Synaptic plasticity onto inhibitory neurons as a mechanism for ocular dominance plasticity

Abstract

Ocular dominance plasticity is a well-documented phenomenon allowing us to study properties of cortical maturation. Understanding this maturation might be an important step towards unravelling how cortical circuits function. However, it is still not fully understood which mechanisms are responsible for the opening and closing of the critical period for ocular dominance and how changes in cortical responsiveness arise after visual deprivation. In this article, we present a theory of ocular dominance plasticity. Following recent experimental work, we propose a framework where a reduction in inhibition is necessary for ocular dominance plasticity in both juvenile and adult animals. In this framework, two ingredients are crucial to observe ocular dominance shifts: a sufficient level of inhibition as well as excitatory-to-inhibitory synaptic plasticity. In our model, the former is responsible for the opening of the critical period, while the latter limits the plasticity in adult animals. Finally, we also provide a possible explanation for the variability in ocular dominance shifts observed in individual neurons and for the counter-intuitive shifts towards the closed eye.

Synapse-Selective Control of Cortical Maturation and Plasticity by Parvalbumin-Autonomous Action of SynCAM 1

“…A recent model proposed that the maturation of inhibition during the critical period selectively decreases spontaneous cortical activity in favor of visually evoked activity, switching the network learning cues to external environment (Toyoizumi et al, 2013). The spontaneous/evoked ratio of SynCAM 1-KO mice is lower than in WT mice already during the critical period (data not shown), which in combination with a significantly lowered feedforward inhibition may shift cortical responses even further toward the open eye (Bono and Clopath, 2018; Kuhlman et al, 2013). The model proposed by Toyoizumi et al (2013) further predicts that MD induces a shift in ocular dominance during the precritical period if thalamic afferents from one eye are mostly blocked.…”

Using psychophysical performance to predict short-term ocular dominance plasticity in human adults

“…For example, monocular deprivation during the critical period leads to long-lasting suppression of the deprived eye, a medical condition called amblyopia (Berardi et al, 2000;Levi, McKee, & Movshon, 2011;Maurer, Lewis, & Mondloch, 2005;Ostrovsky, Andalman, & Sinha, 2006). These forms of neuroplasticity decrease with age, in parallel with the development of intracortical inhibitory signaling, particularly GABAergic (Bono & Clopath, 2019;Spolidoro, Sale, Berardi, & Maffei, 2009). Consequently, when deprivation occurs in the adult individual, long-lasting effects are not usually seen.…”