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Unipolar brush cells subtypes, classified by their excitatory or inhibitory response to glutamate, form circuits with one another that may enhance the capacity of the cerebellum to transform input signals.

Electrophysiological study in human brain slices reveals that short-term synaptic plasticity from presynaptic pyramidal neuron to postsynaptic interneuron connections are target-cell specific based on their subclass interneuron identity.

For the first time, the strength of homeostatic plasticity has been shown to be negatively regulated and the transcription factors responsible for this regulation have been identified.

Microglia that presumably sense neuronal activity via detection of glutamate at synapses in the hippocampus show higher fine process motility and increased contact rates associated with formation and elimination of dendritic spines under conditions of elevated neuronal activity.

Synaptic silencing-induced homeostatic enhancement of presynaptic glutamate release is mediated by the postsynaptic retinoic acid-dependent brain-derived neurotrophic factor (BDNF) synthesis from dendritically targeted BDNF transcripts, leading to retrograde activation of presynaptic tropomyosin receptor kinase B receptors.

Mapping neuronal circuits is made substantially faster, simpler and more accurate with this extended toolkit of novel cell lines and vectors.

The p75 neurotrophin receptor prevents the migration of the granule cell precursors away from its mitogenic niche in the external granule layer of the cerebellum, by maintaining a pool of undifferentiated cells capable of responding to mitogenic signals.