The adult cerebral cortex can adapt to environmental change. Using monocular deprivation as a paradigm, we find that rapid experience-dependent plasticity exists even in the mature primary visual cortex. However, adult cortical plasticity differs from developmental plasticity in two important ways. First, the effect of adult, but not juvenile monocular deprivation is strongly suppressed by administration of barbiturate just prior to recording visual evoked potentials, suggesting that the effect of adult experience can be inactivated acutely. Second, the effect of deprivation is less persistent over time in adults than in juveniles. This correlates with the known decline in CREB function during maturation of the visual cortex. To compensate for this decline in CREB function, we expressed persistently active VP16-CREB and find that it causes adult plasticity to become persistent. These results suggest that in development and adulthood, the regulation of a trans-synaptic signaling pathway controls the adaptive potential of cortical circuits.A primary function of the brain is to integrate the individual into a continually changing environment. Some aspects of this integration are accomplished through developmental processes, other aspects through learning. Although learning can occur throughout life, many behaviors, from language to sexual behavior, are shaped profoundly by early life experience. In this study, we have examined how the adaptive capacity of the cerebral cortex changes with maturation.A classical model of developmental plasticity is ocular dominance plasticity (Wiesel and Hubel 1963;Hubel and Wiesel 1998). Hubel and Wiesel showed that closing one eye of an infant cat produced a visual cortex dominated by the nondeprived eye. Closing an eye of an adult cat was ineffective. Single-unit studies in a number of mammalian systems, ranging from rodents to primates, have found that ocular dominance plasticity is restricted to a period prior to puberty (Hubel and Wiesel 1970;Blakemore et al. 1978;Olson and Freeman 1980;Issa et al. 1999;Fagiolini and Hensch 2000). The amount of deprivation required to alter the responses of visual cortical neurons depends on the animal's age. In the cat, during the peak of the critical period (4-5 wk of age), as little as 1 d of deprivation is sufficient to cause ocular dominance changes (Olson and Freeman 1975). Near the age of puberty, weeks or months of deprivation are necessary to induce changes observable by single-unit recordings, and the changes are thought to occur only in layers 2 and 3 of the visual cortex (Daw et al. 1992).In the clinical literature, however, there are reports suggesting that improvement of visual acuity can occur in adult patients with amblyopia, a central disorder of visual acuity, following patching of the normal eye (Selenow and Ciuffreda 1986; Saulles 1987; Rutstein and Fuhr 1992; Wick and Wingard 1992). Furthermore, a lengthy period of monocular occlusion caused by a dense cataract (Sloper and Collins 1995) can cause significant changes in visu...
Rats and mice are the species most frequently used for cellular and biochemical studies of plasticity, but only a few studies have examined developmentally regulated visual plasticity in these species. Here we report a study of the critical period for monocular deprivation in Long-Evans rats in which visual pattern sweep evoked potentials (sweep VEP) was used. Successful recording of sweep VEPs depended on establishing a stable light plane of anesthesia. We found a mixture of halothane and NO2 to be suitable. During a single trial lasting 10 s, anesthetized rats (n = 28) viewed a sinusoidal contrast grating (spatial frequency of 0.13 cycles/deg) that reversed phase at 3 Hz. During the trial, the grating contrast increased logarithmically from 1 to 70%. Extracellular recording pipettes were placed bilaterally in layers II/III of the binocular regions of primary visual cortex. Stimulating the right and left eye on alternate trials, sweep VEP amplitudes were collected for 30 trials from each eye. In monocularly deprived animals, the right eyelid had been sutured for 5 days before recording. Age at suture varied from P19 to P86. In 12 of 13 rats sutured between P19 and P50, the crossed response from the deprived eye was smaller than the crossed response from the nondeprived eye. The same relation prevailed for the uncrossed responses in 11 of 13 animals. There was no significant monocular deprivation effect in animals sutured between P55 and P86 (n = 9). Dark rearing until approximately P90 followed by 5 days of eyelid suture resulted in a strong monocular deprivation effect in both crossed and uncrossed pathways (n = 3). There was little effect of dark rearing alone on the size the sweep VEPs (n = 3). The critical period reported here lasts at least 2 wk longer than reported for rats by Fagliolini et al. and for mice by Gordon and Stryker. Both previous studies used single unit recording rather than the sweep VEP method.
It has been discovered recently that monocular deprivation in young adult mice induces ocular dominance plasticity (ODP). This contradicts the traditional belief that ODP is restricted to a juvenile critical period. However, questions remain. ODP of young adults has been observed only using methods that are indirectly related to vision, and the plasticity of young adults appears diminished in comparison with juveniles. Therefore, we asked whether the newly discovered adult ODP broadly reflects plasticity of visual cortical function and whether it persists into full maturity. Single-unit activity is the standard physiological marker of visual cortical function. Using a more optimized protocol for recording single-units, we find evidence of adult ODP of single-units and show that it is most pronounced in deep cortical layers. Furthermore, using visual evoked potentials (VEP), we find that ODP is equally robust in young adults and mature adults and is observable after just one day of monocular deprivation. Finally, we find that monocular deprivation in adults changes spatial frequency thresholds of the VEP, decreasing the acuity of the deprived pathway and improving the acuity of the non-deprived pathway. Thus, in mice, the primary visual cortex is capable of remarkable adaptation throughout life.
Previous studies implicate the caudate nucleus as a subcortical mediating structure for frontal and anterior limbic inhibitory effects. On active and passive avoidance tasks caudate-lesioned cats were significantly deficient in ability to inhibit an instrumental feeding response following shock at the food dish but showed normal acquisition of a shuttle-box avoidance response. Septal-area lesioned cats clearly failed to inhibit the passive avoidance response but, in contrast to the caudate group, showed more rapid acquisition of the active avoidance response than did the normal controls. Findings are related to earlier studies of effects of perigenual lesions on these 2 types of avoidance response, and a possible anatomical basis for the present findings is discussed.
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