Activity-dependent mitochondrial ROS signaling regulates recruitment of glutamate receptors to synapses.

Our understanding of mitochondrial signaling in the nervous system has been limited by the technical challenge of analyzing mitochondrial function in vivo. In the transparent genetic model we were able to manipulate and measure mitochondrial reactive oxygen species (mitoROS) signaling of individual mitochondria as well as neuronal activity of single neurons in vivo. Using this approach, we provide evidence supporting a novel role for mitoROS signaling in dendrites of excitatory glutamatergic interneurons.

A Necessary Role for PKC-2 and TPA-1 in Olfactory Memory and Synaptic AMPAR Trafficking in .

Protein kinase C (PKC) functions are essential for synaptic plasticity, learning, and memory. However, the roles of specific members of the PKC family in synaptic function, learning, and memory are poorly understood. Here, we investigated the role of individual PKC homologs for synaptic plasticity in and found a differential role for and , but not and in associative olfactory learning and memory.

Surface acoustic wave microfluidics for repetitive and reversible temporary immobilization of .

is an important genetic model for neuroscience studies, used for analyses of how genes control connectivity, neuronal function, and behavior. To date, however, most studies of neuronal function in are incapable of obtaining microscopy imaging with subcellular resolution and behavior analysis in the same set of animals. This constraint stems from the immobilization requirement for high-resolution imaging that is incompatible with behavioral analysis using conventional immobilization techniques.

Decreased Reactive Oxygen Species Signaling Alters Glutamate Receptor Transport to Synapses in AVA Neurons.

Reactive oxygen species (ROS) are chemically reactive molecules normally produced during cellular respiration. High ROS levels negatively impact forms of synaptic plasticity that rely on changes in the number of ionotropic glutamate receptors (iGluRs) at synapses. More recently, we have shown that physiological increases in ROS reduce iGluR transport to synapses by acting on activity-dependent calcium signaling.

MAPK signaling and a mobile scaffold complex regulate AMPA receptor transport to modulate synaptic strength.

Synaptic plasticity depends on rapid experience-dependent changes in the number of neurotransmitter receptors. Previously, we demonstrated that motor-mediated transport of AMPA receptors (AMPARs) to and from synapses is a critical determinant of synaptic strength. Here, we describe two convergent signaling pathways that coordinate the loading of synaptic AMPARs onto scaffolds, and scaffolds onto motors, thus providing a mechanism for experience-dependent changes in synaptic strength.

Regulation of neuronal excitability by reactive oxygen species and calcium signaling: Insights into brain aging.

Altered cognition and inefficient learning and memory are hallmarks of brain aging resulting from many small changes in the structure and function of neurons. One such change is a decrease in excitatory synaptic transmission mediated by glutamate and its binding to the AMPA and NMDA subtypes of glutamate receptors. Why there is decreased glutamatergic transmission in aging is not well understood.

Spontaneous motor-behavior abnormalities in two models of neurodevelopmental disorders.

Mutations in hundreds of genes cause neurodevelopmental disorders with abnormal motor behavior alongside cognitive deficits. Boys with fragile X syndrome (FXS), a leading monogenic cause of intellectual disability, often display repetitive behaviors, a core feature of autism. By direct observation and manual analysis, we characterized spontaneous-motor-behavior phenotypes of mutants, an established model for FXS.

Reactive Oxygen Species Modulate Activity-Dependent AMPA Receptor Transport in .

The AMPA subtype of synaptic glutamate receptors (AMPARs) plays an essential role in cognition. Their function, numbers, and change at synapses during synaptic plasticity are tightly regulated by neuronal activity. Although we know that long-distance transport of AMPARs is essential for this regulation, we do not understand the associated regulatory mechanisms of it.