Hebbian and Homeostatic Plasticity Mechanisms in Regular Spiking and Intrinsic Bursting Cells of Cortical Layer 5

Stuart David Greenhill,Adam Ranson,Kevin Fox

doi:10.1016/j.neuron.2015.09.025

Abstract

SummaryLayer 5 contains the major projection neurons of the neocortex and is composed of two major cell types: regular spiking (RS) cells, which have cortico-cortical projections, and intrinsic bursting cells (IB), which have subcortical projections. Little is known about the plasticity processes and specifically the molecular mechanisms by which these two cell classes develop and maintain their unique integrative properties. In this study, we find that RS and IB cells show fundementally different experience-dependent plasticity processes and integrate Hebbian and homeostatic components of plasticity differently. Both RS and IB cells showed TNFα-dependent homeostatic plasticity in response to sensory deprivation, but IB cells were capable of a much faster synaptic depression and homeostatic rebound than RS cells. Only IB cells showed input-specific potentiation that depended on CaMKII autophosphorylation. Our findings demonstrate that plasticity mechanisms are not uniform within the neocortex, even within a cortical layer, but are specialized within subcircuits.

Highlights

The cerebral cortex shows a remarkable capacity for functional plasticity (Feldman, 2009; Fox et al, 2000; Fox and Wong, 2005)
Input-specific plasticity can be explained by Hebbian LTP and LTD and their spike timing-dependent forms (STDP), while input-agnostic plasticity can be explained by homeostatic synaptic scaling
intrinsic bursting cells (IB) cells on the other hand showed Hebbian potentiation of spared whisker inputs in combination with homeostatic rebound of depressed inputs, which overall increased their synaptic drive in an uncompensated way, over the 10-day period we studied the process

Summary

Introduction

The cerebral cortex shows a remarkable capacity for functional plasticity (Feldman, 2009; Fox et al, 2000; Fox and Wong, 2005). In the visual cortex, monocular deprivation leads to rapid depression of cortical responses to closed eye input followed by slower potentiation of responses to both open and closed eye input (Kaneko et al, 2008). Input-specific plasticity can be explained by Hebbian LTP and LTD and their spike timing-dependent forms (STDP), while input-agnostic plasticity can be explained by homeostatic synaptic scaling. Evidence for this view derives from studies where factors that are required for a particular form of plasticity are blocked or knocked out. While other forms of plasticity exist, such as changes in inhibition and changes in intrinsic membrane properties, LTP, LTD, and homeostatic mechanisms are demonstrably present in cortex and affect excitatory transmission within the cortex

Results

Discussion

Conclusion