# Non-Synaptic Mechanism of Ocular Dominance Plasticity

## TL;DR

The study reveals a new non-synaptic mechanism in the brain's visual system that changes how eyes influence vision, involving myelin changes rather than just synaptic connections.

## Contribution

The paper introduces a non-synaptic mechanism of ocular dominance plasticity mediated by myelin-forming cells.

## Key findings

- Monocular visual disruption alters spike time arrival in the visual cortex.
- Morphological changes in myelin on axons are associated with this disruption.
- This non-synaptic mechanism may drive or supplement synaptic plasticity.

## Abstract

Classic experiments showing that monocular visual disruption alters synaptic connections to binocular neurons established the fundamental concept of synaptic plasticity. Synaptic inputs that are activated coincidently with postsynaptic action potential firing are strengthened, and inputs from cells firing before or after the postsynaptic action potential are weakened. An implicit assumption, however, is that the speed of impulse transmission is not altered by visual deprivation. If so, spike time arrival at binocular neurons would be affected, thereby inducing synaptic plasticity. This possibility is tested here in adult mice by monocular eyelid suture and monocular action potential inhibition in retinal axons. The results show that spike time arrival in visual cortex is altered by monocular visual disruption in association with morphological changes in myelin (nodes of Ranvier) on axons in optic nerve and optic tract. This non-synaptic mechanism of ocular dominance plasticity, mediated by myelin-forming cells, supplements and may drive synaptic plasticity.