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.

Spontaneous theta oscillations and interneuron-specific phase preferences emerge spontaneously in a full-scale model of the isolated hippocampal CA1 subfield, corroborating and extending recent experimental findings.

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

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

A combination of signal processing and machine learning form a new approach to classify oscillatory coupling in single cycles without averaging over time and to capture cycle-by-cycle changes in coupling.

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.

In the CA1 region of the hippocampus, VTA inputs signal reward proximity while LC inputs respond to novelty, illustrating distinct catecholaminergic roles in hippocampal processing during navigation and learning.

Human hippocampal cornu ammonis 3 damage impairs both recent and remote autobiographical episodic memory, and disrupts functional integration in medial temporal lobe subsystem regions of the default network.

Volume electron microscopy reveals the synaptic organization of the neuropil of the human hippocampal CA1 field.

Specific inhibition of cyclin-dependent kinase-like 5 (CDKL5), a kinase linked to a severe neurodevelopmental disorder, demonstrates an important role in the regulation of excitatory hippocampal synapses and synaptic plasticity that was not previously appreciated in rodent knock-out models.