Add to ORKGSynapses are specialized communication points between neurons, and their number is a major determinant of cognitive abilities. These dynamic structures undergo developmental- and activity-dependent changes. During brain aging and certain diseases, synapses are gradually lost, causing mental decline. It is, thus, critical to identify the molecular mechanisms controlling synapse number. We show here that the levels of phosphoinositide 3kinase (PI3K) regulate synapsenumber inbothDrosophila larvalmotorneuronsandadult brain projection neurons. The supernumerary synapses induced by PI3K overexpression are functional and elicit changes in behavior. Re-markably, PI3K activation induces synaptogenesis in aged adult neurons as well. We demonstrate th...
Complexity in the processing of the Amyloid Precursor Protein, which generates a mixture of βamyloid...
Abstract Peripheral nervous system (PNS) neurons support axon regeneration into adulthood, whereas c...
The mechanisms by which long-term changes in synaptic efficacy (e.g., long-term potentiation) are ma...
PI3K activation is the starting point of signaling pathways relaying on changes in the phosphorylati...
The number of synapses is a major determinant of behavior and many neural diseases exhibit deviation...
Excess of Aβ42 peptide is considered a hallmark of the disease. Here we express the human Aβ42 pepti...
SCIENTIFIC SUMMARYSynapses are specialized connections between nerve cells or between a nerve and a ...
The number of synapses is a major determinant of behavior and many neural diseases exhibit deviation...
<div><p>The number of synapses is a major determinant of behavior and many neural diseases exhibit d...
The mechanisms regulating synapse numbers during development and ageing are essential for normal bra...
The PI3K-dependent activation of AKT results in the inhibition of GSK3β in most signaling pathways. ...
<div><p>The PI3K-dependent activation of AKT results in the inhibition of GSK3β in most signaling pa...
Use-dependent downregulation of neuronal activity (negative feedback) can act as a homeostatic mecha...
Phosphatidylinositol 3-kinase (PI3K) has been implicated in synaptic plasticity and other neural fun...
Phosphoinositide 3-kinase (PI3K) signaling contributes to a variety of processes, mediating many asp...
Complexity in the processing of the Amyloid Precursor Protein, which generates a mixture of βamyloid...
Abstract Peripheral nervous system (PNS) neurons support axon regeneration into adulthood, whereas c...
The mechanisms by which long-term changes in synaptic efficacy (e.g., long-term potentiation) are ma...
PI3K activation is the starting point of signaling pathways relaying on changes in the phosphorylati...
The number of synapses is a major determinant of behavior and many neural diseases exhibit deviation...
Excess of Aβ42 peptide is considered a hallmark of the disease. Here we express the human Aβ42 pepti...
SCIENTIFIC SUMMARYSynapses are specialized connections between nerve cells or between a nerve and a ...
The number of synapses is a major determinant of behavior and many neural diseases exhibit deviation...
<div><p>The number of synapses is a major determinant of behavior and many neural diseases exhibit d...
The mechanisms regulating synapse numbers during development and ageing are essential for normal bra...
The PI3K-dependent activation of AKT results in the inhibition of GSK3β in most signaling pathways. ...
<div><p>The PI3K-dependent activation of AKT results in the inhibition of GSK3β in most signaling pa...
Use-dependent downregulation of neuronal activity (negative feedback) can act as a homeostatic mecha...
Phosphatidylinositol 3-kinase (PI3K) has been implicated in synaptic plasticity and other neural fun...
Phosphoinositide 3-kinase (PI3K) signaling contributes to a variety of processes, mediating many asp...
Complexity in the processing of the Amyloid Precursor Protein, which generates a mixture of βamyloid...
Abstract Peripheral nervous system (PNS) neurons support axon regeneration into adulthood, whereas c...
The mechanisms by which long-term changes in synaptic efficacy (e.g., long-term potentiation) are ma...