Mechanisms of Homeostatic Plasticity in the Mouse Visual Cortex

Abstract

During development, newly established cortical circuits are undergoing a period of experience dependent refinement. Visual deprivation during this time leads to the induction of plasticity mechanisms, including homeostatic plasticity measures. These are a distinct set of plasticity mechanisms thought to play a role in maintaining stability within networks, and preventing large perturbations in overall activity levels. Homeostatic plasticity mechanisms can be divided into synaptic and intrinsic mechanisms. While details of individual mechanisms are reasonably well understood, details of how these different mechanisms are linked to one another are much less clear. In this thesis, I investigate the relationship between structural and functional forms of synaptic and intrinsic plasticity in layer 2/3 neurons in the monocular visual cortex, before and after induction of plasticity via monocular enucleation. I find that while axon initial segment (AIS) plasticity takes place following deprivation, in both pyramidal neurons, and a subset of inhibitory neurons, it does not correlate with functional measures of excitability. However, in control conditions, I do find a relationship between the synaptic inputs of a neuron, and its intrinsic excitability. Following deprivation, this relationship is altered. Specifically, I find that the activity status of the neuron affects the level of intrinsic excitability, and to some extent, the synaptic input to the cell. Putatively inactive neurons show increased excitability, and trend towards stronger synaptic input in comparison to their active counterparts. These differences between active and inactive cells may reflect the engagement of homeostatic mechanisms in inactive cells, in order to restore their activity levels.

Date of Award	2016
Original language	English
Awarding Institution	King's College London
Supervisor	Tara Keck (Supervisor) & Matthew Grubb (Supervisor)