Multiple shared mechanisms for homeostatic plasticity in rodent somatosensory and visual cortex

Abstract

We compare the circuit and cellular mechanisms for homeostatic plasticity that have been discovered in rodent somatosensory (S1) and visual (V1) cortex. Both areas use similar mechanisms to restore mean firing rate after sensory deprivation. Two time scales of homeostasis are evident, with distinct mechanisms. Slow homeostasis occurs over several days, and is mediated by homeostatic synaptic scaling in excitatory networks and, in some cases, homeostatic adjustment of pyramidal cell intrinsic excitability. Fast homeostasis occurs within less than 1 day, and is mediated by rapid disinhibition, implemented by activity-dependent plasticity in parvalbumin interneuron circuits. These processes interact with Hebbian synaptic plasticity to maintain cortical firing rates during learned adjustments in sensory representations. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

Functional and structural properties of highly responsive somatosensory neurons in mouse barrel cortex

“…7). These findings indicate that HRs may down-regulate their intrinsic excitability in response to elevated excitatory inputs in order to maintain their homeostatic balance (Gainey and Feldman 2017;Lambo and Turrigiano 2013), as previously suggested (Elstrott et al 2014;Yassin et al 2010). The highly skewed distribution of EPSC amplitudes, with many small-amplitude and few large-amplitude events, is in close agreement with previous data on excitatory postsynaptic potentials (EPSPs) in barrel cortex L2/3 (Feldmeyer et al 2006;Holmgren et al 2003;Lefort et al 2009).…”

Integrating Hebbian and homeostatic plasticity: introduction

“…slower homeostatic plasticity of excitatory responses found in both visual and somatosensory cortex [24]. Could this be the solution to the question posed by Zenke & Gerstner [13]?…”

“…Because synaptic scaling is itself a homeostatic mechanism, it would appear that homeostatic synaptic scaling is sufficient to explain the increase in closed eye response. As discussed above ( §6), the disinhibitory response of inhibitory interneurons to monocular deprivation also needs to be taken into account in ocular dominance plasticity [24] as it would also tend to act in a homeostatic fashion in its own right and could additionally gate Hebbian plasticity.…”

Hebbian plasticity requires compensatory processes on multiple timescales

“…Suppose we are dealing with a fast negative feedback processes, what are the functional consequences for plasticity and circuit dynamics? To do so, we focus on commonly found forms of firing rate homeostasis (FRH) with a single firing rate set point [15,16,95]. …”

“…Some theoretical forms of ISP are known to implement a rapid form of FRH for individual neurons [14,111]. With accumulating experimental evidence for ISP [95,112,113], it therefore seems likely that synaptic inhibition influences plasticity of excitatory synapses at least indirectly through changes in activity. However, in experiments, the timescale of FRH mediated through ISP appears to be relatively slow [95] and it remains to be seen whether biological forms of ISP can act as RCPs or whether they have a rather homeostatic role.…”