Abstract
Homeostatic plasticity is a form of plasticity in which neurons compensate for changes in neuronal activity through the control of key physiological parameters such as the number and the strength of their synaptic inputs and intrinsic excitability. Recent studies revealed that miRNAs, which are small non-coding RNAs repressing mRNA translation, participate in this process by controlling the translation of multiple effectors such as glutamate transporters, receptors, signaling molecules and voltage-gated ion channels. In this review, we present and discuss the role of miRNAs in both cell-wide and compartmentalized forms of homeostatic plasticity as well as their implication in pathological processes associated with homeostatic failure.
Highlights
Frontiers in Cellular NeuroscienceReceived: 05 September 2019 Accepted: 19 November 2019 Published: 05 December 2019
Neurons employ a variety of homeostatic mechanisms to maintain network activity within physiological ranges in response to a wide range of remodeling events
One important feature shared among the multiple forms of homeostatic plasticity is that they are slow as compared to Hebbian forms of plasticity, i.e., long-term potentiation (LTP) or depression (LTD), in which synaptic strengths are rapidly and durably potentiated or depressed, respectively
Summary
Received: 05 September 2019 Accepted: 19 November 2019 Published: 05 December 2019. Homeostatic plasticity is a form of plasticity in which neurons compensate for changes in neuronal activity through the control of key physiological parameters such as the number and the strength of their synaptic inputs and intrinsic excitability. Recent studies revealed that miRNAs, which are small non-coding RNAs repressing mRNA translation, participate in this process by controlling the translation of multiple effectors such as glutamate transporters, receptors, signaling molecules and voltage-gated ion channels. We present and discuss the role of miRNAs in both cell-wide and compartmentalized forms of homeostatic plasticity as well as their implication in pathological processes associated with homeostatic failure
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