Acetylcholine, released from cholinergic fibers originating from the medial septum, shapes social memory, and controls the CA2 hippocampal circuit via nicotinic receptors localized on GABAergic interneurons.

Structures of a TMEM16 phospholipid scramblase reveal that its Ca²⁺-dependent activation entails global conformational changes and how these rearrangements affect the membrane to enable transbilayer lipid transfer.

C-terminus mediated inhibition is one emerging modality of intervention for L-type Ca²⁺ channels, which coordinate multiple motifs to acutely tune Ca²⁺ current and Ca²⁺ influx down to the lower limits preset by end-stage Ca²⁺-dependent inactivation.

Group III metabotropic glutamate receptor inhibition facilitates synaptic plasticity in the plasticity-resistant synapses of hippocampal area CA2, a brain region critical for social memory.

Input conveying social novelty information from the hypothalamus controls hippocampal activity by recruiting a novel inhibitory circuit in hippocampal area CA2.

External calcium regulates neuronal excitability via its actions on voltage-gated sodium channels but not by regulating NALCN via the calcium-sensing receptor.

Sea anemones use adapted ion channels to control stinging behavior.

Hippocampal area CA2 controls low gamma and ripple oscillations, brain waves known to be impaired in schizophrenia, implicating this important brain region in cognition.

Three distinct AKT isoforms are found in the brain and show dissimilar patterns of expression, differential roles in the expression of synaptic plasticity, and different roles in neuronal signaling.

Spontaneous fusion of vesicles at synapses is regulated independently of fusion triggered by action potentials, adding to evidence that the two types of fusion have distinct functions.