Synaptic plasticity, a change in the efficacy of synaptic signaling, is a key property of synaptic communication that is vital to many brain functions. Hebbian forms of long-lasting synaptic plasticity—long-term potentiation (LTP) and long-term depression (LTD)—have been well studied and are considered to be the cellular basis for particular types of memory. Recently, homeostatic synaptic plasticity, a compensatory form of synaptic strength change, has attracted attention as a cellular mechanism that counteracts changes brought about by LTP and LTD to help stabilize neuronal network activity. New findings on the cellular mechanisms and molecular players of the two forms of plasticity are uncovering the interplay between them in individual neurons.
Brain function requires neuronal activity-dependent energy consumption. neuronal energy supply is controlled by molecular mechanisms that regulate mitochondrial dynamics, including Kinesin motors and mitofusins, miro1-2 and Trak2 proteins. Here we show a new protein family that localizes to the mitochondria and controls mitochondrial dynamics. This family of proteins is encoded by an array of armadillo (Arm) repeat-containing genes located on the X chromosome. The Armcx cluster is unique to Eutherian mammals and evolved from a single ancestor gene (Armc10). We show that these genes are highly expressed in the developing and adult nervous system. Furthermore, we demonstrate that Armcx3 expression levels regulate mitochondrial dynamics and trafficking in neurons, and that Alex3 interacts with the Kinesin/miro/Trak2 complex in a Ca 2 + -dependent manner. our data provide evidence of a new Eutherian-specific family of mitochondrial proteins that controls mitochondrial dynamics and indicate that this key process is differentially regulated in the brain of higher vertebrates.
Homeostatic synaptic plasticity remains an enigmatic form of synaptic plasticity. Increasing interest on the topic has fuelled a surge of recent studies that have identified key molecular players and the signaling pathways involved. However, the new findings also highlight our lack of knowledge concerning some of the basic properties of homeostatic synaptic plasticity. In this review we address how homeostatic mechanisms balance synaptic strengths between the presynaptic and the postsynaptic terminals and across synapses that share the same postsynaptic neuron.
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