Following sensory deprivation in adult mice, homeostatic synaptic strengthening occurs in non-sensory network responsive synapses, but not in sensory responsive synapses, despite homeostatic increases to the global sensory-evoked responses.

Synapses employ distinct acute and chronic signaling processes in order to maintain physiologically appropriate levels of function.

Experiments at synapses between nerve and muscle cells in genetically modified fruit flies reveal how neurons compensate for perturbations that would otherwise cause excessive synaptic transmission.

An accurate and efficient biologically plausible statistical model of the spiking activity of neural populations shows computational benefits of homeostatic synaptic scaling in learning large neural population codes.

Synaptic scaling maintains motor output from the respiratory network of bullfrogs after months of inactivity in the winter, providing evidence for homeostatic plasticity in response to large ecologically relevant perturbations in neuronal activity.

Genetic and electrophysiological experiments define how homeostatic signaling stabilizes both the gain and short-term dynamic properties of neurotransmitter release, ensuring that synaptic information transfer remains robust to external perturbation.

MCTP is a novel presynaptic calcium sensor, resident within the endoplasmic reticulum, that is required for normal baseline neurotransmission, short-term synaptic plasticity and presynaptic homeostatic plasticity.

Skeletal muscle cells constantly monitor their own activity and that of their partner neuron at synapses, enabling them to provide the neuron with feedback regarding neurotransmitter release.

The synaptic structure in mouse V1 is explained by a synergy of homeostatic plasticity in incoming and outgoing synapses of inhibitory interneurons, establishing a stimulus-specific balance of excitation and inhibition.

Individual neurons can adjust the strength of their synapses by using spontaneous calcium influx through NMDA receptors to trigger the release of additional calcium from intracellular stores, which can in turn be used to regulate protein synthesis.