Multiple shared mechanisms for homeostatic plasticity in rodent somatosensory and visual cortex
Author(s) -
Melanie Gainey,
Daniel E. Feldman
Publication year - 2017
Publication title -
philosophical transactions of the royal society b biological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.753
H-Index - 272
eISSN - 1471-2970
pISSN - 0962-8436
DOI - 10.1098/rstb.2016.0157
Subject(s) - homeostatic plasticity , neuroscience , somatosensory system , hebbian theory , synaptic scaling , sensory system , neuroplasticity , homeostasis , visual cortex , metaplasticity , biology , sensory deprivation , synaptic plasticity , perineuronal net , interneuron , inhibitory postsynaptic potential , microbiology and biotechnology , biochemistry , receptor , machine learning , artificial neural network , computer science
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’.
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