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Takuji Kasamatsu, Kazuyuki Imamura; Ocular dominance plasticity maintained by cyclic amp-dependent protein kinase activation: A general mechanism in visual cortex. Journal of Vision 2006;6(6):402. doi: 10.1167/6.6.402.
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© ARVO (1962-2015); The Authors (2016-present)
Animals learn throughout life. Noteworthy is their innate capacity to shape individually brain function through own experience. This experience-guided modification of behavior is especially strong early in life and becomes substantially weak after the animal's maturation. Neural mechanisms underlying cortical plasticity have been extensively investigated till today, using changes in ocular dominance of binocular cells in visual cortex (ocular dominance plasticity, ODP). Higher mammals such as cats and monkeys have provided us with the best animal model of a developmental disorder of spatial vision in human called amblyopia-ex-anopsia, which affects ∼3 % of the global population. Cortical infusion of an inhibitor of cyclic AMP-dependent protein kinase blocks shift in ocular dominance in young kittens following brief monocular deprivation. ODP is also lost in kitten cortex infused with either a catecholaminergic neurotoxin or a β-adrenoreceptor blocker. Activation of protein kinase A enhances ODP in adult cortex, which is usually not plastic. We then asked whether the same mechanisms could enhance ODP in kitten visual cortex that once lost the expression of plasticity due to prior pharmacological treatments. Cortical infusion of cyclic AMP-related drugs (cholera toxin A-subunit or dibutyryl cyclic AMP) in two types of aplastic kitten visual cortex, concurrently with monocular deprivation, resulted in clear shift in ocular dominance to the non-deprived eye. We conclude that, irrespective of the age of animals, activation of protein kinase A cascades is a general mechanism to enhance ODP, its strength being substantially higher in the immature than mature cortex.
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