocular deprivation=1.2±0.16, *p<<0.0001, paired t–test), whereas Arc−/− mice exhibit no significant shift in the C/I ratio (n=8; Day 0=1.4±0.12, 3 Day monocular deprivation=1.5±0.33, p>0.8, paired t–test). Arc−/− mice exhibit a significantly smaller baseline C/I ratio than WT mice (WT n=11, C/I ratio 2.22±0.16; Arc−/− n=8, C/I ratio 1.37±0.12, #p<0.001, t–test). (Error bars represent SEM).
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Figure 3: Chronic VEP recordings show that Arc−/− mice do not exhibit ocular dominance plasticity after short–term monocular deprivation. (a) WT mice exhibit a significant depression in contralateral (deprived eye) responses (n=11; Day 0=149±8.8 µV, 3 Day monocular deprivation=75.4±8.8 µV, *p< <0.0001, paired t–test). No significant change was observed in ipsilateral responses (n=11; Day 0=70.4±6.4 µV, 3 Day monocular deprivation=68.8±8 µV, p>0.8, paired t–test). Averaged waveforms across all mice are shown at top. (b)Arc−/− mice exhibit no changes in contralateral responses (n=8; Day 0=121±14.7 µV, 3 Day monocular deprivation=111.3±13.5 µV, p>0.2, paired t–test) or in ipsilateral responses (n=8; Day 0=92.5±15 µV, 3 Day monocular deprivation=85.8±10.7 µV, p>0.7, paired t–test). Averaged waveforms are shown at top. (c) WT mice exhibit a significant shift in the C/I ratio (n=11; Day 0=2.2±0.16, 3 Day monocular deprivation=1.2±0.16, *p<<0.0001, paired t–test), whereas Arc−/− mice exhibit no significant shift in the C/I ratio (n=8; Day 0=1.4±0.12, 3 Day monocular deprivation=1.5±0.33, p>0.8, paired t–test). Arc−/− mice exhibit a significantly smaller baseline C/I ratio than WT mice (WT n=11, C/I ratio 2.22±0.16; Arc−/− n=8, C/I ratio 1.37±0.12, #p<0.001, t–test). (Error bars represent SEM).

Mentions: To determine how loss of Arc protein might influence cortical plasticity we deprived mice of vision through one eye by suturing the eyelid closed for 3–4 days during the period of heightened plasticity in mice (P25–32). We then used intrinsic signal imaging to measure the cortical response to visual stimulation within the binocular zone of V1, contralateral to the deprived eye. As described above, stimuli were shown to each eye alternately, and the strength of response to contralateral or ipsilateral stimulation was assessed and an ocular dominance index (ODI) calculated. This method has been shown to reliably detect the changes in ocular dominance that can be induced by monocular deprivation in WT animals35. In keeping with previous reports, WT mice show a robust decrease in ODI after brief deprivation (Fig. 2a). By assessing the magnitude of response in deprived and nondeprived animals, this shift appeared to be mediated by a diminished response to the deprived eye (Fig. 2b). By contrast, Arc−/− mice did not exhibit a change in ODI (Fig. 2a) and cortical responses to the deprived eye remained unchanged (Fig. 2c). These results indicate that Arc protein is required for the deprived eye depression induced by brief monocular deprivation. In addition to intrinsic signal optical imaging, which mainly measures responses in superficial cortical layers, we used chronic VEP recordings to monitor changes in the strength of cortical responses in layer 4 prior to and after monocular deprivation27, 34. Electrodes were implanted at a depth corresponding to layer 4 in V1 at P24–P25. After habituation to the restraint apparatus, VEPs were recorded at P28 in fully awake, head–restrained mice in response to square wave–reversing sinusoidal gratings. We collected baseline recordings, and then monocularly deprived animals for 3 days by lid suture. After opening the sutured eye we gathered post monocular deprivation recordings. WT mice showed a robust ocular dominance shift (Fig. 3a, c), whereas Arc−/− mice did not exhibit a change in ocular dominance (Fig. 3b, c). The shift in WT mice was due to a significant depression in deprived eye responses (Fig. 3a), which was not observed in Arc−/− mice (Fig. 3b).


