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Free keywords:
MOUSE VISUAL-CORTEX; OCULAR DOMINANCE PLASTICITY; FIRING RATE
HOMEOSTASIS; LONG-TERM POTENTIATION; AXON INITIAL SEGMENT; IN-VIVO;
MONOCULAR DEPRIVATION; DENDRITIC SPINES; AMPA RECEPTOR; DEPENDENT
PLASTICITYNeurosciences & Neurology;
Abstract:
Homeostatic plasticity is proposed to be mediated by synaptic changes, such as synaptic scaling and shifts in the excitation/inhibition balance. These mechanisms are thought to be separate from the Bienenstock, Cooper, Munro (BCM) learning rule, where the threshold for the induction of long-term potentiation and long-term depression slides in response to changes in activity levels. Yet, both sets of mechanisms produce a homeostatic response of a relative increase (or decrease) in strength of excitatory synapses in response to overall activity-level changes. Here we review recent studies, with a focus on in vivo experiments, to re-examine the overlap and differences between these two mechanisms and we suggest how they may interact to facilitate firing-rate homeostasis, while maintaining functional properties of neurons.
