CB₁-receptor-mediated inhibitory long-term depression (LTD) relies on both protein synthesis and ubiquitination to elicit structural changes that underlie long-term reduction of GABA release.

Electrophysiological and optical analysis of neurotransmitter release at central synapses reveals that glutamate signalling is not required for the long-term potentiation (LTP) of presynaptic function, and instead only promotes presynaptic long-term depression (LTD).

Vulnerability to cocaine addiction during adolescence depends on translational control.

Non-invasive optogenetic induction of synaptic plasticity revealed that long-term potentiation and long-term depression alter the chances of a synapse to survive the next seven days.

Motor training decreased the unit synaptic response and suppressed induction of long-term depression at parallel fiber to Purkinje cell synapses in the cerebellum, supporting involvement of long-term depression in motor learning.

There are at least two separate pathways for AMPA receptor recycling, which are regulated by synaptic activity.

Taking advantage of awell-established learning paradigm, conditioned taste aversion (CTA), change of hedonic value of a palatable tastant revealed the neural mechanisms encoding this learning process.

The molecular mechanisms beyond the bidirectionality (tTLP and tLTD) of endocanabinoid spike-timing dependent synaptic plasticity have been identified.

Patients with DYT1 dystonia show aberrant risk-aversion in a simple decision-making task, in accordance with predictions of a reinforcement learning model of corticostriatal trial-and-error learning.

Somatostatin-expressing interneurons of the rodent dentate gyrus fall into at least two functionally distinct interneuron types with different synaptic integrations into the local dentate gyrus and the more distant medial septum neuronal network.