Mutations in presenilin, which cleaves amyloid precursor protein, cause familial Alzheimer’s Disease. Here, the authors show that loss of presenilin leads to loss of synaptotagmin 7, leading to impaired presynaptic release.

The function of receptor desensitization in vivo is not well understood. Here, the authors show that deletion of CKAMP44, an AMPAR auxiliary protein that modulates desensitization of AMPAR currents, affects synaptic facilitation at retinogeniculate synapses and visually-evoked firing in awake mice.

The calcium-sensing protein synaptotagmin 7 mediates facilitation that is masked by depression, but supports frequency-invariant transmission in mouse cerebellar and vestibular synapses.

The circuitry of the hippocampal CA3 region has long been hypothesized to be well suited to the storage of memories. Mulle and colleagues provide an update on the known types and mechanisms of synaptic plasticity in CA3 and describe evidence for their roles in memory formation and retrieval.