Critical period ocular dominance plasticity and Adult ocular dominance plasticity show different time courses and response changes. (A) Time course of OD shifts in the critical period after varying lengths of MD. Data indicated by open circles were taken from Fig.1 for comparison (n=3-6; * p<0.05; ** p<0.01). (B) Maximum magnitude of responses elicited by the stimulus to the contralateral (black bars) or ipsilateral (white bars) after varying length of MD in critical period mice. For statistical comparison, data from groups which were qualitatively indistinguishable were pooled as indicated (n=6-17, *p<0.05). (C) Time course of OD shift in adult mice after varying length of MD. Data indicated in open circles were taken from Fig.1 for comparison (n=4-7, *p<0.05, **p<0.01). (D) Maximum magnitude of responses elicited by the stimulus to the contralateral (black bars) or ipsilateral eye (white bars) in adult mice. Data from groups that did not show qualitative difference were pooled as indicated for statistical comparison (n=10-11; ** p<0.01) (E) Polar maps of cortical responses in critical period and adult mice with or without 7-day MD. Scale bar = 1mm.

CPP-mediated suppression of NMDA receptor function in visual cortex and NMDA receptor-dependent ocular dominance plasticity in the critical period. (A) Suppression of Zif268 expression in visual cortex at 24 h after CPP injection in juvenile and adult mice. CPP or control saline (Cont) were injected into mice in the critical period at P28 (left panels) and in adulthood at P80 (middle panels) and the amount of zif268 (upper panels) and beta III tubulin (lower panels) proteins at 24 h after injection was quantified by immunoblotting. Right panel shows summary data (n=3 each, * p<0.05, ** p<0.01) (B) Mice in the critical period were treated with CPP 4-6 h prior to MD on Day 0 and every 24 h thereafter and were imaged at 4 days after MD. (C) OD shifts after 4-day MD were blocked by daily CPP treatment in critical period mice (n= 3-6; * p<0.05, ** p<0.01). Data indicated in open circles were taken from Fig.1 for comparison. (D) Decrease in the deprived eye’s response after 4-day MD was prevented by daily CPP treatment in critical period mice (n=3-6). (E) Polar maps of cortical responses of critical period mice with or without CPP treatment and MD.

Different functional consequences for binocular responsiveness in the critical period and adult visual cortices after monocular and binocular deprivation. (A) In juvenile mice, brief (4-day) MD causes robust shift in ocular dominance toward the open eye in both the contralateral and ipsilateral hemispheres. These processes are mediated primarily by rapid decreases in the deprived eyes’ responsiveness. The degree of plasticity is equal in the two hemispheres. (B) BD has no effect on ocular dominance, suggesting that OD shifts produced by brief MD in the critical period are based on competition between inputs from the two eyes. (C) By contrast, in adult mice, longer (7-day) MD causes a significantly large shift in the contralateral hemisphere to the deprived eye and only a hint of OD shift in the ipsilateral hemisphere. These shifts are mediated by transient small decreases in the deprived eye’s response at 4 day after MD followed by recovery from the depression of the deprived eye’s response and an increase in the response to the non-deprived eye at 7 days after MD. This asymmetry suggests that the degree of plasticity is determined by the strength of the deprived input. (D) 7-day BD causes a mild and atypical OD shift. This implies that the OD shifts in adult visual cortex are not based purely on competition in the conventional sense.

The effects of brief MD on mice of different ages. (A) (a) A short sweeping bar moving upward or downward was presented in the binocular visual field of a mouse and the evoked cortical activity was imaged with a CCD camera. (b) Occipital cortex of left hemisphere was exposed (upper left) and cortical blood vessel pattern was captured under green light (lower left). Activity maps of retinotopy (upper right) and magnitude (lower light) were imaged under red light to create polar maps as seen hereafter. (B) OD index following brief (4-5 d) MD of the contralateral eye in pre-critical period mice (a; pre-CP, n=3 each), critical period mice (b; CP, n=5-6) or adult mice (c; Adult; n=5 each). Y-axis shows OD index as described in Methods. The mice subjected to brief MD (MD) showed a significantly lower OD index in CP, but neither in pre-CP nor adulthood. The downward arrow shown to right illustrates that a lower OD index after MD indicates greater plasticity. ** p<0.01; n.s., not significant (C) Maximum response magnitude expressed as fractional change in light reflectance elicited by stimulation of the contralateral (black bars) or ipsilateral (white bars) eye of mice deprived (a) before or (b) during the critical period or (c) in adulthood. Brief MD reduced responsiveness of the deprived eye significantly only in CP, but not pre-CP or in adulthood. * p<0.05. (D) Polar maps of responses in binocular visual cortex of mice of different ages with or without brief MD. Scale bar, 1 mm.

Effects of ipsilateral MD and BD in juvenile and adult mice. (A) OD shifts after 4-day ipsilateral-eye MD and BD in critical period mice. The OD bias shifted towards the contralateral non-deprived eye after 4-day ipsilateral MD. BD did not change OD (n=3-6, *p<0.05, **p<0.01). Data indicated in open circles were taken from Fig. 1 for comparison. (B) Maximum response magnitude for each eye after 4-day ipsilateral-eye MD and BD. The value for the ipsilateral closed eye response of mice with 4-day ipsilateral MD was significantly smaller than that of control mice (*p<0.05, Cont Ipsi vs. Ipsi MD Ipsi n=3-6). (C) Polar maps of cortical responses in critical period mice with no MD, 4-day ipsilateral MD and BD. (D) OD after 7-15 day ipsilateral-eye MD and 7-day BD in adult mice. OD changed only very slightly toward the contralateral non-deprived eye after ipsilateral-eye MD. BD caused moderate and significant ODI shift toward the ipsilateral eye (n=3-7, *p<0.05). Data indicated in open circles were taken from Fig.1 for comparison. (E) Maximum response magnitude for each eye after 7-15 day ipsilateral MD and 7-day BD in adult mice. The ipsilateral eye’s response magnitude after BD is significantly larger than that of mice without deprivation (n=4-5, *p<0.05). (F) Polar maps of cortical responses in adult mice with no MD, 7-day ipsilateral MD and BD.

Role of NMDA receptor activation in adult ocular dominance plasticity. (A) In 7-day CPP treatment (Day 0-6), adult mice were treated with CPP 4-6 hour prior to MD on Day 0 and every 24 h thereafter and were imaged at 7 days after MD. In 3-day CPP treatment (Day 4-6), adult mice were subjected to 7-day MD with no CPP treatment for the first 4 days. Daily CPP injection was then started from Day 4 to Day 6. (B) OD shifts after 7-day MD in adult mice were fully blocked by 7-day CPP treatment (n= 4-7; * p<0.05). Mice with 3-day CPP treatment showed partial blockade of OD shifts compared to the full effect produced by 7-day MD (n= 4-7, * p<0.05). Data indicated in open circles were taken from Figs. 1 and 2 for comparison. (C) Polar maps of cortical responses in adult mice with or without CPP treatment and MD.