Editorial: Homeostatic Synaptic Plasticity: From Synaptic Circuit Assembly to Neurological Disorders

Abstract

Neuronal networks can be viewed as learning and memory storage devices. They are highly “plastic,” changing the way they process information in response to external stimuli. Yet, they are also highly “tenacious,” with many neuronal networks retaining their functional identity over many years. Hebbian forms of synaptic plasticity, such as long-term potentiation (LTP) and long-term depression (LTD), use positive feedback mechanisms to either reinforce the more active synapses or weaken those that are less active, thus contributing to neuronal networks tuning their outputs to ever-changing external stimuli. By contrast, homeostatic forms of plasticity use negative feedback mechanisms to maintain the overall neuronal output as close as possible to an “internal” prefixed set point, thus restraining neuronal networks from becoming either silent or hyper-excitable. Recent findings have clearly shown that there is not one but multiple forms of homeostatic plasticity occurring at different levels of organization of the brain, from single synapses to dendritic branches to individual neurons to full neuronal networks (Davis, [1]; Nelson and Valakh, [8]; Mullins et al., [7]). This ebook presents a collection of articles covering molecular and cellular mechanisms that drive forms of homeostatic plasticity whose dysfunction has been proposed to underlie the pathophysiology of many neurological disorders, such as autism spectrum disorder (ASD), schizophrenia, Alzheimer's disease, addiction, intellectual disability, depression and epilepsy (Wondolowski and Dickman, [9]; Fernandes and Carvalho, [2]; Jaudon et al., [3]; Kavalali and Monteggia, [4]). In particular, the Research Topic explores two possibilities to interpret the diseased brain in light of homeostatic plasticity mechanisms. First, neurological disorders could arise because homeostatic plasticity fails to compensate for genetic defects. This can occur either when the genetic mutation directly impairs built-in feedback control systems or when it is so disruptive to overwhelm the buffering capacity of homeostatic plasticity.