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)

Chronic VEP recordings show that Arc−/− mice do not exhibit ocular dominance plasticity after short–term monocular deprivation. (a) WT mice exhibit a significant depression in contralateral (deprived eye) responses (n=11; Day 0=149±8.8 µV, 3 Day monocular deprivation=75.4±8.8 µV, *p< <0.0001, paired t–test). No significant change was observed in ipsilateral responses (n=11; Day 0=70.4±6.4 µV, 3 Day monocular deprivation=68.8±8 µV, p>0.8, paired t–test). Averaged waveforms across all mice are shown at top. (b)Arc−/− mice exhibit no changes in contralateral responses (n=8; Day 0=121±14.7 µV, 3 Day monocular deprivation=111.3±13.5 µV, p>0.2, paired t–test) or in ipsilateral responses (n=8; Day 0=92.5±15 µV, 3 Day monocular deprivation=85.8±10.7 µV, p>0.7, paired t–test). Averaged waveforms are shown at top. (c) WT mice exhibit a significant shift in the C/I ratio (n=11; Day 0=2.2±0.16, 3 Day monocular deprivation=1.2±0.16, *p<<0.0001, paired t–test), whereas Arc−/− mice exhibit no significant shift in the C/I ratio (n=8; Day 0=1.4±0.12, 3 Day monocular deprivation=1.5±0.33, p>0.8, paired t–test). Arc−/− mice exhibit a significantly smaller baseline C/I ratio than WT mice (WT n=11, C/I ratio 2.22±0.16; Arc−/− n=8, C/I ratio 1.37±0.12, #p<0.001, t–test). (Error bars represent SEM).
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Figure 3: Chronic VEP recordings show that Arc−/− mice do not exhibit ocular dominance plasticity after short–term monocular deprivation. (a) WT mice exhibit a significant depression in contralateral (deprived eye) responses (n=11; Day 0=149±8.8 µV, 3 Day monocular deprivation=75.4±8.8 µV, *p< <0.0001, paired t–test). No significant change was observed in ipsilateral responses (n=11; Day 0=70.4±6.4 µV, 3 Day monocular deprivation=68.8±8 µV, p>0.8, paired t–test). Averaged waveforms across all mice are shown at top. (b)Arc−/− mice exhibit no changes in contralateral responses (n=8; Day 0=121±14.7 µV, 3 Day monocular deprivation=111.3±13.5 µV, p>0.2, paired t–test) or in ipsilateral responses (n=8; Day 0=92.5±15 µV, 3 Day monocular deprivation=85.8±10.7 µV, p>0.7, paired t–test). Averaged waveforms are shown at top. (c) WT mice exhibit a significant shift in the C/I ratio (n=11; Day 0=2.2±0.16, 3 Day monocular deprivation=1.2±0.16, *p<<0.0001, paired t–test), whereas Arc−/− mice exhibit no significant shift in the C/I ratio (n=8; Day 0=1.4±0.12, 3 Day monocular deprivation=1.5±0.33, p>0.8, paired t–test). Arc−/− mice exhibit a significantly smaller baseline C/I ratio than WT mice (WT n=11, C/I ratio 2.22±0.16; Arc−/− n=8, C/I ratio 1.37±0.12, #p<0.001, t–test). (Error bars represent SEM).
Mentions: To determine how loss of Arc protein might influence cortical plasticity we deprived mice of vision through one eye by suturing the eyelid closed for 3–4 days during the period of heightened plasticity in mice (P25–32). We then used intrinsic signal imaging to measure the cortical response to visual stimulation within the binocular zone of V1, contralateral to the deprived eye. As described above, stimuli were shown to each eye alternately, and the strength of response to contralateral or ipsilateral stimulation was assessed and an ocular dominance index (ODI) calculated. This method has been shown to reliably detect the changes in ocular dominance that can be induced by monocular deprivation in WT animals35. In keeping with previous reports, WT mice show a robust decrease in ODI after brief deprivation (Fig. 2a). By assessing the magnitude of response in deprived and nondeprived animals, this shift appeared to be mediated by a diminished response to the deprived eye (Fig. 2b). By contrast, Arc−/− mice did not exhibit a change in ODI (Fig. 2a) and cortical responses to the deprived eye remained unchanged (Fig. 2c). These results indicate that Arc protein is required for the deprived eye depression induced by brief monocular deprivation. In addition to intrinsic signal optical imaging, which mainly measures responses in superficial cortical layers, we used chronic VEP recordings to monitor changes in the strength of cortical responses in layer 4 prior to and after monocular deprivation27, 34. Electrodes were implanted at a depth corresponding to layer 4 in V1 at P24–P25. After habituation to the restraint apparatus, VEPs were recorded at P28 in fully awake, head–restrained mice in response to square wave–reversing sinusoidal gratings. We collected baseline recordings, and then monocularly deprived animals for 3 days by lid suture. After opening the sutured eye we gathered post monocular deprivation recordings. WT mice showed a robust ocular dominance shift (Fig. 3a, c), whereas Arc−/− mice did not exhibit a change in ocular dominance (Fig. 3b, c). The shift in WT mice was due to a significant depression in deprived eye responses (Fig. 3a), which was not observed in Arc−/− mice (Fig. 3b).

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