| Neural plasticity, the modification of neural circuitry that accompanies learning and experience, is essential for the functional wiring of neurons and is no longer thought to be restricted to a developmental time window. The most widely studied form of experience dependent plasticity is ocular dominance plasticity and monocular deprivation has been a central paradigm in understanding, what happens to neurons in the visual cortex when they are deprived of sensory stimulation. With growing evidence for adult plasticity and the interest in deciphering the underlying mechanisms, it is imperative to question what qualifies as 'visual experience' to a normally developed adult visual system. Recent studies on adult humans have reported a shift in sensory eye dominance towards the deprived eye after short periods of monocular deprivation. These effects are opposite and counterintuitive to what deprivation is known to cause early in development. Regardless of what might guide these effects, the shifts in sensory dominance are considered evidence for adult plasticity. Under this framework the goal of our study is twofold: Firstly, we investigated the time course of the deprivation effect by monocularly depriving participants for 10 hours. Consistent with previous work we found shifts in sensory eye dominance towards the deprived eye along with a decrease in sensitivity of the open eye. These effects increased monotonically as a function of deprivation duration up until 5 hours, after which they showed a suggestive decrease with further deprivation. This inflection may reflect the point at which the rapid homeostatic response has saturated, and is overtaken by a slower, opposing mechanism. Secondly, we performed a meta-analysis of all short-term deprivation studies in an effort to understand the key determinant of deprivation. We hypothesized that the key aspect of deprivation is not in the nature of manipulation to the deprived eye's image per se, but whether that manipulation facilitates its suppression during deprivation. We demonstrate this by using a novel form of deprivation that retained all low-level image features while obliterating usefulness for visually guided behavior. Under this explanation, the resulting interocular contrast gain control can be explained by: adaptation-to-suppression instead of a compensatory homeostatic mechanism. |
