Cortical Plasticity under Ketamine: From Synapse to Map

Summary

Ketamine influences neuroplasticity in the primary visual cortex (V1) of mice and cats by altering neuronal orientation selectivity and functional connectivity among V1 cells. The findings indicate that ketamine can induce short-term plasticity, suggesting that antidepressants may optimize cortical processing in response to varying stimuli.

Study at a glance

Abstract

Sensory systems need to process signals in a highly dynamic way to efficiently respond to variations in the animal’s environment. For instance, several studies showed that the visual system is subject to neuroplasticity since the neurons’ firing changes according to stimulus properties. This dynamic information processing might be supported by a network reorganization. Since antidepressants influence neurotransmission, they can be used to explore synaptic plasticity sustaining cortical map reorganization. To this goal, we investigated in the primary visual cortex (V1 of mouse and cat), the impact of ketamine on neuroplasticity through changes in neuronal orientation selectivity and the functional connectivity between V1 cells, using cross correlation analyses. We found that ketamine affects cortical orientation selectivity and alters the functional connectivity within an assembly. These data clearly highlight the role of the antidepressant drugs in inducing or modeling short-term plasticity in V1 which suggests that cortical processing is optimized and adapted to the properties of the stimulus.