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D.S. Liao, A.F. Mower, C. Sato-Bigbee, R.L. Neve, A.S. Ramoa; Mechanisms of Cortical Recovery of Binocularity from Monocular Deprivation . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4108.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Activity dependent modulation of cAMP/Ca2+ binding protein (CREB) function is thought to be essential for plasticity in the visual cortex during monocular deprivation (MD). The present study tests the hypothesis that the same, activity-dependent molecular mechanisms mediate loss and recovery of function in the visual cortex following MD. Methods: Ferrets were monocularly deprived for five days during the peak of the critical period. Binocular vision was then restored resulting in full recovery of cortical binocularity as determined by quantitative single-unit recording techniques. To test whether recovery depends on neuronal activity in the visual cortex, either tetrodotoxin or citrate buffer control was infused into the cortex by osmotic minipump during the period of binocular vision. To test whether recovery depends on CREB activity, we suppressed cortical CREB function by expressing a dominant negative mutant (mCREB) carried in a herpes simplex vector during the period of binocular vision. Suppression of CREB function was verified by DNA binding assays and immunoblotting for C/EBPbeta. Results: Ferrets can recover a normal pattern of cortical binocularity if MD is followed by a period of binocular vision (n=228 neurons in 5 animals). Infusion of tetrodotoxin (n=80 neurons in 5 animals), but not citrate buffer control (n=80 neurons in 5 animals), prevented recovery of cortical binocularity following restoration of binocular vision (p<0.01, Mann Whitney U test). Surprisingly, recovery of binocularity was unaffected in mCREB treated regions of cortex (n=92 neurons in 5 animals), which were indistinguishable from untreated regions of cortex in the same animals (n=93 neurons in 5 animals, p>0.05, Mann Whiteney U test). Conclusions: These results show that cortical activity is required for recovery of binocularity following MD. In addition, they show that the activity dependent mechanisms regulating recovery of binocularity are independent of CREB function.
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