A slow and stable memory unit instructs fast and transient units by activating dopaminergic neurons via an excitatory hub interneuron connecting those units during second-order conditioning in Drosophila.

Preconditioned cues provide information about an associative model but do not, by default, trigger representations of value, either model-based or model-free.

Five mouse models of autism show deficits in delay eyeblink conditioning, a form of split-second sensory learning that involves the cerebellum, a frequent site of disruption in autistic brains.

Associative and non-associative learning mechanisms summate to produce robust and complex conditioned behavior profiles, opening new avenues to in-depth investigations of defensive responses and threat evaluation.

The coactivity of cortical neurons in associative learning recruits them as associative memory cells based on their synapse interconnections by neuroligin-3-mediated synapse formation, which endorses the first order and the second order of associative memory.

Temporal associative learning enhances persistent firing in lateral entorhinal cortex (LEC) layer III neurons, while aging decreases persistent firing, leading to cognitive impairments.

The retrieval of recent memories and very remote memories may rely on distinct regions of the hippocampus.

When new and past experiences are similar, the memories of those experiences are stored together, and when new and past experiences are different, the memories of those experiences are stored separately.

Neuron ensembles in the medial prefrontal cortex gradually develop codes for relevant, latent variables common across multiple experiences while – apparently independently – losing information about irrelevant, contextual variables unique to each experience.

Stimulus-reward learning sharpens the local representation of the visual space while leaving the overall retinotopic map intact.